SRB's Manual of Surgery Sriram Bhat M
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General SurgeryChapter 1

 
A. Wounds and Wound Healing
One having a wound in his eyebrow. An ailment which I will treat. Treatment [of a wound in the eyebrow]: Now after thou hast stitched it, [thou shouldst bind] fresh meat upon [it] the first day. If thou findest that the stitching of this wound is loose, thou shouldst draw it together for him with two strips (of plaster), and thou shouldst treat it with grease and honey every day until he recovers.
—[Anonymous], circa 2500 BC
CHAPTER OUTLINE
  • ❖ Wounds
  • ❖ Classification of Wounds
  • ❖ Wound Healing
  • ❖ Compartment Syndrome
  • ❖ Crush Injury
  • ❖ Crush Syndrome
  • ❖ Degloving Injuries
  • ❖ Keloid
  • ❖ Hypertrophic Scar
  • ❖ Problems with Wound Healing
 
WOUNDS
 
Wound Definition
A wound is a break in the integrity of the skin or tissues often, which may be associated with disruption of the structure and function.
Wound is simply a disruption of any tissues—soft tissue or bone or internal organs. Ulcer is disruption or break in the continuity of any lining—may be skin, mucous membrane or others. Ulcer is one of the types of wounds.
 
CLASSIFICATION OF WOUNDS
I. Rank and Wakefield classification
  1. Tidy wounds
    • They are wounds like surgical incisions and wounds caused by sharp objects.
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      Fig. 1.1A: Tidy wound
    • It is incised, clean, healthy wound without any tissue loss.
    • Usually primary suturing is done. Healing is by primary intention.
  2. 2Untidy wounds
    • They are due to:
      • Crushing.
      • Tearing.
      • Avulsion.
      • Devitalised injury.
      • Vascular injury.
      • Multiple irregular wounds.
      • Burns.
    • Fracture of the underlying bone may be present.
      Wound dehiscence, infection, delayed healing are common.
    • Liberal excision of devitalised tissue and allowing to heal by secondary intention is the management.
    • Secondary suturing, skin graft or flap may be needed.
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      Fig. 1.1B: Untidy wound
II. Classification based on the type of the wound
Clean incised wound: It is a tidy, simple, clean cut wound with linear cut edges; usually due to a sharp object like blade, glass piece or knife. It is treated by primary suturing.
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Fig. 1.2: Clean incised wound.
Lacerated wound: It has ragged edges with some part of the tissues getting devitalized; viability of the tissues may be impaired; depth of the injury and tissue damage should be carefully assessed. Proper adequate wound excision, thorough warm saline wash and suturing of the wound layer-by-layer is required.
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Figs 1.3A and B: Lacerated wounds.
Bruise or contusion: It is due to blow or blunt force to the skin and tissues underneath wherein blood vessels or capillaries are damaged underneath. There is skin discolouration without breaking of the skin; broken vessels cause seepage of blood underneath; minor soft tissue injury crushes small vessels without breaking the skin accumulating trapped blood underneath. It is more on the skin over the bones; lax area like face, scrotum, eyes; vascular areas; children, old aged, fair skin people.
Haematoma: It is a localized collection of blood after blunt trauma or after surgery. Collected fluid blood in few minutes to hours gets clotted; later eventually it gets liquefied and shows discoloured fluid. It may be subcutaneous/ intramuscular/subfascial/intra-articular. Large haematoma may get infected to form an abscess; so large haematoma needs drainage under general or regional anaesthesia. Small haematoma usually gets absorbed (like scalp haematoma). Often haematoma contains reddish plasmatic fluid which should be aspirated using wide bore needle. Complications are—pressure effects and abscess formation; both needs incision and drainage under anaesthesia. Haematoma causing cosmetic problems may require needle aspiration. Haematoma can occur spontaneously in coagulation disorders (haemophilia) or in individuals who are on anticoagulant drug therapy.
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Fig. 1.4: Haematoma of eyelid.
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Fig. 1.5: Haematoma in the groin being aspirated. Haematoma may get infected or can compress adjacent structures.
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Fig. 1.6: Subungual haematoma. Often nail may need to be removed to evacuate the blood clot.
Abrasion: It is superficial injury (scratch/graze/pressure/contact) and is due to shearing of the skin where the surface is rubbed off. This tangential force causes loss of epidermis exposing dermal vessels and nerves leading into profuse painful oozing. Abrasion heals by epithelialisation. Any dirt or foreign body on the abrasion should be removed to avoid formation of poor tattoo like scar.
Puncture wounds and bites: It is usually a stab wound with a pointed object; here depth of the wound is more than the width. Deeper vital structures or organs may be injured, so should be assessed; foreign body or object may be present in the depth of the wound. Wound should be explored under general or regional anaesthesia to assess the depth and severity of the injury and sutured layer by layer after through saline wash.
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Fig. 1.7: Typical look of abrasion in face.
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Fig. 1.8: Multiple abrasions.
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Fig. 1.9: Penetrating wound of the abdomen.
Penetrating wounds: They are similar like puncture wounds; due to stab. Abdomen and chest are common sites. Liver, bowel, spleen, major vessels and other visceral organs may be 4involved. Ultrasound and CT scan should be done to evaluate deeper organ injuries. Under general anaesthesia wound should be explored properly.
Traction and avulsion injuries: these are complex injuries with tissues getting displaced from its normal anatomical position and alignment. It can occur in single plane like in subcutaneous tissue or in multiple planes like in machinery injuries, major injuries or degloving injuries. Ischaemia, bleeding, sepsis, loss of wide tissue area are common problems. Open traction injury occurs on the surface. Closed traction injury can occur in deeper plane like brachial plexus injury or traction bowel injury. After initial resuscitation, definitive treatment like skin graft or nerve repair should be done.
Crush injury: It is due to major wounds, war wounds, natural disaster like earth quake injuries, tourniquet injury. It leads into—compartment syndrome; muscle ischaemia; loss of tissues; gangrene; sepsis. Muscle will lose its viability which is identified by its colour (dark coloured with loss of shining); loss of contractility; turgid, and will not bleed on cutting.
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Fig. 1.10: Severe crush injury leg.
Gunshot injuries: These injuries may be superficial or deep. Usually entry wound and exit wound will be present. It causes explosive and destructive injuries along with burn injuries in the deeper planes and organs. It can be high velocity injuries with massive bleeding and major organ injuries.
Injuries to bones and joints: It is common in all major injuries; should be identified clinically and confirmed radiologically. It needs specialized management like reduction, plating etc.
Injuries to nerves, arteries, veins (major vessels), deeper organs: It needs initial resuscitation, later staged management as per individual patient basis depending on the severity and extent of injury and loss of function.
Closed blunt injury: It may be due to fall, blunt injury wherein no obvious external injury may be seen but deeper injury occurs; it may be often severe enough to cause major injury like in blunt abdominal injury causing bowel/liver/spleen/renal injuries.
Note:
Wound may be closed (bruise, haematoma, blunt injury); open (abrasion, incised, lacerated, penetrating) or complex (traction/avulsion, crush or gunshot injuries).
III. Classification based on thickness of the wound
  • Superficial wound involving only epidermis and dermal papillae.
  • Partial thickness wound with skin loss up to deep dermis with only deepest part of the dermis, hair follicle shafts and sweat glands are left behind.
  • Full thickness wound with loss of entire skin and subcutaneous tissue causing spacing out of the skin edges.
  • Deep wounds are the one extending deeper, across deep fascia into muscles or deeper structures.
  • Complicated wounds are one associated with injury to vessels or nerves.
  • Penetrating wound is one which penetrates into either natural cavities or organs.
IV. Classification based on involvement of structures
  • Simple wounds are one involving only one organ or tissue.
  • Combined/complex wounds are one involving mixed tissues.
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    Fig. 1.11: Complex wound exposed tendons.
V. Classification based on the time elapsed
Acute wounds are generally defined as those that progress through the normal phases of healing and typically show signs of healing in less than 4 weeks; examples are—surgical or traumatic or burn wounds; progress through the healing phases in a timely and orderly fashion - haemostasis, inflammation, proliferation, and remodeling or maturation.
Chronic wounds are defined as those that do not follow the normal healing process and show no signs of healing in 4 weeks. It fails to progress through the normal phases of healing but with prolonged inflammatory phase. Diabetes, venous/arterial diseases, nutritional deficiencies are the causes. Hypoxia initially is a potent stimulus for fibroblast activity and angiogenesis; persisting hypoxia impedes fibroblast and collagen activity and also allows bacterial invasion to make wounds chronic. Chronic wounds are chronically infected with biofilms which interfere mainly with the inflammatory phase of healing, contributing to the non-healing. A biofilm is a complex structure of microorganisms contained in an extracellular matrix of proteins and polysaccharides that adhere to a surface, creating a protected environment for the organisms. Chronic ulcers are unresponsive to dressing treatment; it requires biopsy, culture study, definitive treatment like wound debridement, VAC (Vacuum Assisted Closure) therapy, skin grafting or flap. Specific conditions like tuberculosis if present should be treated. Malignancy if confirmed is treated by wide local excision and skin graft.
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Fig. 1.12: Chronic wounds over the scalp
VI. Classification of surgical wounds
  1. Clean wound
    • Herniorrhaphy.
    • Excisions.
    • Surgeries of the brain, joints, heart, transplant.
    • Infective rate is less than 2%.
  2. Clean contaminated wound
    • Appendicectomy.
    • Bowel surgeries, gastrojejunostomy.
    • Gallbladder, biliary and pancreatic surgeries.
    • Infective rate is 10%.
  3. Contaminated wound
    • Acute abdominal conditions.
    • Open fresh accidental wounds.
    • Infective rate is 15–30%.
  4. Dirty infected wound
    • Abscess drainage.
    • Pyocele.
    • Empyema gallbladder.
    • Faecal peritonitis.
    • Infective rate is 40–70%.
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Fig. 1.13: Clean wound of thyroidectomy surgery.
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Fig. 1.14: Appendicectomy wound, which is a clean contaminated wound.
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Fig. 1.15: Contaminated wound—burst appendicitis.
Wound classifications
  • Simple wounds: Only skin is involved
  • Tidy wounds
  • Complex wounds: Vessels, nerves, tendons or bones are involved
  • Untidy wounds
  • Closed wounds:
  • Clean wound.
  • Contusion
  • Clean contaminated wound
  • Abrasion
  • Contaminated wound
  • Haematoma
  • Dirty wound
  • Open wounds:
  • Incised wounds
  • Lacerated wounds
  • Crush injuries
  • Penetrating wounds
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Figs 1.16A and B: Acute peritonitis with frank pus in peritoneal cavity due to bowel perforation is a dirty wound.
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Fig. 1.17: Wound causing extensive skin loss and necrosis.
 
WOUND HEALING
Wound healing is complex method to achieve anatomical and functional integrity of disrupted tissue by various components like neutrophils, macrophages, lymphocytes, fibroblasts, collagen; in an organised staged pathways—haemostasis → inflammation → proliferation → matrix synthesis (collagen and proteoglycan ground substance) → maturation → remodelling → epithelialisation → wound contraction (by myofibroblasts).
 
Types of Wound Healing
 
Primary Healing (First Intention)
  • It occurs in a clean incised wound or surgical wound. Wound edges are approximated with sutures. There is more epithelial regeneration than fibrosis. Wound heals rapidly with complete closure. Scar will be linear, smooth, and supple.
 
Secondary Healing (Second Intention)
  • It occurs in a wound with extensive soft tissue loss like in major trauma, burns and wound with sepsis. It heals slowly with fibrosis. It leads into a wide scar, often hypertrophied and contracted. It may lead into disability.
  • Re-epithelialisation occurs from remaining dermal elements or wound margins.
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Fig. 1.18: Wound in the abdomen healing with second intention which requires secondary suturing once it granulates well. Secondary suturing is done after 10–14 days, once wound granulates well with proper control of infection. Scar in such type is prone to form incisional hernia.
 
Healing by Third Intention (Tertiary Wound Healing or Delayed Primary Closure)
After wound debridement and control of local infection, wound is closed with sutures or covered using skin graft. Primary contaminated or mixed tissue wounds heal by tertiary intention.
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Phases of Wound Healing
 
Inflammatory phase (Lag or Substrate or Exudative Phase)
  • It begins immediately after formation and lasts for 72 hours.
  • There is initial arteriolar vasoconstriction, thrombus formation, platelet aggregation due to endothelial damage and release of adenosine diphosphate (ADP).
  • Later vasodilatation and increased vascular permeability develops.
  • Here haemostasis, coagulation and chemotaxis occur.
Note:
Coagulation begins at wound haematoma → formation of platelet fibrin thrombus → release of cytokines, PDGF (platelet-derived growth factor), epidermal growth factor (EGF), transforming growth factor β (TGF – β), platelet activating factor and platelet factor IV, fibrin, serotonin. Chemotaxis causes first neutrophil migration, and then activation of macrophages, lymphocytes leading into phagocytosis, wound debridement, matrix activation, angiogenesis. Chemotaxis factors are complement factors, interleukin-1, TNF-α (tumour necrosis factor-α) TGF–β and platelet factor. Activated macrophages produce free radicals and nitric oxide; release cytokine to activate lymphocytes which release interferon and interleukin (called as lymphokines). These factors attract polymorpho nuclear leucocytes (PMN—poly morphonuclear cells–neutrophills) in 48 hours secreting inflammatory mediators and bactericidal oxygen derived-free radicals. Injured tissues and platelet release histamine, serotonin and prostaglandins which increases the vascular permeability by vasodilatation. These actions are reduced in diabetes mellitus, Cushing's syndrome and immunosuppression increasing the sepsis rate.
  • All these cause features of acute inflammation—rubor, calor, tumour, dolor and loss of function.
 
Proliferative phase (Collagen/fibroblastic phase)
  • It begins from 3rd day and lasts for 3–6 weeks. There will be formation of granulation tissue and repair of the wound. Granulation tissue contains fibroblasts, neocapillaries, collagen, fibronectin and hyaluronic acid.
  • (1) Initial angiogenesis (growth of new blood vessels) occurs by release of vascular endothelial cell growth factor (VEGF) by keratinocytes; by release of TNF-α, TGF–β, PDGF, FGF by macrophages. (2) Eventual fibroplasia develops by fibroblast activity with formation of the collagen and ground substance/glycosaminoglycans. Type III collagen is deposited initially in a random fashion. (3) Later re-epithelialisation of the wound surface occurs by migration of basal layer of the retained epidermis which proliferates, differentiates and stratifies to form wound closure.
 
Remodelling phase (Maturation Phase)
  • It begins at 6 weeks and lasts for 6 months to 1 or 2 years.
  • There is maturation of collagen by cross linking and realignment of collagen fibers along the line of tension, which is responsible for tensile strength of the scar. There is reduced wound vascularity. Fibroblast and myofibroblast activity causes wound contraction. Type III collagen is replaced by type I collagen causing maturation of the collagen. Ratio of type I collagen to type III collagen becomes 4:1.
  • Early extracellular matrix contains fibronectin and collagen type III; eventually it contains glycosaminoglycans and proteoglycans; final matrix contains type I collagen.
  • Scar strength is 3% in 1 week; 20% in 3 weeks; 80% in 12 weeks. Final matured scar is acellular and avascular.
Note:
Initially fibrin, fibronectin, proteoglycans deposition occurs; later collagen protein develops to form scar. Normal dermal skin contains 80% type I (20% type III) collagen; granulation tissue contains mainly type III collagen; scar contains both type I and III collagen, initially in equal proportion, later becomes 4:1. Basic essential components of collagen are proline and lysine. Hydroxylation of lysine and later glycosylation of this hydroxylysine decides the type of collagen molecule. Hydroxylation of both proline and lysine as essential step needs adequate concentration of vitamin C, iron and α ketogluteric acid. Collagen deposition in the wound is assessed by quantity of hydroxyproline excreted in urine. There is a balanced activity of collagen production and degradation of collagen (collagenolysis). Collagen is broken down by collagenase and MMPs (matrix metallo- proteinases). Procollagen through procollagenase → collagen fibril → cross linking → collagen fiber → deposition. Deposited collagen → through collagenase → degradation and collagenolysis.
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Fig. 1.19: Healing ulcer with healthy granulation tissue which is ready for skin grafting.
 
Factors affecting Wound Healing
Age: In younger age group wound healing is faster and better. In elderly healing is delayed due to reduction in collagen synthesis, epithelialisation, growth factors and angiogenesis. But final scar will be excellent in old individuals.
Nutrition: Adequate vitamin, trace elements, fatty acids and proteins are essential for wound healing. Vitamin A deficiency affects monocyte activation, inflammatory phase, collagen synthesis and growth factor actions. Vitamin K deficiency affects synthesis of prothrombin (II), factors VII, IX and X. Vitamin E, being an antioxidant stabilizes the cell membrane. Vitamin C deficiency impairs collagen synthesis, fibroblast proliferation and angiogenesis; increases the capillary fragility and susceptibility for infection. Zinc is an essential cofactor for RNA and DNA polymerase; magnesium is a co-factor for synthesis of proteins and collagen; copper is a required co-factor for cytochrome oxidase, for cytosolic anti-oxidant superoxide dismutase, and for the optimal cross-linking of collagen; Iron is required for the hydroxylation of proline and lysine. Glutamine is the most abundant amino acid in plasma; is a major source of energy for rapidly proliferating cells such as fibroblasts, lymphocytes, epithelial cells, and macrophages. The serum concentration of glutamine is reduced after major surgery, trauma, and sepsis, and supplementation of this amino acid improves nitrogen balance and diminishes immunosuppression. Glutamine stimulates the inflammatory immune response in early wound healing. Oral glutamine supplementation improves wound breaking strength and of mature collagen. Arginine is a semi-essential amino acid that is required in growth, severe stress, and injury. Arginine modulates immune function, wound healing, hormone secretion, vascular tone, and endothelial function. Arginine is a precursor to proline; supports collagen deposition, angiogenesis, and wound contraction. Under psychological stress situations, the metabolic demand of arginine increases, and its supplementation hastens the wound healing. Serum albumin level less than 2 g/dl causes prolonged inflammatory phase, decreased fibroplasia, neovascularisation and cell synthesis and wound remodeling and hence decreased wound healing. Wounds in patients who remain in catabolic state will not heal. Collagen is the major protein component of connective tissue; it contains mainly glycine, proline, and hydroxyproline. Collagen synthesis requires hydroxylation of lysine and proline, and co-factors such as ferrous iron and vitamin C. Polyunsaturated fatty acids which cannot be synthesized de novo by mammals, consist mainly of omega-6 (found in soybean oil) and omega-3 (found in fish oil—fatty acids such as eicosapentaenoic acid [EPA] and docosahexaenoic acid [DHA]). They affect pro-inflammatory cytokine production, cell metabolism, gene expression and angiogenesis; improve the systemic immune function of the host, thus reducing infectious complications.
Wound infection: Infection prolongs inflammatory phase, releases toxins and utilizes vital nutrients thereby prevents wound epithelialisation. The β-haemolytic streptococci more than 105 per gram of tissue prevent wounds healing. Formation of biofilms on the wound surface by microorganisms prevents wound healing.
Anaemia: Haemoglobin less than 8g % causes poor oxygenation of tissues preventing healing of the wounds.
Hypoxia: Hypoxia prevents fibroblast proliferation and collagen synthesis; it also promotes bacterial invasion into the wound. Causes of hypoxia are—arterial diseases, cardiac failure, respiratory causes, hypotension, smoking, tobacco, infection, diabetes mellitus and radiation.
Radiotherapy: Both external radiotherapy or ionizing radiation cause endarteritis, fibrosis and delay in wound healing. Radiation may itself cause local tissue necrosis, sepsis and hypoxia.
Systemic and metabolic causes: Diabetes mellitus affects all stages of wound healing. Cardiac, renal, hepatic, respiratory diseases prevent wound healing. Tissue oedema impairs wound healing. HIV and immunosuppression of varying causes, malignancy leads into poor wound healing. Jaundice interferes with wound healing. Obesity causes hypoperfusion, reduced microcirculation, increased wound tension and hence prevents wound healing.
Drugs: Steroids interfere with activation of macrophages, fibroblasts and angiogenesis in the early phase of healing (proliferative). Non-steroidal anti-inflammatory drugs (NSAIDs) decrease collagen production. Chemotherapeutic agents used in oncology inhibit cellular proliferation, protein synthesis. Alcohol consumption decreases the phagocyte response and pro-inflammatory cytokine release; diminishes host response and thus increasing the infection rate.
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Management of Wounds
 
Wound cleaning
Wound cleaning is needed to optimize the healing environment. It is achieved by removing visible devitalized tissues or dressing materials or excess exudates or crusts.
Absolute aseptic technique should be used while cleaning the wound; warm sterile isotonic normal saline (37°C—this is optimum temperature to support cellular activity) is ideal; normal exudates in the wound should be removed; gentle cleaning of the wound is important to minimize the interference of the wound-healing process. Cleaning agent should be of neutral pH and nontoxic; delipidising agents, antiseptics, alkaline soaps should be avoided. Gentle irrigation of warm saline using a sterile syringe on the wound surface is ideal; rubbing with undue force using cotton or gauze may cause mechanical damage on the process of wound healing.
Wound is measured either in two dimensions (length and width) or in three dimensions (length, width and depth).
 
Specific management
  • Wound is inspected and classified as per the type of wounds.
  • If it is in the vital area, then:
    • The airway should be maintained.
    • The bleeding, if present, should be controlled.
    • Intravenous fluids are started.
    • Oxygen, if required, may be given.
    • Deeper communicating injuries and fractures, etc. should be looked for.
  • If it is an incised wound then primary suturing is done after thorough cleaning.
  • If it is a lacerated wound then the wound is excised and primary suturing is done.
  • If it is a crushed or devitalised wound there will be oedema and tension in the wound. So after wound debridement or wound excision by excising all devitalised tissue, the oedema is allowed to subside for 2–6 days. Then delayed primary suturing is done.
  • If it is a deep devitalised wound, after wound debridement it is allowed to granulate completely. Later, if the wound is small secondary suturing is done. If the wound is large a split skin graft (Thiersch graft) is used to cover the defect.
  • In a wound with tension, fasciotomy is done so as to prevent the development of compartment syndrome.
  • Vascular or nerve injuries are dealt with accordingly. Vessels are sutured with 6-zero polypropylene nonabsorbable suture material. If the nerves are having clean cut wounds it can be sutured primarily with polypropylene 6-zero or 7-zero suture material. If there is difficulty in identifying the nerve ends or if there are crushed cut ends of nerves then marker stitches are placed using silk at the site and later secondary repair of the nerve is done.
  • Internal injuries (intracranial by craniotomy, intrathoracic by intercostal tube drainage, intra-abdominal by laparotomy) has to be dealt with accordingly. Fractured bone is also identified and properly dealt with.
  • Antibiotics, fluid and electrolyte balance, blood transfusion, tetanus toxoid (0.5 ml intramuscular to deltoid muscle), or antitetanus globulin (ATG) injection.
Later definitive management is done with:
Wound debridement (wound toilet, or wound excision) is liberal excision of all devitalised tissue at regular intervals (of 48-72 hours) until healthy, bleeding, vascular tidy wound is created.
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Figs 1.20A and B: Delayed primary suturing is done once oedema over the wound subsides. It is done as single layer interrupted deep sutures using monofilament polypropylene or polyethylene.
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Fig. 1.21A:
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Figs 1.21A and B: Secondary suturing is done once wound is healthy after control of wound infection.
 
COMPARTMENT SYNDROME
Compartment syndrome is a special entity; common in leg, forearm, thigh and arm; is a syndrome due to increased intracompartmental pressure within a limited space area.
Causes are—narrowed space due to tight dressings/plaster cast, lying on one limb in comatous patient; increased content within the compartment due to trauma like fractures, oedema, ischaemic injury, haematoma, positioning after trauma, burn injury, etc.; high pressure injection injuries like gun injury, oil based material injury, extravasation of chemotherapeutic drugs; snake bite.
Features are—It compromises circulation and function mainly of muscles and nerves. It often maintains the normal colour and temperature of the fingers and distal pulses may not be obliterated in spite of severe muscle ischaemia. Muscle ischaemia more than 4 hours causes muscle death and myoglobinuria. Irreversible nerve damage develops if ischaemia persists for 8 hours. Progressive, persistent severe pain which is aggravated by passive muscle stretching is the diagnostic sign. Tense tender regional lymph node is typical. Pulse will be usually normally felt in compartment syndrome; but may become absent if there is associated arterial injury. Compartment pressure more than 30 mmHg is an indication for fasciotomy.
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Fig. 1.22: Necrotizing fasciitis with extensive skin involvement which requires adequate wound excision and eventual skin coverage.
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Fig. 1.23: Fasciotomy for compartment syndrome should be longitudinal, deep and lengthy and should decompress the compartment to expose the underlying muscle. It should be done early.
It is common in calf and forearm. Closed injuries cause haematoma leading to increased pressure. It is often associated with fracture of the underlying bone which in turn compresses the major vessel further aggravating the ischaemia causing pallor, pulselessness, pain, paraesthesia, diffuse swelling and cold limb.
If allowed to progress it may eventually lead to gangrene or chronic ischaemic contracture with deformed, disabled limb.
Muscle necrosis releases myoglobulin which is excreted in the urine, damages the kidneys leading into renal failure.
Note:
Affected muscle when passively stretched worsens the pain—the most reliable clinical sign.
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Treatment
  • Compartment pressure will be persistently more than 30 mm Hg. It can be measured by placing a fine catheter in the compartment and using a pressure monitor. This is an indication for fasciotomy. Adequate lengthy incision involving skin, fat and deep fascia should be done until underneath muscle bulges out properly. Multiple incisions should be made if needed. Separate incision in each compartment should be done.
Fasciotomy done in forearm anterior compartment is a specific method. Carpal tunnel should be released by cutting flexor retinaculum. Incision begins at the junction of the thenar and hypothenar area; extends proximally initially transverse across flexion crease of the wrist at the ulnar border; then across forearm towards radial side of forearm; then in proximal forearm towards medial side creating convex flap towards lateral side. In the elbow it crosses along the medial border to reach the arm where it runs in arm along the medial part of the anterior arm. Injury to major nerves, palmar cutaneous branch of median nerve should be avoided while placing the incision. Incision should be deepened by cutting the deep fascia along the entire length of the incision. Dorsal fasciotomy should be added by placing longitudinal lengthy incision in the midline. Two longitudinal incisions on the dorsum of the hand also should be made.
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Fig. 1.24: Incision for fasciotomy in upper limb begins at flexor retinaculum extending into the forearm with a convex flap towards radial side eventually leading towards medial epicondyle of the elbow joint.
  • Antibiotics.
  • Catheterisation.
  • Mannitol or diuretics to cause diuresis, so as to flush the kidney.
  • Fresh blood transfusion.
  • Hyperbaric oxygen.
 
CRUSH INJURY
Crush injury is one where a part of the body is being squeezed/compressed between two high force or pressure systems. It causes extensive lacerations, bruising, compartment syndrome, crush syndrome, fractures, haemorrhage, etc. with extensive tissue destruction and devitalisation. Renal failure, hypovolaemic shock and sepsis are the most dreaded problems in crush injuries.
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Fig. 1.25A:
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Figs 1.25A and B: Traumatic crush injury pelvis exposing testis and iliac vessels. Patient underwent hemipelvectomy.
 
CRUSH SYNDROME
It is due to crushing of muscles causing extravasation of blood and release of myohaemoglobin into the circulation leading to acute tubular necrosis and acute renal failure.
 
Causes
  • Earthquakes.
  • Mining and industrial accidents.
  • Air crash.
  • Tourniquet.
Initially tension increases in the muscle compartment commonly in the limb, which itself impedes the circulation and increases the ischaemic damage. In 3 days, urine becomes discoloured and scanty, patient becomes restless, apathy and delirious with onset of uraemia. Crush syndrome is often life- threatening. Injury is much worser than initial look.
 
Treatment
  • Tension in the muscle compartment is relieved by placing multiple parallel deep incisions in the limb so as to prevent further damage—Fasciotomy.
  • Rheomacrodex, or mannitol is given to improve the urine output by improving the renal function.
  • Alkalisation of urine is done by giving sodium citrate or sodium bicarbonate. It increases the solubility of acid haematin in the urine and so promotes its excretion. Urinary pH should be above 6.5 until urine does not show any myoglobin. Mannitol-alkaline diuresis should be 8 litre/day.
  • Initial aggressive volume load using saline about 1-1.5 litres/hour is ideal in these patients.
  • Haemodialysis is done sometimes as a life-saving procedure.
  • 12Other measures:
    • Catheterization.
    • Oxygen therapy.
    • Antibiotics.
    • Blood transfusion.
    • Correction of severe hyperkalaemia.
Note:
Doing fasciotomy several days after crush injury may not be safe as it may lead to sudden release of myoglobulin causing myoglobulinuria and renal failure.
 
DEGLOVING INJURIES
  • It occurs due to shearing force between tissue planes as traction—avulsion injury. It usually occurs between subcutaneous tissue and deep fascia or between muscle and bone. It can be localised or circumferential.
  • Avulsion injury strips off the superficial tissues exposing the neurovascular bundle, muscles, tendons, and bone. Degloving injury can be open or closed.
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    Fig. 1.26: Degloving injury wherein skin often with soft tissues gets avulsed off the deeper plane to create extensive raw area which may bleed/get infected.
  • It can be in one plane or multiple planes.
  • It is commonly observed in machinery injuries or major road traffic accidents. It is much more extensive than of on initial presentation.
  • Under anaesthesia fluoroscein is injected intravenously and viable skin is visible as fluorescent yellowish—green colour under ultraviolet light. As injection of fluoroscein is not fully safer, serial excision is better to look for dermal punctate bleeding.
  • It needs examination under general anaesthesia, wound excision/radical excision, flap coverage, microflap surgeries, skin grafting, with proper asepsis, and blood transfusion as there is significant blood loss in these injuries.
 
SCAR
Initially immature scar is formed during remodeling phase; this scar is disorganized contains type III collagen. Such scar is itchy, raised, hard and pink in colour. Over the pan of 12 months scar gets matured fully by making disorganised collagen getting aligned along the stress lines and formation of more type I collagen. This matured scar is soft, supple, pale and flat without any itch. Hypertrophic scar and keloid persists to have more type III collagen than type I collagen unlike in matured scar.
 
KELOID: ‘Like a claw’
  • Keloid is common in blacks. Common in females.
  • Genetically predisposed. Often familial. Very rare in Caucasians.
  • There is defect in maturation and stabilization of collagen fibrils. Normal collagen bundles are absent.
  • Keloid continues to grow even after 6 months, may be for many years. It extends into adjacent normal skin. It is brownish black/pinkish black (due to vascularity) in colour, painful, tender and sometimes hyperaesthetic; spreads and causes itching.
  • Keloid may be associated with Ehlers-Danlos syndrome or scleroderma.
  • When keloid occurs following an unnoticed trauma without scar formation is called as spontaneous keloid, commonly seen in Negroes.
  • Some keloids occasionally become non-progressive after initial growth.
  • Pathologically keloid contains proliferating immature fibroblasts, proliferating immature blood vessels and type III thick collagen stroma.
Site: Common over the sternum. Other sites are upper arm, chest wall, lower neck in front.
Differential diagnosis: Hypertrophic scar.
Treatment: Controversial.
  • Steroid injection—intrakeloidal triamcinolone, is injected at regular intervals, may be once in 7–10 days, of 6–8 injections.
  • Steroid injection—excision—steroid injection.
  • Triamcinolone reduces the fibroblast proliferation and collagen synthesis; it is the first line of therapy for keloid
  • Methotrexate and vitamin A therapy into the keloid.
  • Silicone gel sheeting; topical retinoids.
  • Laser therapy.
  • Vitamin E/palm oil massage.
  • Intralesional excision retaining the scar margin may prevent recurrence. It is ideal and better than just excision.
  • 13Excision and irradiation or irradiation alone.
  • Excision and skin grafting may be done.
Note:
Excision and primary suturing has got high recurrence rate; hence it is not usually practiced.
Recurrence rate is very highmore than 50%.
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Figs 1.27A and B: Keloid over the sternum (butterfly shaped; commonest site) and upper part of the arm near shoulder—common sites of occurrence.
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Figs 1.28A and B: Keloid in the ear lobule and chest wall near shoulder.
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Fig. 1.29: Keloid in the upper part of the scar. It is the previous parotidectomy scar.
 
HYPERTROPHIC SCAR
  • Occurs anywhere in the body.
  • Not genetically predisposed. Not familial.
  • Growth usually limits up to 6 months.
  • It is limited to the scar tissue only. It will not extend to normal skin.
  • Spontaneous improvement with time occurs commonly.
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    Fig. 1.30: Diagrammatic representation of linear, hypertrophic and keloid scar.
  • It is pale brown in colour, not painful, nontender.
  • Often self-limiting also. It responds very well for steroid injection.
  • Recurrence is uncommon.
  • It is common in wounds crossing tension lines, deep dermal burns, wounds healed by secondary intention.
 
Complications
  • Often this scar breaks repeatedly and causes infection, pain.
  • After repeated breakdown it may turn into Marjolin's ulcer.
 
Treatment
  • It is controlled by pressure garments or often revision excision of scar and closure, if required with skin graft.
  • Triamcinolone injection is the 2nd line of therapy for hypertrophic scar.
14
Differences between keloid and hypertrophic scar
Keloid
Hypertrophic scar
a.
Genetic predisposition
Yes
No
b.
Site of occurrence
Chest wall, upper arm, lower neck, ear
Anywhere in the body, common in flexor surfaces
c.
Growth
Continues to grow without time limit
Growth limits for 6 months
Extends to normal skin
Limited to scar tissue only
d.
Treatment
Poor response
Good response to steroids
e.
Recurrence
Very high
Is uncommon
f.
Collagen synthesis
20 times more than normal skin (Type III thick)
3-6 times more than normal skin (Type III fine collagen)
g.
Relation of size of injury and lesion
No relation. Small healed scar can form large keloid
Related to size of injury and duration of healing
h.
Age
Adolescents, middle age
Children
i.
Sex
Common in females
Equal in both
j.
Race
More in blacks (15 times)
No racial relation
k.
Structure
Thick collagen with increased epidermal hyaluronic acid
Fine collagen with increased alpha actin
l.
Features
Vascular, tender, itching
Not vascular, nontender, no itching
m.
Natural history
Progressive
Shows regression
n.
Problems
Hyperaesthesia, ulceration
Not much
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Fig. 1.31A:
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Figs 1.31A and B: Different contractures in hypertrophic scars over forearm, finger and neck.
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Fig. 1.32: Hypertrophied scar in the abdominal healed wound
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Fig. 1.33: ‘Z’ plasty is very useful method to release small contractures.
 
PROBLEMS WITH WOUND HEALING
  • Wound infection is common in devitalized deep difficult wounds. Diabetes, immunosuppression, cytotoxic drugs, anaemia, malnutrition, malignancy increases the chances of wound infection.
  • Wound dehiscence is common in all above said adverse factors. Wound suddenly gives away with pain causing copious serosanguineous discharge. After laparotomy when done specially as an emergency in trauma, acute abdomen and also in malignancy, abdominal closed wound may burst in 5–7 days. Usually all layers of abdomen give away causing discharge, occasionally bowel will extrude out. It needs emergency closure of the abdominal wound using specialized sutures or retention sutures.
  • Hypertrophic scar or keloid formation due to altered collagen synthesis in the wound healing process. Collagen synthesis is increased 3–6 times in hypertrophic scar and 20 times in keloid.
  • Deeper wound will cause specified problems like paraesthesia, ischaemia, paralysis, etc.
15B. Ulcer
CHAPTER OUTLINE
  • ❖ Ulcer
  • ❖ Granulation Tissue
  • ❖ Investigations for an Ulcer
  • ❖ Traumatic Ulcer
  • ❖ Trophic Ulcer
  • ❖ Ulcer due to Chilblains
  • ❖ Ulcer due to Frostbite
  • ❖ Martorell's Ulcer
  • ❖ Arterial/ischaemic Ulcer
  • ❖ Bairnsdale Ulcer Carcinomatous Ulcer
  • ❖ Marjolin's Ulcer
  • ❖ Rodent Ulcer
  • ❖ Melanotic Ulcer
  • ❖ Diabetic Ulcer
  • ❖ Meleney's Ulcer
  • ❖ Lupus Vulgaris
  • ❖ Tuberculous Ulcer
  • ❖ Bazin's disease
  • ❖ Tropical Ulcer
  • ❖ Venous Ulcer
  • ❖ Syphilitic Ulcer Soft Chancre/Soft Sore/Ducrey's Ulcer/Chancroid/Bubo
  • ❖ Climatic bubo/Tropical bubo
 
ULCER
 
Definition
An ulcer is a break in the continuity of the covering epithelium, either skin or mucous membrane due to molecular death.
 
Parts of an Ulcer
  1. Margin: It may be regular or irregular. It may be rounded or oval.
  2. Edge: Edge is the one which connects floor of the ulcer to the margin. Different edges are:
    Sloping edge. It is seen in a healing ulcer.
    • Its inner part is red because of red, healthy granulation tissue.
    • Its outer part is white due to scar/fibrous tissue.
    • Its middle part is blue due to epithelial proliferation.
    Undermined edge is seen in a tuberculous ulcer. Disease process advances in deeper plane (in subcutaneous tissue) whereas (skin) epidermis proliferates inwards.
    Punched out edge is seen in a gummatous (syphilitic) ulcer and trophic ulcer. It is due to endarteritis.
    Raised and beaded edge (pearly white) is seen in a rodent ulcer (BCC). Beads are due to proliferating active cells.
    Everted edge (rolled out edge): It is seen in a carcinomatous ulcer due to spill of the proliferating malignant tissues over the normal skin.
  3. Floor: It is the one which is seen. Floor may contain discharge, granulation tissue or slough.
  4. Base: Base is the one on which ulcer rests. It may be bone or soft tissue.
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Fig. 1.34: Parts of an ulcer.
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Fig. 1.35: Ulcer edges.
 
Induration of an Ulcer
Induration is a clinical palpatory sign which means a specific type of hardness in the diseased tissue. It is obvious in well-differentiated carcinomas. It is better felt in squamous cell carcinoma. It is also observed in long standing ulcer with underlying fibrosis. It is absent or less in poorly differentiated carcinomas and malignant melanoma. Less indurated carcinoma is more aggressive. Specific types of indurations are observed in venous diseases and chronic deep venous thrombosis. Brawny induration is a feature of an abscess. Induration is felt at edge, base and surrounding area of an ulcer. Induration at surrounding area signifies the extent of disease (tumour). Outermost part of the indurated area is taken as the point from where clearance of wide excision is planned.
 
Classifications
 
Classification I (Clinical)
  1. Spreading ulcer: Here edge is inflamed, irregular and oedematous. It is an acute painful ulcer; floor does not contain healthy granulation tissue (or granulation tissue is absent) but with profuse purulent discharge and slough; surrounding area is red and edematous. Regional (draining) 16lymph nodes are enlarged and tender due to inflammation. There will be associated fever, pain, impairment of functions with local tissue destruction and with little evidence of regeneration.
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    Fig. 1.36: Spreading ulcer copious purulent discharge with slough.
  2. Healing ulcer: Edge is sloping with healthy pink/red healthy granulation tissue with scanty/minimal serous discharge in the floor; slough is absent; regional lymph nodes may or may not be enlarged but when enlarged always non-tender. Surrounding area does not show any signs of inflammation or induration; base is not indurated. Three zones are observed in healing ulcer. Innermost red zone of healthy granulation tissue; middle bluish zone of growing epithelium; outer whitish zone of fibrosis and scar formation.
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    Fig. 1.37: Healing ulcer with healthy granulation tissue in the floor.
  3. Non-healing ulcer: It may be a chronic ulcer depending on the cause of the ulcer; here edge will be depending on the cause—punched out (trophic), undermined (tuberculous), rolled out (carcinomatous ulcer), beaded (rodent ulcer); floor contains unhealthy granulation tissue and slough, and serosanguineous/purulent/bloody discharge; regional draining lymph nodes may be enlarged but non-tender.
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    Fig. 1.38: Non-healing ulcer with pale unhealthy granulation tissue with slough.
  4. Callous (stationary) ulcer: It is also a chronic non-healing ulcer; floor contains pale unhealthy, flabby, whitish yellow granulation tissue and thin scanty serous discharge or often with copious serosanguinous discharge, with indurated non- tender edge; base is indurated, nontender and often fixed. Ulcer does not show any tendency to heal. It lasts for many months to years. Tissue destruction is more with absence of or only minimal regeneration. Induration and pigmentation may be seen in the surrounding area. There is no/less discharge. Regional lymph nodes may be enlarged; are firm/hard and nontender. It is callousness towards healing; word callous means—insensitive and cruel; and also it means— hard skinned.
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    Fig. 1.39: Callous ulcer without any sign of healing and, without any granulation tissue.
 
Classification II (Based on Duration)
  1. Acute ulcer—duration is less than 2 weeks.
  2. Chronic ulcer—duration is more than 2 weeks (long).
 
Classification III (Pathological)
  1. Specific ulcers:
    • Tuberculous ulcer.
    • Syphilitic ulcer: It is punched out, deep, with “wash-leather” slough in the floor and with indurated base.
    • Actinomycosis.
    • Meleney's ulcer.
    17
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    Figs 1.40A and B: Maggots seen in a chronic ulcer
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    Fig. 1.41: Tuberculous ulcer ankle area. Note the undermined edge. Discharge study, biopsy and later antituberculous drugs are the treatment. They are usually painless.
  2. Malignant ulcers:
    • Carcinomatous ulcer
    • Rodent ulcer.
    • Melanotic ulcer.
  3. Non-specific ulcers:
    • Traumatic ulcer: It may be mechanical, physical, chemical—common.
    • Arterial ulcer: Atherosclerosis, TAO
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      Fig. 1.42: Basal cell carcinoma of face (rodent ulcer). Ulcer edge is raised and beaded in appearance.
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      Fig. 1.43: Squamous cell carcinoma (SCC/epithelioma) leg with typical everted edge. SCC can be ulcerative, ulceroproliferative or proliferative ulcer on clinical look.
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      Fig. 1.44: Squamous cell carcinoma in the arm with secondaries in the axillary lymph node. Friable tumour tissues in the floor cause bleeding after trauma. Secondaries are fixed with ulceration. It is advanced disease.
    • Venous ulcer: Gravitational ulcer, post-phlebitic ulcer.
    • Trophic ulcer/Pressure sore.
    • Infective ulcers: Pyogenic ulcer.
    • Tropical ulcers: It occurs in tropical countries. It is callous type of ulcer, e.g. Vincent's ulcer.
    • Ulcers due to chilblains and frostbite (cryopathic ulcer).
    • Martorell's hypertensive ulcer.
    • 18 Bazin's ulcer.
    • Diabetic ulcer.
    • Ulcers due to leucaemia, polycythemia, jaundice, collagen diseases, lymphoedema.
    • Cortisol ulcers are due to long-time application of cortisol (steroid) creams to certain skin diseases. These ulcers are callous ulcers last for long time and require excision and skin grafting.
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Fig. 1.45: Ischaemic ulcer foot. Middle three toes are already amputated because of gangrene.
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Fig. 1.46: Venous ulcers in both feet. Site is around ankle (Gaiter's zone). There are healthy granulation tissues. It needs skin grafting and definitive procedure for varicose veins after evaluation.
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Fig. 1.47: Infective ulcer in the foot. Note the quantity of slough, exposed tendon and gangrenous toes. Patient requires below or above knee amputation.
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Fig. 1.48: Large ulcer in the foot and leg with exposed tendon.
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Fig. 1.49: Nonhealing ulcer foot in a diabetic patient with Pseudomonas infection. Note the greenish discharge in the wound. Pseudomonas infection is commonly hospital acquired.
 
Wagner's Grading/Classification of Ulcer
Grade 0 – Preulcerative lesion/healed ulcer
Grade 1 – Superficial ulcer
Grade 2 – Ulcer deeper to subcutaneous tissue exposing soft tissues or bone
Grade 3 – Abscess formation underneath/osteomyelitis
Grade 4 – Gangrene of part of the tissues/limb/foot
Grade 5 – Gangrene of entire one area/foot
 
GRANULATION TISSUE
It is proliferation of new capillaries and fibroblasts intermingled with red blood cells and white blood cells with thin fibrin cover over it.
 
Types
  • 19Healthy granulation tissue: It occurs in a healing ulcer. It has got sloping edge. It bleeds on touch. It has got serous discharge. 5 Ps of granulation tissue—Pink, Punctate haemorrhages, Pulseful, Painless, Pin head granulation. Skin grafting takes up well with healthy granulation tissue. Streptococci growth in culture should be less than 105/gram of tissue before skin grafting.
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Fig. 1.50: Healing ulcer with healthy granulation tissue. Note the sloping edge.
  • Unhealthy granulation tissue: It is pale with purulent discharge. Its floor is covered with slough. Its edge is inflamed and oedematous. It is a spreading ulcer.
  • Unhealthy, pale, flat granulation tissue: It is seen in chronic nonhealing ulcer (callous ulcer).
  • Exuberant granulation tissue (Proud flesh): It occurs in a sinus or ulcer wherein granulation tissue protrudes out of the sinus opening or ulcer bed like a proliferating mass. It is commonly associated with a retained foreign body in the sinus cavity.
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    Fig. 1.51: Exuberant granulation tissue (proud flesh) in an ulcer. It should be scooped out using Volkmann's scoop prior to skin grafting.
  • Sprouting granulation tissue of sinus.
  • Pyogenic granuloma: It is a type of exuberant granulation tissue. Here granulation tissue from an infected wound or ulcer bed protrudes out, presenting as a well-localised, red swelling which bleeds on touching.
    Differential diagnosis: Papilloma, skin adnexal tumours.
    Treatment: Antibiotics, excision and sent for biopsy.
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    Fig. 1.52: Pyogenic granuloma.
 
INVESTIGATIONS FOR AN ULCER
  • Study of discharge: Culture and sensitivity, AFB study, cytology.
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    Fig. 1.53: Typical greenish coloured ulcer due to Pseudomonas infection.
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    Fig. 1.54: X-ray showing osteomyelitis with sequestrum inside. Osteomyelitis prevents ulcer healing. Bone thickening on clinical examination is typical.
  • 20Wedge biopsy: Biopsy is taken from the edge because edge contains multiplying cells. Usually two biopsies are taken. Biopsy taken from the centre may be inadequate because of central necrosis.
  • X-ray of the part to look for periostitis/osteomyelitis.
  • FNAC of the lymph node.
  • Chest X-ray, Mantoux test in suspected case of tuberculous ulcer.
  • Haemoglobin, ESR, total WBC count, serum protein estimation (albumin).
Note:
Ulcer will not granulate if haemoglobin is less than 8 gm% and serum albumin is <3 gm%.
 
MANAGEMENT OF AN ULCER
  • Cause should be found and treated.
  • Correction of the anaemia, deficiencies like of protein and vitamins.
  • Proper investigation as needed.
  • Transfusion of the blood if required.
  • Control the pain and infection.
  • Rest, immobilization, elevation, avoidance of repeated trauma.
  • Care of the ulcer by debridement, ulcer cleaning and dressing. Desloughing is done either mechanically or chemically. Mechanically it is done using scissor by excising the slough. Hydrogen peroxide which releases nascent oxygen is used as chemical agent. Acriflavine is antiseptic and irritant and so desloughs the area and promotes granulation tissue formation. Eusol (Edinburgh University Solution) which contains sodium hypochlorite releases nascent chlorine which forms a water soluble complex with slough to dissolve it. Use of povidone iodine in ulcer cleaning is controversial (open wound is not suitable; it is mainly for cleaning the surgical field prior to incision). Maggots if present in the wound will cause crawling sensation and are removed using turpentine solution.
  • Removal of the exuberant granulation tissue is also required when present.
  • Ulcer cleaning and dressing is done daily or twice daily or once in 2–3 days depending on the type of ulcer and type of dressing used. Normal saline is ideal for ulcer cleaning. Various dressings are available. Films (opsite/semipermeable polyurethane), hydrocolloids (duoderm), hydrogels (polyethylene oxide with water), hydroactives (nonpectin-based polyurethane matrix), foams (polyurethane hydrophilic or hydrophobic non-occlusive), impregnates (non-adherent fine mesh impregnated with antibacterials), calcium alginates etc.
  • Topical antibiotics for infected ulcers are not essential but like framycetin, silver sulphadiazine, mupirocin may be used.
  • Vacuum assisted closure (VAC) therapy: It is by creation of negative pressure (25–200 mmHg), continuous or intermittent over the wound surface; it causes reduced fluid in the interstitial space, reduces oedema, increases the cell proliferation and protein matrix synthesis, promotes formation of healthy granulation tissue. Sterile foam is placed over the ulcer bed covering widely; tube drain with multiple holes is kept within it and end of the tube comes out significantly away; foam is sealed airtight using a sterile adhesive film. Tube is connected to suction system. Suction is maintained initially continuously later intermittently. Redressing is done only after 4–7 days.
  • Therapy using infrared/short wave/ultraviolet rays to decrease the ulcer size is often used but their benefits are not proved. Amnion to promote re-epithelialisation, chorion to promote granulation tissue formation is also often used.
  • Antibiotics are not required once healthy granulation tissues are formed.
  • Maggot debridement therapy: It is used as biotherapy (but not commonly) by placing cultured live disinfected maggots. Maggots are larvae of the green bottle fly, also known as the green blowfly (Lucilia sericata). They act by dissolving and engulfing dead necrotic tissues; they may reduce the bacterial content in the wound. They can inhibit many bacteria including MRSA (methicillin resistant bacteria), anaerobic and aerobic bacteria. They secrete proteolytic enzymes to have mechanical effects; secretion of ammonia alters the pH in the ulcer bed which inhibits bacterial growth. They increase the granulation tissue formation also.
  • Once ulcer granulates, defect is closed with secondary suturing, skin graft or flaps.
  • Autologous bone marrow monocytes injection into the ulcer area is new concept by Professor Sribatsa Mohapatra but yet to confirm.
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Figs 1.55A and B: Ulcer in the foot, initially with slough; later after slough excision and regular dressings. Area requires skin grafting.
21
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Figs 1.56A to C: Ulcer leg with exposed bone. Patient underwent local rotation flap to cover. Area from where flap is rotated is covered with split skin graft. When the bone is exposed, skin grafting is not possible.
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Figs 1.57A and B: Solutions commonly used for ulcer and surrounding area cleaning and dressing—povidone iodine (brownish); EUSOL (colourless); hydrogen peroxide and normal saline. Note the EUSOL bath. Dilute EUSOL solution in a basin is used wherein ulcer foot is dipped and kept in place for 20–30 minutes. EUSOL removes the slough and cleans the ulcer bed. Hydrogen peroxide releases nascent oxygen and helps in removing necrotic material. Povidone iodine is not used for open wound; it is only a surface antiseptic
Note:
Debridement can be surgical, mechanical, autolytic or enzymatic.
22
 
TRAUMATIC ULCER
  • Such ulcer occurs after trauma. It may be mechanical—dental ulcer along the margin of the tongue due to tooth injury; physical like by electrical burn; chemical like by alkali injury.
  • Such ulcer is acute, superficial, painful and tender. Secondary infection or poor blood supply of the area make it chronic and deep.
  • Footballer's ulcer is a traumatic ulcer occurring over the shin of males due to direct knocks on the shin. It is staphylococcal infection with a chronic and deep ulcer.
  • Traumatic ulcers can occur anywhere in the body due to trauma.
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    Fig. 1.58: Traumatic ulcers in the upper limb.
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    Fig. 1.59: Degloving ulcer with devitalised exposed tendons on the dorsum of the hand.
  • Trauma causes infection, necrosis, fasciitis, crush injury, endarteritis of the skin leading into formation of large/deep nonhealing ulcer.
  • Treatment depends on size and extent of ulcer. Regular dressing, later skin grafting is done.
 
TROPHIC ULCER (PRESSURE SORE/DECUBITUS ULCER)
Pressure sore is tissue necrosis and ulceration due to prolonged pressure. Blood flow to the skin stops once external pressure becomes more than 30 mmHg (more than capillary occlusive pressure) and this causes tissue hypoxia, necrosis and ulceration. It is more prominent between bony prominence and an external surface.
It is due to:
  • Impaired nutrition.
  • Defective blood supply.
  • Neurological deficit.
 
Sites
  • Over the ischial tuberosity.
  • Sacrum.
  • In the heel.
  • In relation to heads of metatarsals.
  • Buttocks.
  • Over the shoulder.
  • Occiput.
    Due to the presence of neurological deficit, trophic ulcer is also called as neurogenic ulcer/neuropathic ulcer. Initially it begins as callosity due to repeated trauma and pressure, under which suppuration occurs and gives way through a central hole which extends down into the deeper plane up to the underlying bone as perforating ulcer (penetrating ulcer).
Bedsores are trophic ulcers.
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Fig. 1.60: Trophic ulcer—heel. It is deep punched out ulcer. It often requires rotation flap/transposition flap.
 
Clinical Features
  • Occurs in 5% of all hospitalised patients.
  • Painless ulcer which is punched out.
  • Ulcer is non-mobile with base formed by bone.
23
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Figs 1.61A to C: Bedsore (decubitus ulcer) over the greater trochanter, ischium and sacrum. Bedsore is a trophic ulcer. It is usually with punched out edge.
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Fig. 1.62: Bedsore over the sacrum with thick black slough on the surface.
 
Investigations
Study of discharge, blood sugar, biopsy from the edge, X-ray of the part, X-ray spine.
 
Treatment
  • Cause should be treated.
  • Nutritional supplementation.
  • Rest, antibiotics, slough excision, regular dressings.
  • Vacuum-assisted closure (VAC): It is the creation of intermittent negative pressure of minus 125 mmHg to promote formation of healthy granulation tissue. Negative pressure reduces tissue oedema, clears the interstitial fluid and improves the perfusion, increases the cell proliferation and so promotes the healing. A perforated drain is kept over the foam dressing covered over the pressure sore. It is sealed with a transparent adhesive sheet. Drain is connected to required vacuum apparatus.
    zoom view
    Fig. 1.63: Vacuum-assisted closure of an ulcer.
  • Once ulcer granulates well, flap cover or skin grafting is done.
  • Excision of the ulcer and skin grafting.
  • Flaps—local rotation or other flaps (transposition flaps).
  • Cultured muscle interposition.
  • Proper care: Change in position once in 2 hours; lifting the limb upwards for 10 seconds once in 10 minutes; nutrition; use of water bed/air bed/air-fluid floatation bed and pressure dispersion cushions to the affected area; urinary and faecal care; hygiene; psychological counselling. Regular skin observation; keeping skin clean and dry (using regular use of talcum powder); oil massaging of the skin and soft tissues using clean, absorbent porous clothing; control and prevention of sepsis helps in the management.
 
ULCER DUE TO CHILBLAINS
  • It is due to exposure to intense cold causing blisters and ulcerations in the feet.
  • These ulcers are superficial.
  • It is due to excessive cutaneous arteriolar constriction.
  • The condition is also called as perniosis.
24
 
ULCER DUE TO FROSTBITE
  • It is due to exposure of a part to wet cold below the freezing point (cold wind).
  • There is arteriolar spasm, denaturation of proteins and cell destruction.
  • It leads to gangrene of the part.
  • Ulcers here are always deep.
 
MARTORELL'S ULCER (1945)
  • It is seen in hypertensive patients often with atherosclerosis.
  • It is seen in calf. Often it is bilateral and painful.
  • Necrosis of calf skin occurs with sloughing away and formation of deep, punched out ulcers extending into the deep fascia.
  • There is sudden obliteration of the arterioles of the calf skin.
  • All peripheral pulses are present.
  • It takes months to heal.
    Treatment: Once ulcer granulates well, skin grafting with lumbar sympathectomy is done.
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Fig. 1.64: Typical Martorell's ulcer.
 
ARTERIAL/ISCHAEMIC ULCER
  • It is common in toes, feet or legs; often can occur in upper limb digits. It is due to poor blood supply following blockage of the digital or medium sized arteries.
  • Atherosclerosis and TAO (Thromboangiitis obliterans) are common causes in lower limb.
  • Cervical rib, Raynaud's phenomenon and vasculitis are common causes in upper limb.
  • Ulcer initially occurs after trauma, soon becomes nonhealing, spreading with scanty granulation tissue.
  • Ulcer is very painful, tender and often hyperaesthetic. Digits may often be gangrenous. Intermittent claudication, rest pain are common. Other features of ischaemia are obvious in the adjacent areas. They are—pallor, dry skin, brittle nail, patchy ulcerations, and loss of hair.
  • Ulcer is usually deep, destructs the deep fascia, exposing tendons, muscles and underlying bone. Dead tendons look pale/greenish with pus over it.
  • Management: Specific investigations like arterial Doppler, angiogram, lipid profile, and blood sugar are done. Treatment is done accordingly—drugs like vasodilators; arterial surgeries may be needed.
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Fig. 1.65: Ischaemic ulcer foot with gangrene of toes without evidence of any bleeding with exposed tendons.
 
BAIRNSDALE ULCER
  • It is a chronic, irregular, undermined ulcer due to Mycobacterium ulcerans infection.
  • Deep severe form, with extensive dermal necrosis is called as ‘Buruli ulcer’.
  • Discharge study will show acid-fast bacilli.
  • Antituberculous drugs resolve the ulcer usually. Skin grafting may be required later.
 
CARCINOMATOUS ULCER (EPITHELIOMA, SQUAMOUS CELL CARCINOMA)
  • It arises from prickle cell layer of skin. It may initially begin as a nodule or ulcer; but later forms an ulcerative lesion with rolled out/everted edge. Floor contains necrotic content, unhealthy (tumour) granulation tissue and blood.
  • Ulcer bleeds on touch and is vascular and friable. Induration is felt at the base and edge. It is usually circular or irregular in shape. Initially ulcer is mobile but becomes nonmobile once it infiltrates into deeper tissues. The typical foul smell is due to necrotic material, infection and release of polyamides from the tumour cells.
  • Hard, discrete regional lymph nodes are often palpable, initially mobile but later become fixed. Lymph nodes can fungate eventually. Ulcer and lymph nodes are initially painless; but becomes painful and tender once there is deeper infiltration or secondary infection. Systemic spread is rare. It is a locoregional malignant disease.
  • Verrucous carcinoma is exophytic, locally malignant well differentiated squamous cell carcinoma without lymphatic spread.
  • Management: Wedge biopsy; FNAC of regional lymph nodes are the investigations. Treated with wide local excision with skin grafting and regional lymph node block dissection.
25
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Fig. 1.66: Squamous cell carcinoma heel. It is proliferative ulcer. Note the raised and everted edge.
 
MARJOLIN'S ULCER (Rene Marjolin, 1828, Paris)
  • It is slow growing locally malignant lesion—a very well differentiated squamous cell carcinoma occurring in an unstable scar of long duration.
  • It is commonly seen in chronic venous ulcer scar. Often it is observed in burns scar and scar of previous snake bite. Lesion is ulcerative/proliferative.
  • Edge may be everted or may not be. It is painless as scar does not contain nerve fibrils. It does not spread into lymphatics as scar is devoid of lymphatics. Induration is felt at the edge and base. There is marked fibrosis also.
  • Once lesion spreads into adjacent normal skin, it can spread into regional lymph nodes behaving like squamous cell carcinoma.
  • Managed by wedge biopsy and wide local excision and grafting.
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Fig. 1.67: Marjolin's ulcer in a chronic unstable scar (of long duration) in the leg. It does not spread through lymphatics.
 
RODENT ULCER
  • It is ulcerative form of basal cell carcinoma which is common in face.
  • Ulcer shows central area of dry scab with peripheral raised active and beaded (pearly white) edge. Often floor is pigmented. It erodes into deeper plane like soft tissues, cartilages and bones hence the name—rodent ulcer.
  • As lymphatics are blocked early in the disease by large tumour cells, it does not spread to regional lymph nodes. Blood spread is absent. It is only locally malignant.
  • It is common in face; rarely can it occur over tibia, external genitalia, mucocutaneous junction. It does not occur in mucosa.
  • Management: Wedge biopsy, CT scan of the part to see the depth, wide excision.
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Fig. 1.68: Typical rodent ulcer face causing destruction with deep erosions.
 
MELANOTIC ULCER
  • It is ulcerative form of melanoma. It can occur in skin as de novo or in a pre-existing mole. Ulcer is pigmented often with a halo around.
  • Ulcer is rapidly growing, often with satellite nodules and ‘in-transit’ lesions. It is very aggressive skin tumour arising from melanocytes.
  • It spreads rapidly to regional lymph nodes which are pigmented. Blood spread to liver, lungs, brain, and bones is common. It can occur in mucosa, genitalia, and eye. It is a systemic malignant disease.
  • Management: Excision biopsy (usually incision biopsy is not done), FNAC lymph node, US abdomen. Treatment is wide local excision, regional node block dissection, chemotherapy.
26
zoom view
Figs 1.69A and B: Melanotic ulcer in the foot with enlarged inguinal lymph nodes.
 
DIABETIC ULCER
 
Causes
  • Increased glucose in the tissue precipitates infection.
  • Diabetic microangiopathy which affects microcirculation.
  • Increased glycosylated haemoglobin decreases the oxygen dissociation.
  • Increased glycosylated tissue protein decreases the oxygen utilization.
  • Diabetic neuropathy involving all sensory, motor and autonomous components.
  • Associated atherosclerosis.
Note:
Diabetic neuropathy is due to conversion of sugar to sorbitol which causes nerve demyelination; neuropathy is distal, diffuse with a stocking distribution; it takes around 10 years to develop diabetic neuropathy. Glucose forms sorbitol by aldose reductase enzyme and galactose forms galactitol. If sorbitol level raises it gets trapped in peripheral nerves, retina and lens causing neuropathy, cataract and retinopathy. There may be formation of abnormal arteriovenous communications under the skin leads into nerve ischaemia and neuropathy. Sensory neuropathy causes loss of vibration sense, sense of position, touch, pain and temperature. Sensation may be absent in the entire sole due to medial and plantar nerve involvement. Foot feels like dead with like walking in the sand and prone for minor repeated traumas which are not noticed by the patient. Motor neuropathy causes paralysis of intrinsic muscles of foot leading into claw toes and hammer toe. Longitudinal arch of the foot becomes flat causing loss of foot curvature; loss of joint position and loss of foot muscle strength leads into altered gait and positions of foot leading into the deep seated trophic ulcers over the heads of the metatarsals. Autonomic neuropathy causes absence of sweating and loss of skin elasticity making more prone for breakdown and infection. Autosympathectomy is common in diabetics involving foot area.
Diabetic angiopathy may be macro-or micro-angiopthy (thickening of the basement membrane of vessels and capillaries).
Sepsis in diabetes: Cellulitis, deep seated abscess, ulcer formation, gangrene foot, osteomyelitis of metatarsals, septicaemia, multiorgan dysfunction syndrome can occur faster in diabetes. Phagocytic activity in diabetes is reduced significantly; granulocyte mobilization is reduced in diabetic ketoacidosis. Neuropathy, angiopathy, high tissue glucose level, associated smoking, hypertension, hyperlipidaemia, reduced immunity increases the chances of sepsis in diabetics. Polymicrobial and fungal infections are common.
 
Sites
 
Investigations
  • Blood sugar both random and fasting.
  • Urine ketone bodies.
  • Discharge for culture and sensitivity.
  • X-ray of the part to see osteomyelitis.
    zoom view
    Figs 1.70A and B: Foot is the most common area for diabetic infective problems. It can cause abscess, ulcer, osteomyelitis, gangrene, septicaemia. Initially patient undergoes toe amputation but later eventually land with below knee or above knee amputation.
  • 27Arterial Doppler of the limb; glycosylated haemoglobin estimation.
 
Treatment
  • Control of diabetes using insulin.
  • Antibiotics.
  • Nutritional supplements.
  • Regular cleaning, debridement, dressing.
  • Once granulates, the ulcer is covered with skin graft or flap.
  • Revascularisation procedure is done by endarterectomy or thrombectomy or balloon angioplasty or arterial bypass graft. But if distal vessels are involved then success rate is less.
  • Toe/foot/leg amputation.
  • Microcellular rubber (MCR) shoes to prevent injuries; care of foot.
    zoom view
    Fig. 1.71: Microcellular rubber (MCR) chappal is used diabetic neuropathy involving foot.
 
MELENEY'S ULCER (POSTOPERATIVE SYNERGISTIC GANGRENE)
  • It is commonly seen in postoperative wounds in abdomen and chest wall like empyema drainage or after surgery for peritonitis.
  • It is an acute rapidly spreading ulcer with destruction and deep burrowing of subcutaneous tissues.
    zoom view
    Fig. 1.72: Meleney's ulcer.
  • Occasional symbiotic infection may develop in leg or hand. This can be as de novo association of ulcerative colitis or on a pre-existing venous ulcer.
 
Aetiology
  • It is common in old age and immunosuppressed individuals and after surgery for infected cases.
  • It is caused by microaerophillic streptococci, Staphylococcus aureus and anaerobes.
 
Sites
  • It is common in abdomen and thorax. It begins in wound margin and spreads rapidly. It can also occur in other areas of skin.
  • Infection is severe, often with endarteritis of the skin leading to ulcer and destruction.
 
Clinical Features
  • Features of toxaemia.
  • Spreading painful ulcer with discharge.
  • Abundant granulation tissue with purple and red zones.
 
Management
  • Random blood sugar is checked, if diabetic it has to be controlled.
  • Antibiotics.
  • Blood transfusion, critical care.
  • Adequate excision of dead tissues until it bleeds.
  • Once healthy granulation tissue is formed skin grafting is done.
 
LUPUS VULGARIS (‘Lupus’—Wolf)
  • It is cutaneous tuberculosis which occurs in young age group.
  • Commonly seen on face, hand and forearm; starts as typical apple-jelly nodule with congestion of skin around. Eventually a superficial ulcer with undermined edge is formed.
  • Glass slide pressed firmly on the diseased area to eliminate the surrounding hyperaemia causes clinically obvious apple-jelly appearance.
  • The ulcer is active and destruction occurs at the periphery with healing takes place at the centre.
  • Often lesion extends into nose and oral cavity involving the mucosa.
    28
    zoom view
    Figs 1.73A and B: Lupus vulgaris in forearm and thumb. Biopsy confirmed tuberculosis. Patient needs antituberculous drugs(Courtesy: Dr Ashfaque, DNB, Surgeon, KMC, Mangaluru).
  • Due to lymphatic obstruction facial oedema can occur.
  • Long-standing lupus vulgaris can turn into squamous cell carcinoma.
  • Investigation: ESR, discharge study, biopsy, chest X-ray.
  • Treatment:
    • Antituberculous drugs.
    • If complete healing does not occur, then excision and skin grafting is required.
 
TUBERCULOUS ULCER
It is due to Mycobacterium tuberculosis. It is usually due to cold abscess later forming ulcer in the neck, chest wall, axilla and groin. It can also be primary tuberculosis of the skin (commonly in face). Ulcer can be single or multiple; oval or rounded; with undermined edge (due to progression of disease outwards underneath and healing inwards by skin), painless with caseating material on the floor. Ulcer is usually not deep. Regional lymph nodes may be enlarged matted, firm, and nontender.
Tuberculous ulcer is usually painless except on the tongue.
zoom view
Fig. 1.74: Tuberculous ulcer is typically undermined.
 
Management
Discharge study for epithelioid cells (modified histiocytes), AFB; edge biopsy, antituberculous drugs.
 
BAZIN'S DISEASE (ERYTHROCYANOSIS FRIGIDA/ERYTHEMA INDURATUM)
(Pierre Bazin, 1850, Paris)
  • It is localised area of fat necrosis with chronic ischaemia of ankle skin affecting exclusively adolescent girls. It may be due to tuberculosis. It is observed in girls with more / thick subcutaneous fat around ankle.
  • Bluish pink leg which becomes bluish mottling in extreme cold season. On warming, skin turns bright red and painful which is typical due to hyperaemia. In these patients perforating arteries perfusing the skin around the ankle are small/poor/not existing causing ischaemia of skin around ankle which becomes hyperaesthetic and sensitive for temperature alteration.
  • Symmetrical, purple nodules develop in ankles and lower leg which later break down forming multiple, small, painful, superficial ulcers often with ankle oedema and pigment scars.
  • Treatment is antitubercular drugs and lumbar sympathectomy.
 
TROPICAL ULCER
  • It is endemic in monsoon hit humid tropics with repeated epidemics but sporadic in subtropics. Trauma or insect bite leads into infection exclusively in the lower part of the leg and foot.
  • It is an acute ulcerative lesion of the skin observed in tropical regions like Africa, India and South America. It is associated with lower socioeconomic group, anaemia, and malnutrition and vitamin deficiency.
  • It is commonly caused by Fusobacterium fusiformis (Vincent's organisms) and Borrelia vincentii.
  • There are abrasions, redness, papule and pustule formation, acute regional lymphadenitis and severe pain.
  • Pustule bursts in 3 days along with necrobiosis and phagedena causing a spreading painful ulcer with an undermined edge, brownish floor and serosanguineous discharge. Spreading stops in few weeks with ulcer persisting for many months to years. Eventually a chronic, large nonhealing/callous ulcer forms with persistent pain, profuse serosanguineous discharge, extremely unpleasant odour, long existing firmly adherent slough in the floor without any obvious constitutional symptoms. During healing it causes a slight pigmented, parchment like round scar.
  • Often destruction is progressive without cessation (phagedena) to extend into entire soft tissues of foot and leg inviting amputation. Phagedena (Greek—to eat) is also seen in chancroid and cancrum oris.
Note:
Phagedena is destruction without proliferation.
  • Occasionally squamous cell carcinoma can develop in it.
  • Treatment: Improvement in nutrition, penicillin, metronidazole, Eusol dressing, skin grafting at a later date.
29
 
VENOUS ULCER (GRAVITATIONAL ULCER)
  • It is common around ankle (gaiter's zone) due to ambulatory chronic venous hypertension. It is due to varicose veins (long saphenous vein/short saphenous vein/perforators) or post- phlebitic limb.
  • Post-phlebitic limb consists of veins that is been partially recanalised following deep venous thrombosis which causes increased venous pressure around ankle through perforators.
  • Varicose veins are common in females. 50% of venous ulcers are due to varicose veins; 50% are due to post-phlebitic limb (previous DVT). Pain, discomfort, pigmentation, dermatitis, lipodermatosclerosis, ulceration, periostitis, ankle joint ankylosis, talipes equinovarus deformity and Marjolin's ulcer are the problems of varicose veins and later of venous ulcer.
  • Ulcer is initially painful; but once chronicity develops it becomes painless. Ulcer is often vertically oval; commonly located on the medial side; occasionally on lateral side; often on both sides of the ankle; but never above the middle third of the leg. Floor is covered with pale or often without any granulation tissue. When well-granulated, edge is sloping. Induration and tenderness is seen often at the base of an ulcer.
  • Venous ulcer is vertically oval with sloping edge and will not penetrate deep fascia.
  • Inguinal lymph nodes (vertical group) are often enlarged. Ulcer often attains very large size which is nonhealing, indolent and callous.
  • Ulcer heals on rest and treatment; but reforms again. Scarring is common due to repeated healing and recurrent ulcer formation. This unstable scar of long duration may lead into squamous cell carcinoma (Marjolin's ulcer).
  • Management: Venous Doppler, regular dressing, skin grafting, specific treatment for varicose veins.
zoom view
Fig. 1.75: Venous ulcer around ankle with skin changes over surrounding area. It is the most common site of venous ulcer.
 
SYPHILITIC ULCER
  • Nowadays it is a rare entity. It is caused by Treponema pallidum bacterium. It is a sexually transmitted disease. It is named as ‘Syphilis’ after a shepherd named Syphilus who acquired the disease as was written in a poem by Francastorius of Verona. Many clinical lesions are observed in different stages of syphilis.
  • John Hunter inoculated himself with syphilis organism to study the clinical features and effects. After 24 years of inoculation, he died from rupture of syphilitic aortic aneurysm at the age of 65.
  • Genital chancre (Hard chancre, Hunterian chanre) is painless, hard, button like, indurated, nonbleeding ulcer; usually seen in corona or frenum of penis, often on lips, breasts and anal region; appears 4 weeks after initial infection in first stage of the disease (primary syphilis). Shotty, painless, firm, discrete groin lymph nodes may get enlarged along with genital chancre. Suppuration in these nodes will not occur. Extragenital chancres in lips and breasts show enlarged neck/axillary nodes which are inflamed, painful and also often may be matted.
  • During second stage (secondary syphilis) white, thickened mucous patches appear commonly in the mouth like small, circular, superficial snail track ulcers. Also there appears raised, flat, hypertrophied, and warty like epithelium at mucocutaneous junctions (mouth, genitalia) called as condyloma lata. Generalised, shotty, hard, discrete, painless lymph nodes are palpable, epitrochlear and suboccipital nodes in particular are enlarged. Epitrochlear nodes are felt 1-2 cm above the medial epicondyle (It is also enlarged in non-Hodgkin's lymphoma/NHL). Iritis, arthritis, hepatitis (massive liver in syphilis is called as hepar lobatum), meninigitis, syphilitic osteitis with ‘ivory’ sequestrum, coppery red skin rash, moth-eaten alopecia are other features of second syphilis.
  • In tertiary/late stage syphilis gummatous ulcer develops. It is deep, punched out, painless, nontender ulcer with wash leather slough in the floor, with ‘silvery tissue paper’ like scar around and occurs over the subcutaneous bones like tibia, sternum, skull, palate or other area. It also can occur over the tongue, anterior aspect of the scrotum. It is due to delayed hypersensitivity reaction with endarteritis obliterans and vasculitis. Perforation of nasal septum/palate can occur. Clutton's joint and Sabre tibia are often seen. Lymph nodes are not affected in tertiary syphilis. Neurosyphilis (tabes dorsalis), aneurysm of arch of aorta are other features of tertiary syphilis.
  • Tabes dorsalis presenting as generalized paralysis of insane is often called as late tertiary or quaternary syphilis.
  • Long quiescent asymptomatic period from secondary to tertiary is called as latent syphilis.
  • Secondary syphilitic stage shows plenty of circulating Treponema spirochaetes in blood where as in tertiary stage spirochaetes are less or absent.
 
SOFT CHANCRE/SOFT SORE/DUCREY'S ULCER/CHANCROID/BUBO
  • These multiple irregular genital ulcers appear 3 days after infection with Haemophillus ducreyi as a venereal disease.
  • They are acute painful, tender, nonindurated ulcers. Floor shows yellowish slough with purulent discharge. Edge is oedematous and inflamed. Acute regional lymphadenitis with suppuration presenting as tender, soft or firm swelling is common. Such soft fluctuant inguinal swelling is termed as bubo.
  • Treatment is by drugs like co-trimoxazole, erythromycin, ciprofloxacillin, ceftriaxone; aspiration of bubo.
 
CLIMATIC BUBO/TROPICAL BUBO
  • It is due to lymphogranuloma inguinale, a venereal spreading organism (LGV, Chlamydia type L1, 2, 3).
  • 30In LGV, lesion of primary genital stage is small, painless and commonly unnoticed.
  • Lesion of secondary stage develops in 2 weeks. In males inguinal lymph nodes; in females intrapelvic and pararectal nodes are involved. Suppuration of inguinal nodes eventually occurs leading into discharging sinuses. Frei intradermal test becomes positive in 6 weeks and remains positive for life time.
  • In tertiary stage, eye, joint, meninges may get involved after many years. Repeated chronic inflammation, lymphatic blockage, scarring can cause rectal stricture and vulval elephantiasis (esthiomene) in females.
  • Treatment is tetracycline for 3 weeks.
 
OTHER ULCERS
  • Ulcers can occur, in various parts like over shin, legs, feet, face, chest wall, in various diseases like anaemia, polycythaemia, sickle cell disease, hereditary spherocytosis, leukemia, vasculitis, autoimmune diseases like rheumatoid arthritis, Paget's disease of bone (deep, nonmobile, fixed to bone; common in tibia), ulcerative colitis, etc.
  • Treponema pertenue causing Yaws (Frambesia) can have multiple painless ulcers in leg and feet due to walking with bare foot (organism enters through abrasion) which heals spontaneously leaving a tissue paper like scar.
  • Poor hygiene and dressings can cause multiple, small, red often scabbed Staphylococcus aureus ulcers on the skin over the leg and feet which is often recurrent and disturbing.
  • Buruli ulcer: It is chronic ulcer caused by Mycobacterium ulcerans (acid fast bacillus). Initially it forms a subcutaneous nodule later forming non-caseous necrosis showing slow healing with severe scarring.
  • Veld sore: It is cutaneous diphtheria through the skin causing vesicles with a straw coloured fluid; once vesicles rupture chronic tender shallow ulcers will form.
  • Delhi boil (Oriental sore): Here Leishmania tropica infection causes indurated papule on the face and exposed body parts causing indolent chronic ulcer which heals producing an ugly pigmented scar.
31C. Sinus and Fistula
CHAPTER OUTLINE
  • ❖ Sinus
  • ❖ Fistula
  • ❖ Median Mental Sinus
  • ❖ Sequestrum
  • ❖ Preauricular Sinus
 
SINUS
It is a blind track lined by granulation tissue leading from an epithelial surface into the surrounding tissues.
Sinus means hollow” or “a bay” (Latin).
zoom view
Fig. 1.76: Sinus.
 
Causes
Congenital: Preauricular sinus.
Acquired: Actinomycosis, tuberculosis, pilonidal sinus, chronic osteomyelitis, median mental sinus.
zoom view
Fig. 1.77: Typical sinus in the thigh due to osteomyelitis of the greater trochanter.
 
FISTULA
It is an abnormal communication between the lumen of one viscus to another or the body surface or between the vessels. Fistula means “flute” or “a pipe or tube.”
zoom view
Fig. 1.78: Fistula.
 
Causes
Congenital:
  • Branchial fistula.
  • Tracheo-oesophageal fistula.
  • Congenital AV fistula.
  • Umbilical fistula (patent vitellointestinal duct).
Acquired:
  1. Traumatic:
    • Following surgery—intestinal fistulas (biliary, pancreatic, faecal).
    • Following instrumental delivery or difficult labour (vesicovaginal fistula, rectovaginal fistula, ureterovaginal fistula).
  2. Inflammatory—intestinal actinomycosis, tuberculosis.
  3. Malignancy—when the growth of one organ penetrates into the nearby organ (Rectovesical fistulas as in carcinoma rectum, vesicouterine fistulas as in uterine cancer).
External fistula
Internal fistula
  • Orocutaneous
  • Branchial fistula
  • Thyroglossal fistula
  • Enterocutaneous fistula
  • Appendicular fistula
  • Tracheo-oesophageal fistula
  • Cholecystoduodenal fistula
  • Colovesical fistula
  • Rectovesical fistula
 
Clinical Features of sinus/fistula
  • Discharge from the opening of sinus.
  • No floor.
  • Raised indurated edge, indurated base, nonmobile.
  • Often sprouting granulation tissue over the sinus opening.
  • Bone thickening in osteomyelitis.
  • Surrounding skin may be erythematous in inflammatory; bluish in tuberculosis; excoriated in faecal fistula; pigmented in chronic sinuses/fistulas.
  • 32Discharge typical of the cause will be evident which will be obvious after applying pressure over surrounding area.
  • Induration is a feature of all chronic fistulas except tuberculosis.
zoom view
Figs 1.79A and B: Faecal fistula through laparotomy wounds. One is through main wound; other is through drain site. It often occurs after surgery for severe peritonitis, tuberculosis, malignancy.
zoom view
Fig. 1.80: Multiple discharging sinus foot. It is commonly due to mycetoma (Madura foot). It could also be due to tuberculosis, chronic pyogenic osteomyelitis or malignancy.
  • Thickening of the bone underneath on palpation if sinus is adherent to bone or if there is osteomyelitis.
  • Enlargement of regional lymph nodes will be evident.
  • Sinus may be single or multiple.
Note:
The most common cause of sinus in neck is tuberculosis. Commonly it is tuberculous lymphadenitis. It shows yellowish cheesy discharge with bluish margin. Usually tuberculous sinus/ulcer does not show any induration.
zoom view
Figs 1.81A and B: Secondaries in neck causing discharging sinus. (A) and (B) in two different patients.
zoom view
Fig. 1.82: Mandibular sinus. It is usually due to infected tooth causing osteomyelitis of mandible. It also could be due to tumour, trauma, actinomycosis and radiation. X-ray (orthopantomogram), study of discharge and biopsy are relevant investigations. Such sinus should be excised with extraction of the causative tooth.
zoom view
Fig. 1.83: Discharging sinus in the neck due to tuberculosis of lymph nodes with a cold abscess underneath.
33
zoom view
Fig. 1.84: Pilonidal sinus showing primary and secondary sinus.
zoom view
Fig. 1.85: Fistula in ano both sides.
zoom view
Fig. 1.86: Post-operative gastrointestinal fistula. Note the skin excoriation. It can be controlled by using zinc oxide cream local application.
Note:
  • Streptococcal pus is watery with blood stain.
  • Staphylococcal pus is yellow and creamy.
  • Green or greenish blue pus is due to pseudomonas aeruginosa infection.
  • Anchovy sauce pus is seen amoebic liver abscess.
  • Gas gangrene produces sickly sweet odour—decayed apple like.
  • E. coli pus is usually odourless.
  • Anaerobic bacteria and proteus vulgaris cause typical odour due to proteolysis. Bacteroids cause typical over ripe Camembert cheese like odour.
  • Faecal fistula causes foul smelling discharge with gas bubble in it.
  • Tuberculous sinus discharges caseating cheesy material.
 
Investigations
  1. Fistulogram/sinusogram using ultrafluid lipiodol or water soluble iodine dye (Lipiodol is poppy seed oil containing 40% iodine).
  2. Discharge for C/S, AFB, cytology, staining.
  3. Biopsy from the edge for tuberculosis and malignancy.
  4. Chest X-ray; X-ray of the part; MRI (most reliable) of the part.
  5. ESR.
  6. CT sinusogram.
  7. Probing gently with care.
  8. Digital examination of the rectum and proctoscopy in fistula in ano.
 
Treatment
  • Treat the cause.
  • Excision of sinus or fistulas. Always specimen should be sent for histology.
  • Antibiotics, antitubercular drugs, rest, adequate drainage.
 
MEDIAN MENTAL SINUS
It is a chronic infective acquired condition wherein there is infection of roots of one or both lower incisor teeth forming root abscess which eventually tracks down between two halves of lower jaw in the midline presenting as discharging sinus on the point of chin at midline.
 
Features
  • Usually painless discharging sinus in the midline on the point of chin.
  • Often incisor infection may be revealed (in many patients clinically tooth looks normal even though root is infected invariably).
zoom view
Fig. 1.87: Median mental sinus. Note the origin of the sinus from the root/roots of the lower incisor/incisors.
  • It is often mistaken for infected sebaceous cyst.
  • Osteomyelitis of the mandible is the possible complication.
  • Differential Diagnosis
    • Infected sebaceous cyst.
    • Tuberculous sinus.
    • Osteomyelitis.
  • 34Investigations:
    • Dental X-ray is diagnostic (Plain X-ray mandible may not reveal the disease).
    • Discharge study—C/S, cytology, AFB.
  • Treatment:
    • Antibiotics, after doing discharge study (C/S).
    • Lay opening and excision of the sinus track with extraction of incisor tooth/teeth.
zoom view
Fig. 1.88: Median mental sinus.
 
SEQUESTRUM
  • Sequestrum is dead bone in situ.
  • It can be pyogenic, tubercular (feathery), Salmonella (granular), syphilitic (ivory), tubular and ring (in amputation stump).
  • It can be unformed—means separation between sequestrum and adjacent normal bone has not occurred or formed— means there is proper adequate separation between normal bone and sequestrum by forming granulation tissue. Radiologically formed sequestrum shows clear lucent area/zone of demarcation.
  • Sequestrum is denser because of the absence of decalcification in the dead bone as there is no blood supply (dead bone is dense bone).
  • Sequestrum should be formed prior to surgical intervention—sequestrectomy and saucerisation.
zoom view
Figs 1.89A and B: Diagram and X-ray showing osteomyelitis with sequestrum and sinus. Sequestrum is dead bone in situ.
zoom view
Figs 1.90A to C: Osteomyelitis patient with scar. Also showing on table photo of sequestrectomy and saucerisation.
zoom view
Figs 1.91A and B: X-ray pictures showing features of osteomyelitis with sequestrum, sinus, cavity.
35
zoom view
Fig. 1.92: X-ray of foot showing osteomyelitis of metatarsal bones. Metatarsal osteomyelitis is commonly seen in diabetes mellitus and trauma.
 
PREAURICULAR SINUS
It is a congenital entity occurring due to imperfect fusion of the six tubercles which form ear cartilage. Sinus opening may be seen at the root of the helix or on the tragus. Track is quiet deep running backwards, slightly upwards towards the helix. It usually ends blindly. Outer opening of the sinus often closed causing formation of a cystic swelling (preauricular cyst) which contains fluid which is often infected. Preauricular sinus in no instance will communicate with the external auditory meatus. Bursting of this swelling leads into formation of ulcer like lesion. It can be unilateral or bilateral. Occasionally multiple sinuses are seen. Opening of the sinus occurs in a small triangular area in front of the ear at the level of the tragus. Scarring is common around the opening due to repeated infection.
 
Features
  • It is seen since childhood.
  • Often swelling appears and apparently disappears repeatedly.
  • Pain and discharge is common.
  • It causes a cosmetic problem in young individual.
  • Discharge study, ESR, sinusogram to assess the track is needed. MR sinusogram is beneficial.
  • Differential diagnosis: Cold abscess, sebaceous cyst.
  • Investigation: Sinusogram, discharge study.
  • Treatment: Excision under general anaesthesia with removal of entire track is essential. If track is not removed properly recurrence will occur.
zoom view
Figs 1.93A and B: Preauricular sinus. During excision, methylene blue is injected into the track initially and later it is excised using elliptical incision.
36D. Infectious Diseases
But however secure and well-regulated civilized life may become, bacteria, protozoa, viruses, infected fleas, lice, ticks, mosquitoes, and bedbugs will always lurk in the shadows ready to pounce when neglect, poverty, famine, or war lets down the defenses.
—Hans Zinsser, 1934
CHAPTER OUTLINE
  • ❖ Surgical Infection
  • ❖ Cellulitis
  • ❖ Erysipelas
  • ❖ Lymphangitis
  • ❖ Abscess
  • ❖ Metastatic and Pyaemic Abscess
  • ❖ Bacteraemia
  • ❖ Septicaemia
  • ❖ Pyaemia
  • ❖ Boil
  • ❖ Hidradenitis Suppurativa
  • ❖ Carbuncle
  • ❖ Pott's Puffy Tumour
  • ❖ Pyogenic Granuloma
  • ❖ Impetigo
  • ❖ Erythrasma
  • ❖ Scrum Pox
  • ❖ Tetanus
  • ❖ Gas Gangrene
  • ❖ Tuberculosis
  • ❖ Leprosy
  • ❖ Syphilis
  • ❖ Actinomycosis
  • ❖ Madura Foot
  • ❖ Rabies
  • ❖ Anthrax
  • ❖ Nosocomial and Opportunistic Infections
  • ❖ Necrotising Fasciitis
  • ❖ Acute Pyomyositis
  • ❖ Surgical Site Infection
  • ❖ Hiv Infection and AIDS
 
SURGICAL INFECTION
  • Surgical infection is major problem in surgical practice. Asepsis (prevention of entry of organisms) and antisepsis (killing of the bacteria in the skin or tissues) has made a difference in surgical practice. Epithelial surfaces act as mechanical barrier and phagocytes, antibodies; complements, macrophages, leukocytes, opsonins, etc. act as protective mechanisms.
  • Malnutrition, diabetes mellitus, obesity, uraemia, jaundice, malignancy, immunosuppression, radiotherapy, chemotherapy, HIV, ischaemia, foreign body, haematoma are the risk factors for surgical infections. Virulence of organisms, blood supply, body immunity and support of antibiotics are the decisive factors in proper response to control infection.
  • Surgical infection can be superficial surgical site infection in the wound or deep surgical site infection in deeper fascio-muscular layers or organ space infection like abdomen/thoracic cavity, etc.
  • Health care associated infection occurs after hospital admission in intensive unit/postoperative ward, etc.
  • Southampton wound grading system for healing and infection:
    • Grade 0 is normal healing;
    • Grade 1 is with bruising/mild erythema;
    • Grade 2 is severe erythema with other features of inflammation at or around wound;
    • Grade 3 is serous or bloody discharge;
    • Grade 4 is presence of pus or deep infection or tissue breakdown or significant haematoma.
ASEPSIS wound score system is used to assess the wound infection.
ASEPSIS wound scoring
Parameters
Score
  • Additional treatment
  1. Antibiotics
10
  2. Pus drainage
05
  3. Wound debridement
10
  • Serous discharge—for 5 days of first 7 days of wound infection
0–5 daily
  • Erythema—for 5 days of first 7 days of wound infection
0–5 daily
  • Purulent fluid—for 5 days of first 7 days of wound infection
0–10 daily
  • Separation of deep tissues—for 5 days of first 7 days of wound infection
0–10 daily
  • Isolation of bacteria
10
  • Stay in the hospital (in-patient) more than 14 days due to infection
05
 
CELLULITIS
  • It is spreading inflammation of subcutaneous and fascial planes.
  • 37Infection may follow a small scratch or wound or incision or insect/snake/scorpion bite.
  • It can be superficial or deep. More common superficial type is easier to diagnose.
  • It is common in diabetics, immunosuppressed people and old age.
  • It is common in face, lower limb, upper limb and scrotum wherein subcutaneous tissue is lax.
Note:
Cellulitis occurring in children is never primary but secondary to an underlying bone infection—Morison's aphorism (James Morison, 1939—Surgeon, Durham, Newcastle).
 
Causative Agents
  • Commonly due to Streptococcus pyogenes and other Gram +ve organisms. Release of streptokinase and hyaluronidase cause spread of infection.
  • Often Gram –ve organisms like Klebsiella, Pseudomonas, E. coli are also involved (usually Gram –ve organisms cause secondary infection).
 
Sequelae
  • Infection can get localised to form pyogenic abscess.
  • Infection can spread to cause bacteraemia, septicaemia, pyaemia.
  • Often infection can lead to local gangrene.
  • Extensive necrosis of skin and subcutaneous tissue— necrotizing fasciitis.
 
Clinical Features
  • Fever, toxicity (tachycardia, hypotension).
  • Swelling is diffuse and spreading in nature.
  • Pain and tenderness, red, shiny area with stretched warm skin.
  • Cellulitis will progress rapidly in diabetic and immunosuppressed individuals.
  • Tender regional lymph nodes may be palpable which signify severity of the infection.
  • No edge; no pus; no fluctuation; no limit.
 
Investigations
  • Total count raises, differential count, platelet count (decreases) to be done.
  • Liver function tests, blood urea and serum creatinine in severe cases.
  • Blood sugar estimation, urine test for ketone bodies, glycosylated haemoglobin estimation.
  • Deep vein thrombosis (DVT) often may mimic cellulitis of lower limb. Venous Doppler and ultrasound of soft tissues of the limb may require in such situation.
 
Treatment
  • Elevation of limb or part to reduce oedema so as to increase the circulation and bandaging.
  • Antibiotics—penicillins, cephalosporins.
  • Dressing (often glycerine dressing is used as it reduces the oedema because of its hygroscopic action glycerine magnesium sulphate dressing).
  • Diabetes to be treated with insulin. Ketosis if present should be confirmed by assessing urine ketone bodies and treated subsequently with intravenous insulin.
  • Often patient may be in septicaemia; patient in such condition should be treated with higher antibiotics, critical care with fluid management, along with maintaining adequate urine output. Catheterization is required; monitoring is done with—renal function tests, haematocrit (platelet count), liver function tests, prothrombin time and serum electrolyte estimation.
 
Cellulitis in Special Areas
 
Orbital Cellulitis
  • Cellulitis in orbit causes proptosis, leading to impairment of ocular movements and blindness.
  • It can spread through ophthalmic veins into cavernous sinus causing cavernous sinus thrombosis.
  • It requires admission and immediate aggressive treatment with higher generation antibiotics (Penicillins, cephalosporins).
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Fig. 1.94: Cellulitis face. Note the oedema of the face and eyelids.
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Figs 1.95A and B:
38
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Figs 1.95A to E: Note the cellulitis in different patients. It is common in lower limbs. There is no edge without any formed pus. It should never be incised with certain exceptions like Ludwig's angina. It is treated by antibiotics. It can cause bacteraemia/septicaemia.
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Fig. 1.96: Dangerous area of face—area of upper lip and lower part of nose. Infection from this area spreads through deep facial vein → pterygoid plexus → communicating vein → cavernous sinus causing its life-threatening thrombosis.
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Fig. 1.97: Severe cellulitis face involving nose, eyelids and facial skin. It can cause septicaemia, cavernous sinus thrombosis or intracranial spread of infection. This area is called as dangerous zone in face. It needs hospitalisation for treatment.
 
Ludwig's Angina (Wilhelm Frederick von Ludwig in 1836)
  • It is a rapidly progressive polymicrobial cellulitis of the sublingual and submandibular spaces involving the floor of the mouth and suprahyoid area on both sides of the neck.
  • Commonest cause is dental infection of 2nd or 3rd molar teeth precipitated by tooth extraction; other causes are submandibular sialadenitis, trauma, peritonsillar abscess, upper respiratory infection, interventions like endotracheal intubation.
  • Predisposing factors are—diabetes mellitus, chemotherapy, oral cancer, alcohol, neutropenia.
  • Commonest organisms are—Streptococcus viridians, Staphylococcus aureus and anaerobes. Gram negative organisms can also be involved.
  • Cellulitis may extend into the pharyngomaxillary space, retropharynx, and superior mediastinum.
 
Features
  • Diffuse painful swelling with woody brawny induration of the mouth and anterior neck. Swelling is non-fluctuant but with redness and tenderness. Bilateral submandibular oedema with marked tenderness on palpation at suprahyoid area with bull's neck appearance.
  • Toxic features like fever, tachycardia, tachypnoea is common.
  • Difficulty in speech, earache, drooling of saliva and putrid halitosis.
  • Involvement of connective tissues, muscles and fascial spaces but not glandular structures.
  • Spread via fascial planes in continuity not by lymphatics; no lymph node enlargement.
  • Oedema of the tongue with pushing against palate (elevation) upwards and backwards causing airway obstruction, dysphagia and odynophagia.
  • Stridor, respiratory distress and cyanosis may develop due to oedema of tongue and larynx.
  • Investigations—CT scan or MRI is useful to identify airway block, fluid collection and presence of gas. Ultrasound neck is simpler method to identify same. Total count, blood sugar, chest X-ray and often blood gas analysis (in severe cases) is done.
  • Differential diagnoses are—angioneurotic oedema, sublingual haematoma, sialadenitis, lymphadenitis.
 
Complications
  • Laryngeal oedema can occur due to spread of inflammation to glottis submucosa via stylohyoid tunnel. It may require emergency tracheostomy to maintain the respiration.
  • Mediastinitis due to spread of infection into mediastinum; aspiration pneumonia.
  • Septicaemia.
  • Spread of infection into the parapharyngeal space leads to thrombosis of the internal jugular vein which may extend above into the sigmoid sinus which may be fatal.
  • Mortality is less than 5% unlike in olden days.
 
Treatment
  • Antibiotics (intravenous) like penicillins, piperazillin, tazobactam, clindamycin, metronidazole should be started at the earliest.
  • If patient is in respiratory distress, tracheostomy is required as a life saving procedure.
  • Whenever distress is severe surgical decompression is required. Submental horizontal incision is placed; mylohyoid muscles are cut (both sides); wound may be closed with a loose sutures with a 39drain or kept open with a dressing cover until oedema and sepsis subsides and later secondary suturing can be done.
  • Initial steroid therapy (dexamethasone) may be beneficial and is often used to reduce oedema even though it is controversial.
 
ERYSIPELAS
Erysipelas is (Greek-red skin, Ignis sacer, holy fire, St Anthony fire) an acute spreading inflammation of the upper (outer) dermis and superficial lymphatics; it has got typical skin rash presenting on legs, toes, face and fingers due to acute infection by beta haemolytic Streptococcus pyogenes, presenting as raised well demarcated skin rash (rash is due to exotoxin). It is more superficial than cellulitis. In olden days, it was more common in face, now it is common in legs. Infection occurs through a minor trauma. It affects all races; more common in females. There will be always cutaneous lymphangitis with development of rose pink rash with cutaneous lymphatic oedema. Vesicles which form eventually will rupture to cause serous discharge.
 
Sites
  • Orbit, face and ear lobule—most common.
  • Hands and scrotum.
  • Umbilicus in infants.
  • Decubitus ulcer of lower limb (legs and feet are now becoming more common site).
 
Clinical Features
  • Toxaemia is always a feature.
  • Rash is fast spreading and blanches on pressure.
  • Rash is raised with sharp margin.
  • Redness becomes brown and later yellow with vesicles.
  • Discharge is serous (In cellulitis discharge is purulent).
  • In the face and orbit it causes severe oedema.
  • Milian's ear sign is a clinical sign used to differentiate erysipelas from cellulitis wherein ear lobule is spared. Skin of ear lobule is adherent to the subcutaneous tissue and so cellulitis cannot occur. Erysipelas being a cutaneous condition can spread into the ear lobule (Gaston Milian—dermatologist Paris, 1945).
  • Tender, regional lymph nodes are usually palpable.
  • Differential diagnoses—herpes zoster, angioneurotic oedema, contact dermatitis.
 
Complications
  • Septicaemia, localized cutaneous and subcutaneous gangrene are dangerous problems.
  • Abscess, pneumonia, meningitis may develop.
  • Lymphoedema of face or eyelid or limbs (when involved) can occur due to lymphatic fibrosis.
  • Glomerulonephritis (not rheumatic fever), septic arthritis, necrotizing fasciitis, can occur occasionally.
  • Recurrence rate is 20%. It causes disfiguring sequelae.
 
Treatment
  • Penicillins, clindamycin, erythromycin, roxithromycin.
  • Recurrent erysipelas may require injection benzathine penicillin (long-term penicillin) monthly for 2 years.
 
ERYSIPELOID DISEASE
  • Also called as ‘Fish handler's disease.
  • Occurs following any cuts or scratches.
  • It has features of both erysipelas and cellulitis.
  • It is self-limiting with relatively mild symptoms.
 
LYMPHANGITIS
  • It is an acute nonsuppurative infection and spreading inflammation of lymphatics of skin and subcutaneous tissues due to beta haemolytic streptococci, staphylococci, clostridial organisms. It is commonly associated with cellulitis. Erysipelas is a type of lymphangitis.
  • In endemic areas, filariasis is the most common cause (coastal India). It is caused by Wuchereria bancrofti. It is transmitted through bites of Culex mosquito. Microfilaria reaches the lymph node forming adult worm which blocks the lymph node causing obstruction, fibrosis and lymphangitis.
  • Usually lymphangitis due to bacterial infection occurs following a small trauma. Rapidly affected area develops warmness and redness.
 
Features
  • Streaky redness which is spreading is typical. On pressure area blanches; on release redness reappears.
  • Oedema of the part, palpable tender regional lymph nodes are obvious.
  • Fever, tachycardia, features of toxaemia.
  • Groin lymph nodes are enlarged and tender in lower limb lymphangitis. In upper limb, as lymphatics are mainly located on the dorsum of hand, oedema and redness develops on the dorsum. Infection in thumb and index finger causes palpable tender axillary nodes; in little and ring finger causes first tender palpable epitrochlear nodes to appear; infection in middle finger causes first deltopectoral nodes to enlarge.
  • Regional lymph nodes (only) may eventually suppurate to form an abscess.
  • Toxaemia, septicaemia may occur. Rapidity may be more in diabetics and immunosuppressed.
  • Chronic lymphangitis occurs due to repeated attacks of acute recurrent lymphangitis leading into acquired lymphoedema.
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Figs 1.98A and B1:
40
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Figs 1.98A to C: (A) Lymphangitis of lower limb showing redness. (B1) Lymphangitis of upper limb; (B2) Blanching is seen immediately after pressure; (C) Typical red streaks in an upper limb lymphangitis.
 
Management
  • Blood count, platelet count, renal and liver function tests, peripheral smear and blood culture—are needed investigations.
  • Antibiotics like penicillin, cloxacillin.
  • Elevation, rest, glycerine magnesium sulphate dressing.
  • Management of toxaemia or septicaemia with critical care.
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Fig. 1.99: Lymphangitis of one leg. Note the typical streaky redness compare to normal side.
 
ABSCESS
 
Pyogenic Abscess
It is a localised collection of pus in a cavity lined by granulation tissue, covered by pyogenic membrane. It contains pus in loculi. Pus contains dead WBC's, multiplying bacteria, toxins and necrotic material.
  • Protein exudation causes fibrin deposition and formation of pyogenic membrane.
  • Macrophages and polymorphs release lysosomal enzymes which cause liquefaction of tissues leading into pus formation.
  • Toxins and enzymes released causes tissue destruction and pus formation.
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Fig. 1.100: Pyogenic abscess—parts.
 
Mode of Infection
 
Bacteria Causing Abscess
  • Staphylococcus aureus.
  • Streptococcus pyogenes.
  • Gram-negative bacteria (E. coli, Pseudomonas, Klebsiella).
  • Anaerobes.
41
 
Clinical Features
  • Fever often with chills and rigors.
  • Localised swelling which is smooth, soft and fluctuant.
  • Visible (pointing) pus.
  • Throbbing pain and pointing tenderness.
  • Brawny induration around.
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Fig. 1.101: Abscess in the face. Note the localisation and redness.
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Fig. 1.102: Abscess in the nape of the neck—suboccipital region. Note the redness and visible pus. Patient is diabetic.
  • Redness and warmth with restricted movement around a joint.
  • Rubor (redness); dolor (pain); calor (warmness); tumour (swelling) and functiolaesa (loss of localised and adjacent tissue/joint function) are quiet obvious.
(Commonly cellulitis occurs first which eventually gets localised to form an abscess.)
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Fig. 1.103A:
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Figs 1.103A and C: Pyogenic abscess in different locations in chest wall; in plantar aspect of the foot and in the thigh. Note the redness and visible pus.
Visible (pointing) pus, tenderness, fluctuation are the features of formed abscess.
Cellulitis
Pyogenic abscess
  • Diffused—no edge
  • Well-localised with clear edge
  • Pus not formed—non- suppurative initially
  • Formed pus
  • Not fluctuant
  • Fluctuant
  • Spreading—SIRS can occur
  • Blood culture may be negative
  • Culture of pus is usually positive
  • Never incise; if done danger of bacteraemia. Antibiotics, elevation, dressing—are treatment
  • Drainage is essential
 
Sites of Abscess
  1. External Sites
    • Fingers and hand.
    • Neck.
    • Axilla.
    • Breast.
    • Foot, thigh—here it is deeply situated with brawny induration.
    • Ischiorectal and perianal region.
    • Abdominal wall.
    • 42Dental abscess, tonsillar abscess and other abscesses in the oral cavity.
    zoom view
    Fig. 1.104: Perineal abscess.
  2. Internal Abscess
    • Abdominal: Subphrenic, pelvic, paracolic, amoebic liver abscess, pyogenic abscess of liver, splenic abscess, pancreatic abscess.
    • Perinephric abscess.
    • Retroperitoneal abscess.
    • Lung abscess.
    • Brain abscess.
    • Retropharyngeal abscess.
 
Investigations
  • Total count is increased.
  • Urine sugar and blood sugar is done to rule out diabetes.
  • USG of the part or abdomen or other region is done when required.
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Fig. 1.105: Abscess in plantar aspect of foot. Note the visible pus.
  • Chest X-ray in case of lung abscess.
  • Gallium isotope scan is very useful.
  • CT scan or MRI is done in cases of brain and thoracic abscess.
  • Investigations, relevant to specific types: Liver function tests, PO2 and PCO2 estimation, blood culture.
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Fig. 1.106: Multiple abscesses in neck, chin, face. It is common in HIV, diabetes and immunosuppressed.
 
Differential Diagnosis
  • Aneurysm: Especially in popliteal, femoral and axillary regions. So before draining the abscess, presence of pus is confirmed by aspirating with a needle. It should be remembered that thrombosed aneurysm may not be pulsatile but can be warm, soft and tender.
  • Soft tissue tumours: Sarcomas may be smooth, soft and warmer.
  • Haematoma.
  • Cold abscess.
43
Differences between pyogenic abscess and cold abscess
Pyogenic abscess
Cold abscess
a. Red, warm, tender, with signs of acute inflammation
a. No signs of acute inflammation
b. Pyogenic bacteria are nonspecific organisms (Streptococcus, Staphylococcus)
b. Tuberculous bacteria
c. For drainage, dependent incision is used
c. Nondependent incision is used
d. Suturing of the wound is not done
d. Wound is sutured
e. Drain is placed
e. Drain is not placed (otherwise sinus will form which is difficult to treat)
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Fig. 1.107: Typical cold abscess and tuberculous sinus in the neck. It does not show signs of acute inflammation. It should be drained (under cover of antituberculous drugs) through nondependent incision and incision should be closed without placing a drain.
 
Treatment of an Abscess
Note:
  • Pus anywhere will come to surface; pus anywhere should be drained.
  • “Pus is like the truth—you have to let it out.”Gareth Morris-Stiff
 
Procedure
Hilton's method of draining an abscess.
  • Initially broad spectrum antibiotics are started (depending on severity, extent and site of the abscess).
  • Under general anaesthesia or regional block anaesthesia,* after cleaning and draping, abscess is aspirated and presence of pus is confirmed.
  • Skin is incised adequately, in the line parallel to the neurovascular bundle in the most dependent position.
  • Next, pyogenic membrane is opened using Sinus forceps** and all loculi are broken up. Abscess cavity is cleared of pus and washed with saline.
  • A drain (either gauze drain or corrugated rubber drain) is placed.
  • Wound is not closed. Wound is allowed to granulate and heal.
  • Pus is sent for culture and sensitivity.
  • Biopsy should be done in suspected tuberculosis or malignancy.
  • Sometimes secondary suturing or skin grafting is required.
  • Antibiotics are continued.
  • Treating the cause is important.
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Fig. 1.108: Scrotal abscess, which is well-localised and ready for drainage. Patient has undergone surgery for hernia earlier.
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Fig. 1.109: Abdominal wall abscess being aspirated. Note the aspirated pus in the syringe. Abscess should be aspirated prior to drainage.
_______________
* As the pus is acidic local anaesthetic agent will not act and hence it is not used.
** Sinus forceps do not have lock and has got serrations in the tip. It is called as sinus forceps because it was initially designed and used to pack sinuses.
44Note:
  • Counter-incision is placed in breast abscess which is placed in upper quadrant.
  • Incision should be deeper while draining pus in radial and ulnar bursae, palmar spaces and tenosynovitis.
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Figs 1.110A to C:
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Figs 1.110A to F: Technique of incision and drainage of a pyogenic abscess. Abscess should be aspirated first to get pus; No. 11 blade is used to incise; using sinus forceps pyogenic membrane is opened; pus is collected for culture; loculi are broken using sinus forceps and little finger; cavity is irrigated with normal saline (ideal); cavity is packed with roller gauze; wound is not sutured.
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Fig. 1.111: Incision for draining an abscess by Hilton's method. Note the longitudinal incision.
45
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Fig. 1.112: Abscess with loculi and breaking of loculi using finger for drainage.
 
METASTATIC AND PYAEMIC ABSCESS
Metastatic abscess
  • It is an abscess which occurs as a spread from other abscess. For example, lung abscess causing metastatic abscess in the brain (common example).
  • Presentation here is of features of focus abscess and of metastatic abscess (localised features).
Pyaemic abscess
  • It is from any infective focus which need not be always from an abscess (from cellulitis or skin infections, etc.) causing pyaemic emboli leading into multiple abscess in different places like brain, kidneys, liver, etc.
  • Presentation here, is mainly of systemic features involving multiple organs with toxicity.
  • These emboli contain bulk of multiplying organisms often derived from infective thrombus or vegetations. Focus may be an abscess, cellulitis, skin infection, acute osteomyelitis, and acute bacterial endocarditis. Acute appendicitis with severe sepsis can cause infective pyaemia in liver called as pyelphlebitis or portal pyaemia.
  • Pyaemic abscess are multiple, deeper, beneath the fascia or in the internal organs. When it is on the surface, it is less tender without any clear signs of inflammation.
  • Pyaemic abscess carries high mortality with SIRS and MODS.
  • Management:
    • Evaluation for focus of infection, pus for culture, blood culture (three samples), antibiotics, critical care, systemic therapy, drainage of surface abscesses.
 
BACTERAEMIA
Presence of bacteria in blood.
 
SEPTICAEMIA
Presence of overwhelming and multiplying bacteria in blood with toxins causing SIRS (Systemic inflammatory response syndrome) or MODS (Multiorgan dysfunction syndrome).
 
Types
  1. Gram +ve septicaemia
    It is due to staphylococci, streptococci, pneumococci, etc. It is common in children, old age, diabetics and after splenectomy. After splenectomy, overwhelming post-splenectomy sepsis (OPSI) is not uncommon. Common origin is skin, respiratory infection.
  2. Gram –ve septicaemia
    It is common in acute abdomen like peritonitis, abscess, urinary infections, biliary infections, postoperative sepsis. It is commonly seen in malnutrition, old age, diabetics, immunosuppressed people. Common bacteria are E. coli, Klebsiella, Pseudomonas, Proteus. Condition is also called endotoxic shock. Common focus of Gram-negative sepsis are urinary infection, abscess or infected wounds, biliary sepsis, postoperative wounds.
 
Stages of Gram-negative Septicaemia
  1. Warm stage is reversible stage. Here existing fever is due to pyrogenic response. Patient is toxic with fever, chills and rigors.
  2. Cold stage is irreversible stage. Here fever is not present due to absence of pyrogenic response. Patient is having renal failure, ARDS, liver failure and multiorgan failure.
 
Investigations
  • Urine/pus/discharge culture.
  • Blood culture.
  • Haematocrit.
  • Electrolyte assessment.
  • PO2 and PCO2 analysis.
  • Blood urea, serum creatinine, liver function tests.
 
Treatment
  • Antibiotics like cefoperazone, ceftazidime, cefotaxime, amikacin, tobramycin, metronidazole.
  • Fresh blood transfusion.
  • Adequate hydration.
  • Oxygen supplementation.
  • Ventilatory support.
  • Electrolyte management.
  • Parenteral nutrition (TPN).
  • CVP line for monitoring and perfusion.
  • FFP or platelets in case of DIC.
 
PYAEMIA
Presence of multiplying bacteria in blood as emboli which spread and lodge in different organs in the body like liver, 46lungs, kidneys, spleen, brain causing pyaemic abscess. This may lead to multiorgan dysfunction syndrome (MODS). It may endanger life if not treated properly.
 
Common Causes
  • Urinary infection (most common).
  • Biliary tract infection.
  • Lower respiratory tract infection.
  • Abdominal sepsis of any cause.
  • Sepsis in diabetics and immunosuppressed individuals like HIV, steroid therapy.
 
Investigations
  • Total leucocyte count, platelet count.
  • C reactive protein.
  • Pus, blood, urine culture depending on need.
  • Blood urea, serum creatinine.
  • Liver function tests, prothrombin time.
  • Chest X-ray, USG abdomen.
  • CT chest/abdomen/brain as needed.
  • Arterial blood gas analysis if needed.
 
Treatment
  • Monitoring of vital parameters.
  • Antibiotics (ceftazidime, cefoperazone, ceftriaxone sodium).
  • IV fluids, maintenance of urine output.
  • Hydrocortisone—200–600 mg IV.
  • Blood and plasma transfusion.
  • Nasal oxygen, ventilator support, monitoring of pulmonary function.
 
BOIL (Furuncle)
It is an acute staphylococcal infection of a hair follicle with perifolliculitis which usually proceeds to suppuration and central necrosis.
  • Often boil opens on its own and subsides (S. aureus infection).
  • Furuncle in external auditary canal is very painful because of rich cutaneous nerves. Here skin is adherent to perichondrium.
  • Boil often heals spontaneously; suppuration will not occur in such boil; it is often called as blind healed dull boil.
  • Boil is common over back, neck, thigh, and forearm even though it can occur anywhere. Boil in eyelash follicle is called as stye. Boil can occur in perianal region which can lead into abscess and fistula. Boil can lead into hidradenitis, common in axilla and pubic region. Boil can cause cellulitis of local area. Overlying skin undergoes necrosis. But during healing re-epithelialisation occurs.
  • Boil commonly subsides spontaneously often with the support of suitable antibiotics; occasionally it requires incision and drainage. Regional enlarged tender lymph nodes may be palpable due to secondary infection.
  • Systemic features are not common unless it is multiple/ recurrent/severe or in diabetics and immunosuppressed.
  • Multiple/recurrent boils are common in diabetics.
 
Treatment
  • Antibiotics given if boil is not resolving spontaneously— cloxacillin/amoxycillin.
  • Rarely drainage of boil is needed in severe persistent form.
 
Complications
  • Cellulitis.
  • Lymphadenitis.
  • Hidradenitis (Infection of group of hair follicles).
  • Boil in dangerous zone in the face, can cause cavernous sinus thrombosis.
    zoom view
    Fig. 1.113: Furuncle/boil are infection of hair follicle with perifolliculitis due to Staphylococcus aureus.
 
HIDRADENITIS SUPPURATIVA
It is a, chronic scarring inflammatory acne like disease of the skin bearing apocrine sweat glands. Apocrine sweat glands are coiled glands which open into the hair follicles.
Hidradenitis suppurativa is also known as ‘acne inversa’. It occurs commonly in women of menstruating age group; smoking is the important aetiological factor. It may be associated with acne, pilonidal sinus or Crohn's disease.
 
Aetiology
  • Smoking, obesity, poor hygiene, polycystic ovarian disease.
  • Diabetes mellitus, steroid therapy.
  • Genetic causes: It is associated with chromosome 15q24-q25. Multiple members of the family may be affected. It may be associated with pyoderma gangrenosum, acne (PASH syndrome) or/and pyogenic arthritis (PAPASH syndrome).
Note:
Lesion is usually sterile; bacterial infection supervenes in deep abscesses and sinus tracks. Staphylococcus aureus and Propionibacterium acnes are the common bacteria.
47
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Figs 1.114A and B: Hidradenitis suppurativa. It is chronic infection of apocrine sweat glands of the skin. It is common in axilla(Courtesy: Dr Achaleshwar Dayal, MS, Itarsi, MP).
 
Pathogenesis
Obstruction of duct of apocrine sweat gland by keratin
Dilatation of the duct of gland
Infection and abscess formation
Involvement of subcutaneous tissue and adjacent apocrine glands
Fibrosis, scarring, sinus formation
Spread to surrounding tissues
 
Clinical Features
  • Common in females 4 : 1.
  • The most common site is axilla. Often it is bilateral.
  • Multiple discharging sinuses, with nodules in the skin which is tender.
  • Induration due to fibrosis.
Note:
Hidradenitis suppurativa in the anal region rarely my turn into squamous cell carcinoma.
 
Investigation
  • Discharge study—culture/sensitivity and AFB.
  • Biopsy to rule out tuberculosis or malignancy.
 
Differential Diagnosis
  • Tuberculous sinus.
  • Malignancy (squamous cell carcinoma of skin).
  • Lymph node mass in the region which are in deeper plane.
 
Treatment
  • Topical clindamycin 1%; topical resorcinol 15% cream.
  • Oral antibiotics like clindamycin, erythromycin, doxycycline – needs longer course.
  • Infliximab, retinoids (isotretinoin 0.25–0.4 mg/kg) may be used in severe cases.
  • Wide excision (radical excision) of the involved area with skin grafting.
  • Antiandrogen therapy in females using oral estrogen or oral contraceptives or spironolactone or cyproterone acetate or finasteride.
  • Ablative laser (CO2 or erbium YAG) therapy is an alternate therapy often used
 
CARBUNCLE
Word meaning of carbuncle is charcoal.
  • It is an infective gangrene of skin and subcutaneous tissue.
  • Staphylococcus aureus is the main culprit.
  • Common site of occurrence is nape of the neck and back. Skin in this area is thick. Condition also can occur in shoulder, cheek, hand, forearm.
  • It is common in diabetics and after forty years of age.
  • It is common in males.
Infection
Development of small vesicles
Sieve like pattern
Red indurated skin with discharging pus
Many fuse together to form a central necrotic ulcer (ash-grey slough) with peripheral fresh vesicle looking like a “rosette” (cribriform)
48Skin becomes black due to blockage of cutaneous vessels
Disease spreads to adjacent skin rapidly
Patient is toxic and in diabetics they are ketotic
In carbuncle, group of hair follicles are involved. Carbuncle is cluster of furuncles connected subcutaneously, causing deeper suppuration and scarring.
 
Investigations
  • Urine sugar and urine ketone bodies.
  • Blood sugar.
  • Discharge for C/S.
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Fig. 1.115: Carbuncle in the nape of the neck—typical site. Note the wide area of involvement and dark area—charcoal like. Ash-grey slough is specific.
 
Treatment
  • Control of diabetes is essential using insulin.
  • Antibiotics like penicillins, cephalosporins or depending on C/S is given.
  • Drainage is done by a cruciate incision and debridement of all dead tissues is done. Excision is done later.
  • Once wound granulates well, skin grafting may be required.
Renal Carbuncle is an entity which occurs in kidney due to infection, forming localized infective mass lesion.
 
POTT'S PUFFY TUMOUR
  • It is a misnomer. It is not a tumour.
  • It is formation of diffuse external swelling in the scalp due to subperiosteal pus formation (abscess) and scalp oedema.
  • It originates commonly in frontal region and may extend into other regions.
  • There is acute osteomyelitis of frontal bone.
 
Causes
  • Chronic frontal sinusitis which eventually suppurates and extends into subperiosteal region.
  • Trauma—subperiosteal haematoma.
  • Chronic suppurative otitis media.
 
Features
  • Pain and boggy swelling in frontal region which is warm, tender.
  • Toxicity and drowsiness.
  • Pitting scalp oedema is typical.
  • Investigations:
    • Total leucocyte count—increased. ESR—raised.
    • X-ray skull. CT scan.
  • Differential diagnosis: Secondaries in the skull or brain.
    zoom view
    Fig. 1.116: Pott's Puffy tumour. Note the swelling over the frontal region and eyelid.
 
Complications
 
Treatment
  • Antibiotics and drainage under general anaesthesia before it spreads into cranial cavity.
  • Once it extends into cranial cavity, it is treated accordingly by formal neurosurgical decompression (often using Dandy's brain cannula).
  • Osteomyelitis of skull bones requires radical removal with reconstruction of skull defect.
 
PYOGENIC GRANULOMA (GRANULOMA PYOGENICUM)
  • It is a common condition which occurs on the face, scalp, fingers and toes.
  • It may be due to minor trauma or minor infection.
  • Infection leads to formation of unhealthy granulation tissue which protrudes through the wound.
    It is also called as acquired lobular capillary haemangioma.
49
 
Clinical Features
  • Usually single, well localised, red, firm, nodule, which bleeds on touch.
  • May or may not be tender.
 
Differential Diagnosis
  • Haemangioma.
  • Papilloma.
  • Skin adnexal tumours.
  • In recurrent cases, haemangioendothelioma and melanoma.
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Figs 1.117A and B: Pyogenic granuloma finger.
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Fig. 1.118: Pyogenic granuloma lower lip.
 
Treatment
  • Excision, laser surgery.
  • Tissue to be sent for histopathological study.
 
IMPETIGO
  • It is highly infectious superficial skin infection caused commonly by staphylococcus but sometimes by streptococcal organisms.
  • It usually occurs in infants and children with formation of multiple blisters in the face, neck and hands that rupture and coalesce to cover with honey coloured crust.
  • Red sores, itchy rashes, tender regional lymph nodes are typical.
  • Impetigo may be non bullous (impetigo contagiosa, most common, common in nose and mouth); bullous (common in < 2 years, common in body/arms/legs); ecthyma (most serious form involving deeper layer of the skin).
  • Staphylococcus aureus causes most nonbullous impetigo and all bullous impetigo.
  • Ecythma is an ulcerative form of impetigo. Ecthyma is characterized by small, purulent, shallow, punched-out ulcers with thick, brown-black crusts and surrounding erythema.
  • For persistent impetigo, culture of the wound (to identify MRSA) and the nose (to identify a causative nasal reservoir) is needed.
  • Treatment is oral antibiotics and topical antiseptics (Mupirocin, fusidic acid).
 
ERYTHRASMA
  • It is the infection caused by Corynebacterium minutissimum involving foot, groin, axilla, subumbilical area and perineum mimicking the tinea or intertrigo.
  • It is common in diabetics, obesity; common in females.
  • Superficial scaling, fissuring and maceration are common. In groin, pink brown marginated patch with fine scaling is common.
  • Erythrasma fluorescences a typical coral red color under a wood light. Absence of hyphae in skin scrapings differentiates it from tinea.
  • Treatment is topical and oral erythromycin or clindamycin.
 
SCRUM POX
  • Scrum pox is a disease seen in rugby players (athletes with close contact sports) wherein infection occurs during scrumming. It is usually caused by Herpes rugbiorum or Herpes rugbiaforum (Herpes simplex virus type 1).
  • Scrum pox like condition can also be caused by Streptococcus pyogenes where it is called as ‘scrum strep’. Similar infection seen in wrestlers caused by Herpes gladiatorum and is called as ‘mat pox’.
  • Rugby players within the scrum (forwards position) are more prone for infection.
  • Vesicular lesions with pain, fever are the usual features.
  • Infection may complicate as keratitis, corneal scarring, sacral ganglionitis and meningitis.
  • Antiviral drug like acyclovir (200 mg 5 times a day for 10 days) is the treatment. Valacyclovir is also used.
 
TETANUS
It is an infective condition caused by Clostridium tetani organisms leading to reflex muscle spasm, often associated with tonic clonic convulsions.
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Predisposing Factors for Tetanus
  • Absence of prior tetanus toxoid immunisation.
  • Trauma with lacerations, deep wounds, crush devitalised wounds, presence of foreign body, wounds with anaerobic environment in the tissues.
  • Chronic suppurative otitis media with perforation, caries teeth.
  • Improper sterilisation in the ward, labour (septic abortion) and operation theatre.
  • Tattooing, rusted nails (there is a myth that only rusted instrument will cause tetanus; this is not true), ear lobe prick, colloquial perianal therapies,
Note:
Tetanus is not communicable from person to person.
 
Organism
  • Clostridium tetani is a Gram-positive, anaerobic, motile, noncapsulated, organism with peritrichous flagella, and terminal spores (Drum stick/tennis racket appearance).
  • Spore is the infective agent. They are found in soil, manure, dust.
  • Spore can gain entry through any wound, pricks, injuries resulting from road traffic accidents, penetrating injuries.
 
Pathogenesis
zoom view
Cranial nerves involved in tetanus – trigeminal (trismus); facial (risus sardonicus); vestibulocochlear nerve (hyperacusis); vagus and hypoglossal (dysphagia).
 
Toxins
  • Exotoxins released by Clostridium tetani are tetanospasmin and tetanolysin (Exotoxin is the one which is released from bacteria without their destruction/death. Endotoxin is the one which is released with death of the bacteria). Tetanus bacteria release only exotoxins.
  • Tetanospasmin, the common exotoxin released by the multiplying bacteria once spore germinates travels along the perineural sheath, lymphatics along the nerve, and through blood to cause various effects.
Tetanospasmin is oxygen stable, heat labile exotoxin (zinc dependent metalloproteinase) and is a single polypeptide chain of 150 KDa which gets cleaved into light (fragment A, 50 KDa) and heavy (fragment B, 100 KDa) parts; fragment B part binds to nerve receptors; fragment A blocks neurotransmitter. It blocks the release of inhibitory neurotransmitters glycine and gamma amino butyric acid (GABA). Loss of inhibition alters (increases) the firing rate of α motor neuron causing rigidity, spasm, sympathetic overactivity. Tetanospasmin rapidly binds to gangliosides at the presynaptic membrane of inhibitory motor nerve endings.
 
Clinical Features
 
Signs
  • Trismus, due to spasm of masseter and pterygoids.
  • Risus sardonicus (smiling facies), a rigid smile due to spasm of the facial muscle—zygomaticus major. Looks as if patient is smiling.
  • Neck rigidity.
  • Spasm and rigidity of all muscles.
  • Hyperreflexia.
  • Respiratory changes—due to laryngeal muscle spasm, infection, aspiration.
  • Tonic clonic convulsions.
  • Abdominal wall rigidity often with haematoma formation.
  • Severe convulsion may often lead to fractures, joint dislocations and tendon ruptures.
  • Fever and tachycardia.
  • Retention of urine (due to spasm of urinary sphincter), constipation (due to rectal spasm).
  • Rarely features of carditis are seen due to involvement of the cardiac muscle, which is dangerous, as it often leads to cardiac arrest and death. Here steroids are very useful. It presents with refractory bradycardia.
  • Symptoms will be aggravated by stimuli like light, noise.
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Effects on Respiratory System
Diaphragm and other muscles of respiration undergo spasm causing tachypnoea, respiratory distress, respiratory infections, aspiration, cyanosis, respiratory failure with altered PO2 and PCO2 levels.
 
Types of Tetanus
  • Early tetanus: It is a severe form with a short incubation period and poor prognosis.
  • Latent tetanus: Wound is healed and forgotten. After a long incubation period, may be years later, under favourable environment, spores release bacteria and cause tetanus. It carries better prognosis. Latent tetanus is often called as delayed tetanus.
  • Late tetanus: Disease develops many months after injury.
  • Ascending tetanus: Symptoms and signs progress from below upwards.
  • Descending tetanus: Symptoms and signs progress from above downwards.
  • Cephalic tetanus: Facial muscles are involved first (3rd, 4th, 6th and 7th cranial nerves can get involved). Facial nerve is commonly involved in this type. Oculomotor nerve—3rd nerve (ophthalmoplegia), hypoglossal nerve—12th nerve (spasm of tongue) are other cranial nerves involved.
  • Localised tetanus: Here muscles adjacent to the wound or muscles of one segment or one area develop spasm. It is due to less virulent toxin or released toxins are of less concentration or only one or few segments of anterior horn cells of the spinal cord are affected.
  • Bulbar tetanus: When muscles of deglutition and respiration are involved. Highly fatal.
  • Tetanus neonatorum (7th day tetanus): Tetanus occurring in neonates. Spread is through umbilical cord. It carries very high, nearly 100% mortality.
  • Urban tetanus. Due to repeated injections in IV drug abusers.
  • Post-operative tetanus due to improper sterilisation.
  • Even though it is classified as acute tetanus (tetanus develops within 10 days) or chronic tetanus (tetanus develops from 10 days to 3 months) it is only of outcome value as therapy will be same in both.
  • Post-abortion or puerperal tetanus develops due to practice of improper sterilisation during abortion or delivery.
  • If patient is not given tetanus toxoid during the first attack, he can develop second attack of tetanus at a later period called as recurrent tetanus as patient who had once tetanus is not immune for development of second attack of tetanus.
  • In children and adolescents chronic suppurative otitis media (CSOM) with perforation of tympanic membrane can cause tetanus—otitis tetanus.
 
Different Postures in Tetanus
  • Opisthotonus: Posterior muscles are acting more, so backward bending.
  • Orthotonus: Straight posture. Both front and back muscles are acting equally.
  • Emprosthotonus: Forward bending as front muscles are acting more.
  • Pleurothotonus: Lateral bending as lateral muscles act more.
    zoom view
    Fig. 1.119: Different types of postures seen in tetanus.
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Culture media for Clostridium tetani are RCM (Robertson's cooked meat) media and nutrient agar.
 
Management of the Tetanus
 
Isolation
  • Isolation is advised in a dark quiet room to have a faster recovery; ventilator and all supportive critical care facilities should be available. Tetanus perse being not a communicable disease does not essentially require isolation.
 
Eliminating the source of the toxin
  • Clostridium tetani are sensitive to penicillins, metronidazole, clindamycin, and erythromycin. Injection crystalline penicillin 20 lac 6th hourly; injection gentamicin and metronidazole are given in secondary infection. Only problem with penicillin is that it is GABA antagonist and may increase the convulsions, but still it is the most commonly used drug. Metronidazole is more effective and choice of drug at present—500 mg intravenously 8th hourly for 10 days.
 
Neutralizing the unbound and circulating toxins
  • It is done ideally by Human Tetanus Immunoglobulin (HTIG/ATG)—3000–6000 units. HTIG is given intramuscularly usually to deltoid as a single dose or often in 2 or 3 divided doses. HTIG (ATG) has got long half life (40 days). There is no risk of hypersensitivity; it does not interfere with antibody production; there is no preservative. It does not penetrate blood brain barrier. Intrathecal injection of antitoxin is of less value (circulating free toxin in the CSF can be neutralized in first 48 hours during initial development of the spasm). It should not be given intravenously. It is 100 times more potent than anti-tetanus serum (ATS, equinus tetanus antitoxin).
  • When HTIG is not available or financial constraint is the matter then as an alternative, equinus tetanus antitoxin serum (ATS, anti-tetanus serum) can be given. Full dose is 1,00,000 units; half is given intramuscular and another half is intravenously after initial checking for anaphylaxis by injecting a test dose of 1000 units intravenously.
 
Control of muscle spasms
  • Benzodiazepines are used mainly; they are GABA agonists but do not restore glycinergic inhibition. Higher doses of diazepam; lorazepam with a longer duration of action; midazolam with shorter duration of action as infusion (15 mg/hour). Diazepam and lorazepam contains propylene glycol which may cause lactic acidosis; but midazolam does not contain propylene glycol. Diazepam has got cumulative effect by it metabolites oxazepam and desmethyldiazepam.
  • Phenobarbitones (anticonvulsants) and chlorpromazines are also used.
  • Therapeutic paralysis with a nondepolarising neuromuscular blocking agent with mechanical ventilation is often required. Vecuronium and atracurium are used; pancuronium is also used but may cause tachycardia and hypertension. Propofol infusion, dantrolene, baclofen are other agents used. Intrathecal baclofen is also often used (500–200 mg infusion) which is a GABA agonist but is invasive.
  • Magnesium sulphate infusion is rapidly emerging as a useful therapeutic technique. It controls the autonomic dysfunction; loading dose of 5 gram in 20 minutes followed by infusion for maintenance should be given; one should observe for hypermagnesaemia by observing ventilation changes.
  • Centrally acting drugs like methocarbamol, mephenesin or meprobamate is useful. Methocarbamol which is long acting with high potency does not suppress respiration. It may cause severe gastritis and haemorrhagic cystitis. Mephenesin causes hypotension and haemoglobinuria. Meprobamate causes thrombosis, haemolysis and uraemia but is most potent muscle relaxant.
 
Control of autonomic dysfunction
  • Autonomic dysfunction in tetanus causes haemodynamic instability. Fluid therapy (8 liters/day), morphine (20–180 mg), phenothiazines (Chloropromazine, phenoxybenzamine, phentolamine [α receptor blocker]), anticholinergics (atropine 100 mg hourly), α2 adrenergic agonists (clonidine, dexmedetomidine) contribute to cardiovascular stability. Beta blockers like propranolol should not be used. Sodium valproate, angiotensin converting enzyme inhibitor, adenosine are other drugs used for this purpose.
  • Magnesium sulphate as presynaptic neuromuscular blocker reduces receptor responsiveness to the catecholamines and also is an anticonvulsant and a vasodilator.
 
Managing respiratory system complications
  • Aspiration, pneumonia, ARDS (Adult respiratory distress syndrome), respiratory failure are common life-threatening complications. Ventilator support (IPPR) with endotracheal intubation; paralyzing the patient; tracheostomy; regular suctioning, respiratory physiotherapy for prevention of bronchopneumonia and ARDS; regular monitoring by doing arterial blood gas analysis (ABG), total count, chest X-ray. Steroids may be beneficial in ARDS and in patients with carditis.
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Active immunization
  • Tetanus toxoid should be given as disease will not give immunity against further infection. To start—1st dose, 2nd dose after one month, 3rd dose after six months.
 
Wound management
Wound debridement, drainage of pus when present and injection of HTIG 500 units into wound area to reduce the effects of toxins locally.
 
Management of complications
  • Respiratory (laryngospasm, aspiration, pneumonia, ARDS, pulmonary oedema), renal (infection, failure), cardiac (arrhythmias, failure), gastrointestinal (stasis, ileus, diarrhoea, haemorrhage), fracture bones and vertebrae, muscle and tendon injuries, DVT, thromboembolism, sepsis should be managed accordingly.
 
Other management
  • Good nursing care, prevention of bedsore and DVT (deep vein thrombosis), nutrition (enteral through nasogastric tube or parenteral using a central line)—are important. Care of urinary catheter, prevention of urosepsis is important.
  • Steroids may be useful in ARDS and carditis.
  • Pyrexia or hyperpyrexia should be treated by tepid sponging, intravenous paracetamol or steroids. It is a poor prognostic indicator.
  • Hyperbaric oxygen even though routinely not used has got beneficial effects in reversing the symptoms.
  • Cardiac pacemaker may be useful in refractory bradycardia and arrhythmias.
  • Following treatment patient may develop muscle spasms or tics which can be prevented by giving oral methocarbamol for one year.
Note:
  • Culture media for Clostridium tetani is RCM (Robertson's Cooked Meat) media and nutrient agar.
  • Serum anti-toxin (antitetanus antibody) level more than 0.01 units/L is protective against tetanus.
 
Monitoring during Therapy
PCO2, PO2, haemotocrit, blood urea, serum electrolytes, chest X-ray, ECG are done at regular intervals.
 
GAS GANGRENE
It is an infective gangrene caused by clostridial organisms involving mainly skeletal muscle as oedematous myonecrosis. Earlier it was called as malignant oedema.
 
Source and Predisposing Factors
  • Contaminated, manured or cultivated soil, intestines are the sources. Faecal flora commonly contains clostridial organisms enters the wound; in presence of calcium from blood clot or silica (silicic acid) of soil, it causes infection.
  • It is common in crush wounds, following road traffic accidents, after amputations, ischaemic limb, gunshot wounds, war wounds. Injury or ischaemia or necrosis of the muscle due to trauma predisposes infection.
  • Anaerobic environments in the wound—initial infection with aerobic organism utilises existing oxygen in tissues creating anaerobic environment to cause clostridial sepsis.
 
Organisms
  • Clostridium welchii (perfringens): Gram-positive, anaerobic central spore bearing, nonmotile, capsulated organisms, most common—60%.
  • 54Clostridium oedematiens.
  • Clostridium septicum.
  • Clostridium histolyticum.
Various strains include—A, B, C, D, E.
‘A’ strain is most common.
Note:
Non-clostridial gas producing organisms like coliforms can also cause gas gangrene.
 
Exotoxins
  • Lecithinase is important toxin which is haemolytic, membranolytic and necrotic causing extensive myositis. It splits lecithin into phosphocholine.
  • Haemolysin causes extensive haemolysis.
  • Hyaluronidase helps in rapid spread of gas gangrene.
  • Proteinase causes breaking down of proteins in an infected tissue.
    Spores enter through the devitalised tissues commonly in road traffic accidents, crush injury
    Spores germinate
    Released bacteria will multiply
    Exotoxins are released
    cause their effects
 
Effects
  • Extensive necrosis of muscle with production of gas (hydrogen sulphide; nitrogen; carbon dioxide) which stains the muscle brown or black anaerobic myositis/myonecrosis.
  • Usually muscle is involved from origin to insertion.
  • Often may extend into thoracic and abdominal muscles.
  • When it affects the liver it causes necrosis with frothy blood—foaming liver, is characteristic.
  • Rapidly spreading infection which is also often fatal.
  • Limbs are commonly involved; but organs like liver can also be affected.
  • Muscle glycogen is broken down into lactic acid, CO2 and hydrogen. Proteinase released by organism forms amino acids which further releases ammonia and hydrogen sulphide. Acid released earlier is neutralised by ammonia and calcium to progress further multiplication of organisms.
 
Clinical Features
Incubation period is 1–2 days.
  • Features of toxaemia, fever, tachycardia (out of proportion to fever) pallor.
  • Wound is under tension with foul smelling discharge (sickly sweety/decaying apple odour).
  • Khaki brown coloured skin due to haemolysis.
  • Crepitus can be felt.
  • Jaundice may be ominous sign and also oliguria signifies renal failure.
  • Frequent sites are adductor region of the lower limb and buttocks and subscapular region in upper limb.
Clostridium welchii can infect limbs, abdominal wall, appendix, gallbladder, common bile duct, intestine, uterus (during septic abortion).
 
Clinical Types
  • Fulminant type causes rapid progress and often death due to toxaemia, renal failure or liver failure or MODS or ARDS.
  • Massive type involving whole of one limb containing fully dark coloured gas filled areas.
  • Group type: Infection of one group of muscles, extensors of thigh, flexors of leg.
  • Single muscle type affecting one single muscle.
  • Subcutaneous type of gas gangrene involves only subcutaneous tissue (i.e. superficial involvement). It is mainly of anaerobic cellulitis type without muscle involvement usually caused by less virulent clostridial organisms other than clostridial welchii. It is usually superficial but may spread and involve fascial planes. It causes necrosis with foul smelling seropurulent discharge.
zoom view
Fig. 1.120: Gas gangrene in upper limb. It is after effect of an assault using an axe by a drunken husband.
zoom view
Fig. 1.121: Gas gangrene involving entire leg extensively. Note the black/khaki coloured area. Patient died of toxaemia.
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Investigations
  • X-ray shows gas in muscle plane or under the skin.
  • Liver function tests, blood urea, serum creatinine, total count, PO2, PCO2.
  • CT scan of the part may be useful especially in chest or abdominal wounds.
  • Gram's stain shows Gram-positive bacilli.
  • Robertson's cooked meat media is used which causes meat to turn pink with sour smell and acid reaction.
  • Clostridium welchii is grown in culture media containing 20% human serum in a plate. Antitoxin is placed in one-half of the bacteria grown plate sparing the other half. Zone of opacity will be seen in that half of the plate where there is no antitoxin. In the other half part of the plate where there is antitoxin there is no opacity—Nagler reaction.
 
Treatment
  • Injection benzyl penicillin 20 lacs 4th hourly + Injection metronidazole 500 mg 8th hourly + Injection aminoglycosides (if blood urea is normal) or third generation cephalosporins or metronidazole.
  • Fresh blood transfusion.
  • Polyvalent antiserum 25,000 units given intravenously after a test dose and repeated after 6 hours (Welchii 10,000 IU, oedematiens 10,000 IU, and septicum 5,000 IU).
  • Hyperbaric oxygen is very useful.
  • Liberal incisions are given. All dead tissues are excised and debridement is done until healthy tissue bleeds.
  • Rehydration and maintaining optimum urine output (30 ml/hour) (0.5 ml/kg/hour).
  • Electrolyte management.
  • In severe cases amputation has to be done as a life-saving procedure stump should never be closed (Guillotine amputation).
  • Often ventilator support is required.
  • Once a ward or operation theatre is used for a patient with gas gangrene, it should be fumigated for 24–48 hours properly to prevent the risk of spread of infection to other patients especially with open wounds.
  • Hypotension in gas gangrene is treated with whole blood transfusion.
  • Therapy should be concentrated in managing dehydration, hypotension, infection, toxaemia by hydration, fresh whole blood transfusion, passive immunisation, antibiotics, and hyperbaric oxygen, doing radical wound excision with removal of all dead tissues with foreign body or amputation with critical care.
 
TUBERCULOSIS
zoom view
Fig. 1.122: Tuberculous lymphadenitis and tuberculous ulcer.
  • It is commonly caused by Mycobacterium tuberculosis; occasionally by Mycobacterium bovis, M. kansasii, M. fortuitum, M. marinum, M. ulcerans.
  • M. tuberculosis is gram neutral, acid fast, alcohol fast straight or slightly curved rods.
  • It is prevalent in most of the developing countries and has made its resurgence in the developed countries with the advent of AIDS.
 
Pathogenesis
  • The characteristic lesion here is ‘tubercle’, which is an avascular granuloma composed of a central zone containing giant cells, with or without caseation necrosis, surrounded by a rim of epithelioid cells, lymphocytes and fibroblasts.
  • It can occur in almost all organs in the body. Presentation may vary depending on the individual sites.
 
General Features
  • Low-grade fever with evening rise of temperature.
  • Loss of appetite.
  • Decreased weight.
 
Investigations
  • ESR is often raised; peripheral smear—lymphocytosis.
  • AFB (Acid fast bacillus) staining using Ziehl-Neelsen stain.
  • Chest X-ray is done to rule out pulmonary tuberculosis.
  • Culture of the organism in Lowenstein Jenson media.
  • Mantoux skin test—read after 48 hours of inoculation.
  • Guinea-pig inoculation.
  • Relevant investigations depending on the site of the tuberculosis.
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Treatment
  • Antituberculous drugs are given for 6 months to one year.
  • Specific treatment is given depending on the site of the tuberculosis.
(Please refer individual chapters for details about tuberculosis at different locations and also chapter drugs for Anti-tuberculous Therapy.)
 
LEPROSY
  • It is caused by Mycobacterium leprae. It is a Gram-positive, acid fast bacillus.
  • It mainly involves skin, nasal mucosa and peripheral neural tissues.
  • It involves only the cooler parts of the body (So axilla, gluteal region are not involved). Testicular involvement is seen but not the ovary. It does not involve the vital organs. Though not acutely fatal, the disease leaves the victim severely deformed and crippled for life.
zoom view
Figs 1.123A to D: A leprosy patient with the typical face (leonine); skin patches; hand deformities and trophic changes; trophic ulcer in heel.
 
Types
 
a. Multibacillary Types
  • Lepromatous leprosy: It denotes little or no host resistance. Bacilli are seen in large numbers in the superficial nodular lesions and the patient is highly infective.
  • Borderline lepromatous.
  • Borderline.
 
b. Paucibacillary Types
  • Borderline tuberculoid.
  • Tuberculoid leprosy: Here strong host resistance is observed. The disease is more localised, but it causes more deformities due to early involvement of nerves. Bacilli are scanty in the lesion and so infectivity is minimal.
 
Investigations
  • Regular checking of sensation of the suspected area.
  • Split skin smear, nerve biopsy.
 
Treatment
  • Dapsone 100 mg daily.
  • Rifampicin 600 mg once a month.
  • Clofazimine 50 mg daily + 300 mg once a month.
For paucibacillary types, treatment is for 6 months.
For multibacillary types, treatment is for 2 years or more.
 
Surgical Complications in Leprosy
 
a. Primary Deformities
  • Leonine facies.
  • Collapsed nasal bridge.
  • Upper branch facial nerve palsy (causes lagophthalmos).
  • Keratitis and blindness.
  • Claw hand either ulnar or combined ulnar and median nerves.
  • Radial nerve palsy—wrist drop (1%).
  • Clawing of toes due to involvement of posterior tibial nerve.
  • Foot drop due to involvement of lateral popliteal nerve.
    (Medial popliteal nerve which supplies the tibialis posterior is never involved.)
 
b. Secondary Deformities
  • Anaesthesia of the part makes it prone to trauma, infection, infective gangrene, destruction, autoamputation and functionless parts.
  • Trophic ulcers in the foot are common.
 
Treatment of Complications
  • Reconstructive surgeries.
  • Release of contractures.
  • Tendon transfers.
  • Arthrodesis.
  • Ulcer management.
  • Physiotherapy and rehabilitation.
 
SYPHILIS (GREAT POX) (FRENCH DISEASE)
It is a venereal infection caused by Treponema pallidum.
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Early syphilis:
It lasts for 2 years and the patient is infective during this period.
Primary syphilis:
It presents as a Hunterian chancre (Hard chancre). It is a shallow, painless, indurated, nonbleeding ulcer usually seen in the genitalia and often on the lips, breasts and anal region. It occurs in 3–4 weeks after the infection. It is confirmed by dark field microscopic study of the discharge for the organism.
Secondary syphilis: It occurs in 6–12 weeks.
It presents as:
  • Cutaneous coppery rashes.
  • Snail-track oral ulcers.
  • Condyloma lata: Raised, flat, white lesions seen at the mucocutaneous junctions (mouth, anus vulva).
  • Painless, shotty lymphadenopathy—epitrochlear suboccipital.
  • Moth-eaten alopecia.
  • Hepatitis, arthritis, iritis, meningitis. Massive, enlarged liver in syphilis is called as hepar lobatum.
  • Syphilitic osteitis with “ivory” sequestrum.
Latent syphilis:
It lasts between 2 years to lifetime. Serum tests are positive.
Late (tertiary) syphilis:
  • Painless, punched out, gummatous ulcers are seen with “wash leather base” and silvery tissue paper scar.
  • It is seen over the tibia, sternum, ulna, skull, scrotum.
  • It is a hypersensitivity reaction occurs as a result vasculitis and obliterative endarteritis.
  • Neurosyphilis.
  • Cardiovascular syphilis—aneurysm of arch of aorta.
 
Investigations
  • VDRL test; Kahn test.
  • Treponema pallidum haemagglutination test (TPHA).
  • Treponema pallidum immobilisation test (TPI).
 
Treatment
Penicillin for 15 days is the drug of choice.
Doxycycline 100 mg can be given thrice daily for 15 days.
Others: Erythromycin, tetracycline, cephalosporins.
Jarisch-Herxheimer reaction is commonly seen after penicillin, which often requires steroid therapy.
 
Congenital Syphilis
Here the infection is transmitted from the mother to foetus through placenta.
Early congenital syphilis: It is seen in newborn.
Late congenital syphilis:
Congenital syphilis is treated with penicillins.
zoom view
Fig. 1.124: Saddle nose.
 
ACTINOMYCOSIS
  • It is caused by Actinomyces israelii.
  • It is an anaerobic Gram-positive fungal like bacterium, which is a branching filamentous organism. It is called as “Ray fungus” because of sun-ray appearance.
 
Clinical Types
  • Facio-cervical: It is the most common type. Infection spreads either from tonsil or from adjacent infected tooth. Initially an induration develops. Nodules form with involvement of skin of face and neck. It softens and bursts through the skin as sinuses which discharge pus which contains sulphur granules (60%).
  • Thorax: Lungs and pleura get infected by direct spread from pharynx or by aspiration. Empyema develops. Later chest wall nodules appear leading to sinuses with discharge (20%).
  • In right iliac fossa: It presents as a mass abdomen with discharging sinus.
  • Liver is infected through portal vein (Honey comb liver).
  • Pelvic: Pelvic actinomycosis can occur due to intra-uterine devices.
 
Pathogenesis
Organism enters through deeper plane of the tissue, causes subacute inflammation with induration and nodule formation. Eventually discharging sinus forms at the surface. Pus collected in a swab or sterile tube will show sulphur granules.
 
Clinical Features
  • Discharging sinus with induration and nodules.
  • No lymph nodal involvement.
  • Through blood spread it may cause pyaemia and endanger life.
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Investigations
  • Pus under microscopy shows branching filaments.
  • Gram's staining shows Gram-positive mycelia in centre with Gram-negative radiating peripheral filaments. These clubs are due to host reaction which are lipoid material (antigen-antibody complex).
  • Cultured in brain heart infusion agar and thioglycolate media.
 
Treatment
  • Penicillins for longer period (6–12 weeks).
  • Tetracyclines, lincomycin, streptomycin.
  • Dapsone and iodides may be useful.
  • Antifungals are often given because it is fungal like bacterium.
  • Surgical debridement is occasionally required.
  • Welsh regimen— Injection amikacin 15 mg/kg IV daily for 21 days; such cycle is repeated 3 times at a gap of 15 days—along with tablet trimothoprim (7 mg/kg)—sulfamethoxazole (35 mg/kg) daily for 6 months.
 
MADURA FOOT (MYCETOMA PEDIS)
  • It is a chronic granulomatous condition of the foot involving subcutaneous and often deeper tissues causing multiple discharging sinuses.
  • It was first identified in Madurai, Tamil Nadu (India) by Gill (1842, Madura mycosis).
  • It is common in India and Africa.
  • It is common in Tamil Nadu.
  • It can be fungal (more common) or bacterial origin.
    • Bacterial can be Actinomyces or Nocardia. Among bacterial Nocardia madurae is most common.
    • Bacterial mycetomas are by Actinomyces (A. israelii or A. bovis) or by Nocardia or Actinomadura (red granules). Occasionally it can be due to pyogenic bacteria like Staphylococcus aureus (Botryomycosis). Bacterial mycetoma shows white/yellow/red granules which on smear delineates thin filaments (1 µm). Nocardia asteroids can primarily involve lungs later spreading to brain, kidney and other organs as metastatic infection.
    • Fungal eumycotic mycetoma is caused by Madurella mycetomi or Madurella grisa. Fungal mycetoma causes black granules, crushed smear of which shows thick stout filaments (5 µm).
 
Pathogenesis
Organism enters through a prick in the foot usually who walks barefoot
Reaches deeper plane in the foot
Evokes chronic granulomatous inflammation
Causes pale, painless, firm nodule
Formation of vesicles
Burst to form a discharging sinuses.
  • Discharging granules may be Black, Red, Yellow.
  • In black type of Madura foot, infection is mainly subcutaneous.
  • In red and yellow types, it burrows into the deeper plane including bone causing bone necrosis (osteomyelitis). Eventually gross swelling of the limb with multiple discharging sinuses with disability will occur.
  • Muscles and bones are involved.
  • Tendons and nerves are spared until very late.
  • Regional lymph nodes are not involved.
  • Condition will deteriorate by secondary bacterial infection.
Note:
If infection occurs in hand, it is called as Madura hand.
 
Clinical Features
  • Painless diffuse swelling in the foot of long duration.
  • Later multiple discharging sinuses develop on the skin.
  • Lymph node involvement will not occur unless secondary bacterial infection is present.
  • Significant limb disability is common.
  • Common in males.
  • Twenty per cent develop pain—due to secondary infection or bone involvement.
59
 
Investigations
  • Discharge study will show branching filamentous appearance of the organism.
  • Culture in Sabouroud's dextrose agar medium.
  • Gram stain for actinomycosis will show sun-ray appearance with Gram +ve centre and Gram –ve clubs.
  • X-ray of the foot is done to look for osteomyelitis.
  • FNAC and biopsy is confirmative as eumycetoma or actinomycetoma.
  • Ultrasound of area; MRI are useful. Dot in circle sign in MRI is characteristic.
  • Immunoelectrophoresis and ELISA are having diagnostic value showing antibody titre against causative organism.
zoom view
Fig. 1.125: Madura foot. Note the multiple sinuses.
zoom view
Figs 1.126A and B: Mycetoma thigh and foot in two different patients. Note the discharging sinuses.
 
Treatment
 
Medical
  • In actinomycetoma, amikacin or streptomycin, co-trimoxazole combined therapy is the first line of treatment (5 weeks therapy). Long-term penicillins are useful. Amoxicillin— clavulanic acid, rifampicin, sulphonamides, gentamicin and kanamycin are second line of drug treatment.
  • In eumycetoma, ketoconazole, itraconazole, voriconazole are the drugs used for long term up to one year.
  • Dapsone and iodides are often used for long term.
 
Surgical
  • Wide surgical excision should be done after initial proper medical line of treatment. Improper excision will cause recurrence. Recurrence rate is up to 50%. After wide excision, drug therapy has to be continued.
  • Amputation is needed in severe refractory cases as a life saving option. Amputation rate is 10–25%.
 
RABIES (HYDROPHOBIA)
It is an acute fatal encephalomyelitis caused by a single stranded RNA virus Lyssa virus type 1.
  • It is a zoonotic disease transmitted to humans by bite/lick/scratch of infected animals (commonly dogs).
  • It is an ancient disease mentioned even in Vedas. Rabies word is derived from Sanskrit word ‘Rabhas’ means ‘to do violence’.
  • Celsus found relation of saliva of infected dog to human disease in 1st century AD. Louis Pasteur developed 1st vaccine against Rabies in 1885.
  • Rabies is uncommon in developed countries. It is mainly seen in Indian subcontinent (80%) and Africa. In India, it is not seen in Lakshadweep, Andaman and Nicobar islands. If disease is not seen for 2 years in humans and animals then that area is termed as rabies free. Maldives country does not have human or animal rabies.
 
Pathogenesis
  • There is no predilection for age or sex even though, it is observed more in children and adult males.
  • Ninety-five per cent of rabies develops due to bite of rabid dog occasionally cat (Urban rabies). Other animals that can transmit rabies are monkey, horse, fox, cows and buffaloes, donkey, pig, sheep, camel, elephant, mongoose, jackal, bear (Wild life/sylvatic rabies). In India, transmission is not observed through bats, rodents and birds. Bat rabies (vampire bat) is seen in parts of USA and Latin American countries.
  • Asymptomatic carrier stage occurs only in animals, but they are unlikely to be infective. Only symptomatic animals are considered to be infective.
  • Rabies virus is bullet shaped envelop virus (75 nm × 180 nm) with numerous glycoprotein spikes to help in attachment of virus and also to induce antibodies. Natural occurring rabies virus is called as street virus which shows long incubation period of 20–60 days. Serial passage of this virus to brain of rabbits creates fixed virus which has got short incubation period of 4–6 days which does not show Negri bodies. This fixed virus which cannot multiply in extraneural tissues is inactivated to prepare vaccine.
  • 60Infection commonly occurs by animal bite, often by licks, scratches. Licks on abraded skin and licks on abraded or unabraded mucosa can cause infection. Licks are often ignored dangerously. Severity of infection depends on viral load in the animal saliva and class of wound. Aerosol transmission is found in bats or in lab workers. Person to person transmission can occur even though it is rare. Rabies may get transmitted through organ/corneal transplantation.
  • Virus multiplies at the site of infection and passes (ascends) through the peripheral nerves into the CNS to develop Negri bodies in the brain leading into fatal encephalomyelitis. From the brain virus descends into different tissues like salivary glands, muscles, heart, adrenals and skin. It also involves salivary glands to get secreted in the saliva to cause infection.
 
Clinical Features
  • Incubation period is 3–6 weeks; but rarely can be up to many years.
  • Prodromal symptoms like fever, headache.
  • Pain, tingling sensation at the site of bite.
  • Hyperexcitability and irritability; increased muscle reflexes and spasms.
  • Increased salivation, sweating, lacrimation.
  • Hydrophobia (fear of water) and aerophobia (fear of air) is pathognomonic.
  • Mental instability, dilatation of pupils.
  • Symptoms are aggravated by swallowing water or blowing air on them.
  • Once disease starts, patient die in 72 hours.
Fear of water is seen only in affected human beings, not in animals.
 
Classification of Wounds
Class I: Touching or feeding the diseased animal, lick over intact skin or scratches without oozing of blood.
Class II: Licks on broken skin, scratches with blood ooze, and all bites except over head, face, palms and fingers. Minor wounds less than five in number.
Class III: All bites over head, face, palms and fingers, lacerated wounds, wounds more than five in number, wild animal bites, and contamination of mucous membrane with saliva.
 
Indications for Antirabies Vaccination
  • All rabid animal bites.
  • If animal is killed or dies during 10 days of observation period.
  • Bite by an unidentified animal.
  • If lab tests in animal show positive for rabies.
  • All wild animal bites.
 
Vaccines for Rabies
 
1. Nervous Tissue Vaccine
(a) BPL inactivated vaccine: It is nervous tissue vaccine. It is 5% emulsion of the infected brain of the sheep containing the inactivated fixed virus. It is Semple vaccine.
Dosage of semple vaccine (as recommended by Pasteur Institute, Coonoor)
Adult
Children
Duration
Class I
2 ml
1 ml
7 days
Class II
3 ml
3 ml
10 days
Class III
5 ml
3 ml
10 days
Mode of administration: Subcutaneously into the abdominal wall using long needle. Joseph Meister received first anti-rabies vaccine (ARV) in 1885. In Olden days, it was given for 15–21 days.
Antibody develops in 7–30 days. Protection lasts only for 6 months. Booster doses are given if needed.
Side effects
  • Headache, palpitation, allergic reactions.
  • Redness, tenderness and swelling at the site of the vaccination.
  • Post-vaccinal neuroparalysis—a dangerous life-threatening complication.
  • During therapy patient should avoid alcohol and steroids.
(b) Nervous tissue vaccine derived from suckling mouse (less than 9 days old) brain (Fuezalida vaccine) is used to reduce neuroparalytic complications as suckling mouse has low myelin neuron. It is given for 10 daily doses then on 20th and 30th day.
 
2. Avian vaccines—Duck Embryo Vaccine (DEV)
It has got less neuroparalytic side effects. It can cause egg protein allergy. Purified duck embryo vaccine (PDEV-1 ml) is available in India.
 
3. Cell Culture Vaccines
They are more potent and safer.
  • Human Diploid Cell Vaccine (HDCV-1 ml): Safest vaccine. It is prepared using fixed virus in human diploid fibroblast cells. But it is costly. It is available in India.
  • Second generation tissue culture vaccines: They are potent and cost-effective. They are derived from nonhuman base sources. Examples are chick embryo fibroblast (Purified Chick Embryo Cell Culture Vaccines—PCECV-1 ml), foetal bovine kidney, hamster kidney cells, vero cells (Purified Vero cell Rabies Vaccine—PVRV-0.5 ml).
Dosage: 2.5 IU in one ml. One ml is given IM into the deltoid on 0, 3, 7, 14, 28 and 90 (optional) days.
Side effects: Headache, redness at the site, fever. No other serious side effects.
Second generation tissue culture vaccine can be given intradermally also. Intradermal dose is one fifth of the intramuscular dose (0.1 ml).
 
Wound Treatment
  • Proper local wound care reduces the chances of rabies infection by 80%. Immediate cleaning and washing of the wound with running water for 15 minutes is essential to reduce the viral load at the wound site. If soap is available soap water is also used. It is better to wash with warm water if available.
  • Wound should be cleaned with virucidal agents like alcohol, tincture, povidone iodine. Savlon or carbolic acid or nitric acid should not be used.
  • Wounds should not be closed. ARS should be injected locally. In deep wounds it may be closed only after 48 hours with loose sutures after thorough washing.
  • ARS (horse or human) should be injected to all wounds locally.
  • One should not scrub the wound.
  • One should not touch the wound with bare hands. One should wear gloves to touch the wound.
 
Passive Immunity
It is used in all severe exposures, class II and class III and in all wild animal exposure. Present recommendation is injection of ARS with vaccine in all exposed patient irrespective of the class.
61
 
Types of Antirabies Serum (ARS)
Horse antirabies serum (horse/equine ARS): It is given on first day with a dose of 40 IU/ kg body weight (maximum up to 3000/units). Half is given into the wound and another half given into the gluteal muscle (IM)—single dose. It prevents the multiplication of the virus at the wound site. It also prolongs the incubation period. Passive immunity should always be combined with vaccine therapy. ARS needs test dose prior to injection of full dose. Side effects: Serum sickness, anaphylaxis.
Human rabies immunoglobulin (HRIG). Dose is 20 units/kg body weight. Part is injected into the wound remaining part into the gluteal muscle (IM)—single dose. Patient should be immunised actively along with serum with additional booster doses. Side effects are rare here.
 
Post-exposure Prophylaxis
Cell culture and purified duck embryo vaccines are used as they are safe and efficacious.
All vaccines should be given to deltoid region (never to gluteal region as due to high fat content vaccine would not get absorbed into circulation rapidly and so immune response may not be optimum). Vaccines should be stored at 4–8°C after reconstitution and should be used immediately.
 
Mode of Injection
  1. Intramuscular into deltoid region—Essen regimen. It is commonly used and technically easier but higher dose is required compared to intradermal. It is injected at a schedule of 0, 3, 7, 14, and 28 days and booster at 90 days. First dose should be combined with ARS preferably HRIG. Multisite IM regime is often used as follows—first dose on day 0 two doses of IM vaccine is injected one on each side deltoid. Later single doses on 7 and 21 days (as 0 {2}, 7 {1}, 21 {1}).
  2. Intradermal route: (1) Two site intradermal method is used. 1/5th of the IM dose of selected vaccine is used. Two sites on the day 0, 3, 7 and one site on the days 28 and 90. PVRV 0.1 ml; PCECV 0.2 ml; PDEV 0.2 ml. (2) Eight site intradermal method is used. On day 0, eight sites intradermal injections at both deltoids, both suprascapular, both thighs, both lower quadrants of abdomen are given. On day 7, on 4 sites—both deltoids, both thighs intradermal injections are given. On days 28 and 90 one dose on each day intradermal vaccine is injected at one site. HDCV 0.2 ml is used. It is like 0 (8); 7 (4); 28 (1); 90 (1). In whatever type, on first day (0) rabies immunoglobulin should be injected locally as well as IM.
Postexposure vaccination if individual has been vaccinated earlier: Doses on days 0, 3, and 7 are given. But ideally assessed by serum antibody level (should be more than 0.5 IU/ml. Passive immunity is not given in individuals who had vaccination earlier.
 
Pre-exposure Prophylaxis
It is given to veterinarians, animal handlers. Dose: 1 ml of cell culture vaccine IM or 0.1 ml intradermally on days 0, 7, 28. Serum titre for antibodies should be assessed after 1 month. If it is less than 0.5 IU/ml then one booster dose is injected. Booster doses are given once in every 2 years.
 
RABIES IN DOGS
Incubation period: 10 days to 8 weeks.
 
Types
  1. Furious type: Here dogs are aggressive like a mad dog. Dog changes its behaviour with loss of fear of human beings; bites objects, eat, mud, etc. Running amok, voice change, inability to bark properly, excessive salivation and foaming, paralysis and death.
  2. Dumb type: Dog is paralytic and sleepy. There is no aggressiveness at all. Dog sleeps for 3 days and dies.
Once symptoms of rabies develop in a dog it rarely survives more than a week.
Dog brain is sent for study in 50% glycerol-saline solution.
 
Laboratory Tests to Confirm Rabies in Dogs/Animals
  • Fluorescent antibody test (FRA test): It is reliable test. If FRA test is negative in brain of animal then even if dog is rabid its saliva does not contain virus. FRA test is positive at any stage of the disease.
  • Microscopic examination of the brain of the infected dead animal to look for NEGRI bodies. It is seen in 90% of dead rabid dogs.
  • Mouse inoculation test is very sensitive test. 10% brain tissue emulsion in saline is centrifuged at 2000 rpm for 10 minutes; 0.03 ml top fluid is injected intracerebrally into the suckling mouse to demonstrate rabies in 8 days in mouse.
  • Corneal test is simpler but negative result does not rule out the infection possibility.
 
Immunisation in Animals
  1. BPL inactivated nervous tissue vaccine (20% infected sheep brain suspension): Single dose 5 ml to dogs; 3 ml to cats. Second dose after 6 months. Then once a year regularly.
  2. Modified live virus vaccine (33% infected chick embryo suspension): Dose—3 ml single dose which is repeated once in 3 years.
  3. Oral vaccines are used successfully to control wild foxes in Canada by placing vaccine in food through baits.
 
ANTHRAX
  • It is caused by Bacillus anthracis, which is a Gram-positive, aerobic, spore forming, capsulated, nonmotile, nonacid-fast bacillus and is resistant to heat and antiseptics.
  • Disease is common in cattle and seen in people who handle carcasses, wool, hairs.
  • It is often used in biological war.
 
Types
  1. Cutaneous type (Hide porter's disease)
    • It is the most common type and occurs within 3–4 days after infection.
    • Indurated papule with black slough surrounded by vesicles—malignant pustule. Itching is common in papule—black colour eschar (Anthrax means charcoal).
    • Regional lymph nodes are involved.
    • Toxaemia is common.
  2. Respiratory type (Wool Sorter's disease) is due to inhalation of spores, causing haemorrhagic pneumonia. It is more dangerous and life-threatening.
  3. Alimentary type due to ingestion of spores.
    • Fatal septicaemia and meningitis can occur in any type.
 
Diagnosis
  • Culture of fluid will show Medusa head appearance.
  • It shows positive M'Fadyean's reaction and positive Ascoli's thermoprecipitation test.
 
Treatment
  • Ciprofloxacillin, doxycycline, penicillins.
  • Alum precipitated Anthrax toxoid is used in humans.
  • Scalvo's serum prepared by active immunisation of asses are used.
 
NOSOCOMIAL AND OPPORTUNISTIC INFECTIONS
 
Nosocomial Infection (Hospital-acquired Infection)
It is an infection acquired because of hospital stay.
 
Sources
  • Contaminated infected wounds.
  • Urinary tract infections.
  • Respiratory tract infections.
  • Opportunistic infections.
  • Abdominal wounds with severe sepsis.
Spread can occur from one patient to another, through nurses or hospital staff who fail to practice strict asepsis.
 
Organisms
  • Staphylococcus aureus is the most common organism causing hospital-acquired wound infection. Others are Pseudomonas, Klebsiella, E. coli, Proteus.
  • Streptococcus pneumoniae, Haemophilus, Herpes, Varicella, Aspergillus, Pneumocystis carinii are the most common pathogens involved in hospital-acquired respiratory tract infection which spreads through droplets.
  • Klebsiella is the most common pathogen involved in hospital acquired UTI which is highly resistant to drugs.
 
Management
Most of the time, organisms involved are multi-drug resistant, virulent and hence, cause severe sepsis.
  • Antibiotics.
  • Isolation.
  • Blood, urine, pus for culture and sensitivity to isolate the organisms.
  • Blood transfusion, plasma or albumin therapy.
  • Ventilator support.
  • Maintaining optimum urine output.
  • Nutritional support.
 
Prevention
  • Isolation of patients with badly infected open wounds, severe RTI/UTI.
  • 63Following strict aseptic measures in OT and in ward by hospital attendants.
  • Proper cleaning and use of disinfectant lotions and sprays for bedpans, toilets and floor.
  • The precipitating causes have to be treated, along with caring for proper nutrition and improving the anaemic status by blood transfusion.
 
Opportunistic Infections
They are normally of low pathogenicity, occur through therapeutic invasive procedures and are common in immune deficiency status.
Therapeutic invasive procedures may be in the form of IV cannula, bladder catheter, tracheostomy and other minor surgical procedures which permit the skin organisms like Staphylococcus epidermidis to penetrate the skin and invade the deeper tissues.
 
Organisms
Bacteria: Gram-negative: E. coli, Pseudomonas, Klebsiella, Proteus, Serratia.
Gram-positive: Staphylococcus epidermidis, Streptococcus pneumoniae.
Viruses: Herpes, CMV, Varicella zoster, may cause fatal pneumonia.
Fungal: Candida, Aspergillus, yeast.
Protozoal: Cryptosporidia (causes diarrhoea), Pneumocystis carinii.
Because of the poor defence mechanism, infection is severe and often life-threatening.
 
Investigations
  • Swab culture, blood culture, pus culture.
 
Treatment
  • These infections are difficult to treat as they are often multi-drug resistant.
  • Combination of broad spectrum antibiotics—cephalosporins, aminoglycosides, metronidazole are given.
  • Depending on culture and sensitivity appropriate antibiotics are given.
  • Often ventilatory support and critical care are necessary.
 
NECROTISING FASCIITIS (Wilson, 1952)
  • It is spreading inflammation of the skin, deep fascia and soft tissues with extensive destruction, toxaemia commonly due to Streptococcus pyogenes infection, but often due to mixed infections like anaerobes, coliforms, Gram-negative organisms.
  • It is common in old age, smoking, diabetics, immunosuppressed, malnourished, obesity, steroid therapy and HIV patients. Trauma is a common precipitating factor/cause—80%.
  • It can occur in limbs, lower abdomen (Meleney‘s infection), groin, perineum. There is acute inflammatory response, oedema, extensive necrosis and cutaneous microvasculature thrombosis.
  • Muscle is usually not involved in necrotising fasciitis.
zoom view
Figs 1.127A and B: Necrotising fasciitis of skin, deep fascia and soft tissues without involvement of muscle.
64 
Clinical Features (See Table)
  • Sudden swelling and pain in the part with oedema, discoloration, necrotic areas, ulceration.
  • Foul smelled discharge.
  • Features of toxaemia with high-grade fever and chills, hypotension.
  • Oliguria often with acute renal failure due to acute tubular necrosis.
  • Jaundice.
  • Rapid spread in short period (in few hours).
  • Features of SIRS, MODS with drowsy, ill-patient.
  • Condition if not treated properly may be life-threatening.
Note:
LRINEC (Laboratory Risk Indicator for Necrotising Fasciitis) scoring system is very useful to assess the severity. Parameters used are – C- reactive protein (less or more than 150 mg/L); TC (less than 15,000; 15,000 to 25,000; more than 25,000); Hb% (> 13.5 g, 11 to 13.5, < 11); serum sodium (> 135 or less than 135); serum creatinine ( less or more than 1.6); blood sugar (less or more than 180 mg). Score > 8 is severe; 6–8 is moderate; < 8 is good.
 
Management
  • IV fluids, fresh blood transfusion.
  • Antibiotics depend on C/S or broad-spectrum antibiotics. High dose penicillins are very effective. Clindamycin, third generation cephalosporins, aminoglycosides are also often needed.
  • Catheterisation and monitoring of hourly urine output.
  • Haematocrit, serum creatinine assessment.
  • Pus culture, blood culture.
  • Electrolyte management and monitoring.
  • Control of diabetes, if patient is diabetic.
  • Oxygen, ventilator support, dopamine, dobutamine supplements whenever required.
  • Radical wound excision of gangrenous skin and necrosed tissues at repeated intervals.
    zoom view
    Figs 1.128A and B: Necrotising fasciitis over chest wall and neck in two different patients.
    zoom view
    Figs 1.129A to C: The typical necrotising fasciitis showing gangrenous skin. In second photo, arm is extensively involved. Also note the granulating area after extensive wound excision of the necrotic skin (debridement).
  • Vacuum assisted dressing is better.
  • Once patient recovers and healthy granulation tissue appears, spilt skin grafting is done. As it commonly involves large area, mesh graft (meshing of SSG) is needed.
 
ACUTE PYOMYOSITIS
  • It is infection and suppuration with destruction of the skeletal muscle, commonly due to Staphylococcus aureus (90%) and Streptococcus pyogenes, occasionally due to Gram-negative organisms.
  • It is common in muscles of thigh, gluteal region, shoulder and arm.
  • Precipitating factors are similar to necrotising fasciitis—trauma, malnutrition, anaemia, and immunosuppression.
  • Pain, oedema, tenderness over the site with apparently normal overlying skin.
  • Induration and muscle spasm is typical.
  • Fever, jaundice, uraemia (acute renal failure) are common.
65
 
Management
  • Creatine phosphokinase will be very high and signifies acute phase (more than 50,000 units); due to rhabdomyolysis.
    zoom view
    Fig. 1.130: Pyomyositis of thigh muscle.
  • MRI is useful. US guided pus aspiration is also done.
  • Treatment is antibiotics, radical wound excision with removal of pus and all necrosed muscle and compartment release. Haemodialysis is needed until recovery if there is renal failure. Later secondary suturing or skin grafting is needed.
 
SURGICAL SITE INFECTION (SSI)
Surgical site infection is the second most common complication following surgical procedures (first being postoperative pneumonia) due to virulent bacterial entry, altered wound microenvironment, and changed host defense. Prevention of SSI can be achieved by better preoperative preparation; proper infection control during surgery; adherence to principles of preventive antibiotic therapy; better surgical techniques to reduce haematoma, tissue injury and foreign bodies within the surgical site; prevention of tissue hypoxia with enhanced oxygen support.
 
Common Sources of Infection
  • Surgical wards, wounds, ulcers, catheters, drains, sputum, urine, faeces, open wounds.
  • Operation room without proper ventilation, nurses, surgeons. Operation methods, sterilisation of instruments.
 
Organisms Causing SSI
  • Commonly Staphylococcus aureus. Any organisms like clostridia, Gram-negative bacteria can cause SSI.
  • Bacteria present in a wound with no signs or symptoms of systemic inflammation is called as colonization, usually less than 105cfu/ml. Transient exposure of a wound to bacteria (usually less than 6 hours) is called as contamination with varying concentration.
 
Sequence of Events (in Surgical Wounds)
  • Activation of inflammation occurs by cuts, incisions, abrasions, burns. This initiates inflammation by protein coagulation, platelet aggregation, mast cell activity, release of complements and bradykinin. Phase I of inflammation begins with vasodilatation, increased bulk flow, increased vascularity. Later Phase II of inflammation proceeds with phagocytic infiltration and bacterial phagocytosis, removal of dead tissue with release of proinflammatory cytokines. Here tissue injury from incision mobilizes phagocytes before bacterial contamination leading into prior preparation against infection. If contamination is controlled monocytes activate to regulate wound healing using myofibrocytes and collagen.
  • If bacterial contamination is not controlled, proinflammatory cells release TNF-α to stimulate neutrophils for phagocytosis. It also causes release of reactive oxygen and acid hydrolases from lysosomal vacuoles to result in lipid peroxidation, release of interleukins, evoking acute inflammatory response with creation of space containing pus which contains necrotic tissue, neutrophils, bacteria and proteinaceous fluid with all signs of inflammation—rubor, dolor, calor, tumour. It is typical surgical site infection (SSI).
 
Factors Related to SSI
  • Bacterial entry (inoculum) into the wound occurs through air in operation room, through instruments, through surgeons and theatre staffs, patient's endogenous bacteria like perineum, urine, etc.
  • Bacterial virulence plays major role in causing SSI.
  • Microenvironment in the wound like haemoglobin level at surgical site; presence of necrosis which interferes with phagocytosis; presence of dead space and or foreign body in the wound.
  • Host defences both natural (Innate) and acquired, when altered SSI occurs. Acquired causes are—shock, hypoxia, chronic illness, hypoalbuminemia, malnutrition, hypothermia, hyperglycemia, corticosteroids, HIV infection, malignancy and certain drugs.
 
Classification of Surgical Wounds
  • Clean wounds—operative procedure does not enter into normally colonised viscus.
  • Clean-contaminated—operation enters into a colonised viscus but under elective controlled circumstances.
  • Contaminated wounds—gross contamination is present at the surgical site in the absence of obvious infection.
  • Dirty wounds—surgical procedures performed when active infection is present.
 
Risk Classification and Identification System
It is based on three categories of variables—(1) Those that estimate intrinsic degree of microbial contamination at the surgical site. (2) Those that measure the duration of operation. (3) Host susceptibility markers.
 
Variables that influence SSI
Variables that influence SSI
Point
1. An abdominal operation.
1
2. Operation lasting more than 2 hours.
1
3. Surgical site classified as contaminated or dirty/ infected.
1
4. Operation performed on a patient with more than three discharge diagnosis.
1
Total index
4
All variables have equal significance. This index twice better at predicting SSI than wound classification. Disadvantage is that it is not operation specific and variables collected at discharge.
66
 
The National Nosocomial Infections Surveillance (NNIS) System as Basic SSI Risk Index
NNIS system
Point
Operation classified as contaminated or dirty.
1
The patient has an ASA (American Society of Anaesthesiology) preoperative assessment score of 3, 4, or 5.
1
Duration exceeds 75th percentile of ‘T’ point.
‘T’ point defined as length of time in hours that represents 75th percentile of procedures in NNIS survey.
1
Note:
T point for common surgical procedures are—coronary artery bypass graft—5; Bile duct, liver or pancreatic surgery, craniotomy, head and neck surgery—4; Colonic surgery, joint prosthesis surgery, vascular surgery—3; Abdominal or vaginal hysterectomy, ventricular shunt, herniorrhaphy—2; Appendicectomy, limb amputation, caesarean section—1.
 
Physical status classification
Class I: A patient in normal health.
Class II: A patient with mild systemic disease resulting in no functional limitations.
Class III: A patient with severe systemic disease that limits activity, but is not incapacitating.
Class IV: A patient with severe systemic disease that is a constant threat to life.
Class V: A moribund patient not likely to survive 24 hours.
 
Classification of Surgical Site Infection (SSI)
 
A. According to the Depth of the Wound Infection
1. Superficial incisional SSI
It occurs within 30 days of operation; involves only skin and subcutaneous tissue; and one of following:
Purulent drainage (culture documentation not required), organisms isolated from fluid/tissue of superficial incision, at least 1 sign of inflammation, wound is deliberately opened by the surgeon, surgeon or attending physician declares that the wound is infected.
A wound is not considered as superficial site infection—if stitch abscess is present; if infection is at episiotomy site; burn wound, SSI extends into the fascia or muscle.
2. Deep incisional SSI
It occurs within 30 days of operation or 1 year if an implant is present; involves deep soft tissues of the incision; and at least one of the following—purulent drainage from the deep incision site without organ/space involvement, fascial dehiscence or deliberate separation by surgeon, deep abscess, identified by—reoperation/histopathology/radiology, surgeon or attending physician declares deep infection present.
3. Organ space infection
It occurs within 30 days or 1 year if an implant is present; involves anatomic structures not opened or manipulated during surgery; and one of the following—pus from a drain placed into organ/space, organism isolated by culture, identification of abscess by direct examination, reoperation, histopathology, radiology, diagnosis by surgeon or attending physician.
zoom view
Fig. 1.131: Surgical site infection classification as—superficial incisional, deep incisional, organ space.
zoom view
Figs 1.132A to C: Surgical site infection (SSI) types: (A) Superficial incisional SSI. (B) Deep incisional SSI. (C) Organ space SSI.
 
B. Classification of Wound Infection According to the Aetiology
  1. Primary infection where the wound is the primary site of infection.
  2. Secondary infection arises following a complication that is not directly related to the wound.
 
C. Classification of Wound Infections According to the Time
  1. An early infection presents within 30 days of a surgical procedure.
  2. An intermediate infection occurs between 1-3 months afterwards.
  3. Late infection occurs in more than three months after surgery.
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D. Classification of Wound Infections According to the Severity
  1. Minor wound infection if there is discharge without cellulitis or deep tissue destruction.
  2. Major if the discharge of pus is associated with tissue breakdown, partial or total dehiscence of the deep fascial layers of the wound, or if systemic illness is present.
Note:
Please refer first page of this Chapter for Southampton wound grading system and Asepsis wound score system.
 
Prevention of SSI
 
1. Preoperative
  • Preoperative cleaning and antiseptic scrub of surgical site. Skin is colonised by various bacteria mainly Staphylococcus aureus (50%). Preoperative skin wash using chlorhexidine decreases bacterial colonisation by 80% and so wound contamination.
  • Surgical site to be shaved or clipped in the operation theatre. Shaving should be done in the theatre itself or within 2 hours of beginning of the surgery otherwise infection rate may raise. Clean wound infection after shaving is 2.3%; after clipping it is 1.7%; without shaving or clipping it is 0.9%. However, selective shaving is definitely needed in area like scalp, axilla, groin, and perineum.
  • Surgery should be avoided or postponed if fingers or hand of surgeon has open wounds or infection.
  • Obvious infection in patient if exists should be treated.
  • Prolonged preoperative admission should be avoided for an elective surgery.
 
2. Care in the Operation Theatre
  • One should ensure that sterile caps, masks, gowns and sterile gloves are used.
  • Proper skin cleaning is needed on table after anaesthesia using antiseptics like povidone iodine. One should ensure that all drapes are dry throughout the procedure and all instruments are thoroughly sterilised.
  • Unimpregnated plastic drapes are avoided as it is found that it does not have any advantage.
  • Gentle tissue handling, absolute haemostasis, holding tissues using instruments as much as possible, using appropriate suture materials, avoiding dead space during closure are certain essential on table tips to reduce SSI.
  • One should consider leaving wounds open if it is severely contaminated.
 
3. Preventive Antibiotic Therapy
  • It is used whenever high-risk of infection is associated with the procedure and consequences of infection if possibly severe and if patient has a high NNIS risk index.
  • Antibiotics should be administered as close to the incision time as possible, before induction of anaesthesia.
  • Selected antibiotic should have activity against likely pathogens.
  • Postoperative systemic antibiotics for 24 hours (beyond 24 hours not shown to reduce SSI).
  • Benefit of preoperative antibiotics in NNIS risk 0 index is difficult to assess and quantify.
  • Proper techniques and wound microenvironment are more important than antibiotics.
  • Preventive systemic antibiotics not to be used to prevent nosocomial infections.
  • Oral antibiotic bowel preparation with appropriate mechanical bowel preparation.
  • If systemic antibiotics are to be used antibiotics of longer half-life are to be chosen.
  • Very long procedures should have a redosing strategy during the procedure.
 
4. Enhancement of Host Defences
  • Increased oxygen delivery facilitates phagocytic eradication of microbes.
  • Optimising core body temperature is important as warmer patients resist bacteria better.
  • Blood glucose control is essential even to nondiabetics as well.
 
Management of SSI
  • SSI is managed depending on the type of SSI—superficial, deep or organ space.
  • All infected material and pus should be removed from the wound site—debridement.
  • Sutures are removed to allow free drainage of infected material.
  • Infected fluid is sent for culture and sensitivity and suitable antibiotics are started.
  • Once wound shows signs of healing by healthy granulation tissue, secondary suturing is done. Often it is allowed to heal by scarring.
Different definitions
Contamination
Bacteria are on the wound surface. No division is occurring
Colonization
Bacteria are dividing
Topical infection (Critical colonization)
Bacteria are dividing and have invaded the wound surface. There may be an increasing variety of bacteria present; Biofilm may be present
Local infection
Bacteria and/or their products have invaded the local tissue
Regional/Spreading infection/Cellulitis
Bacteria and/or their products have invaded the surrounding tissue
Sepsis
Bacteria and/or their products have entered the blood stream and may have spread to distant sites or organs
 
HIV INFECTION AND AIDS (Acquired Immunodeficiency Syndrome)
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Definition of AIDS
Confirmed HIV infection with CD4 T lymphocyte count < 0.2 × 106/L with symptoms.
 
Human Immunodeficiency Virus
It was discovered by Barre-Sinoussi and Montagnier in 1983.
 
Types
It is classified under HTLV Type III. HIV is subdivided into Type 1 and Type 2.
They are retroviruses.
 
Mode of Transmission
  • Sexual intercourse—vaginal or anal.
  • Needle pricks—using unsterilised needles for injections, in IV drug abusers, careless handling.
  • Mother to child—during birth through vaginal secretion, transplacental, through breast milk.
  • Blood transfusions, organ transplantations.
Disease is common in Africa and Asian countries.
HIV mainly harbours in semen, genital secretions, blood, pus, sputum, saliva and other body fluids.
 
Tests for HIV
  1. ELISA test (screening test).
  2. Western blot test (diagnostic test).
  3. Polymerase Chain Reaction (PCR).
  4. Anti-HIV antibody detection.
  5. Viraemia quantification—to start treatment and to see the response of antiviral drugs (useful if it is within 0.5 log 10).
  6. CD4+ count
    • Normal value > 500/mm3.
    • Values between 200–500/mm3 is seen in Kaposi sarcoma, Candida infection, Mycobacterium tuberculosis.
    • Values between 50–200/mm3 is seen in Pneumocystis carinii and Toxoplasma infections.
    • Values < 50/mm3 is seen in atypical mycobacteria, cytomegalovirus, lymphomas.
After HIV infection, there is a time gap for the patient to become reactive to tests. This time gap is called as “Window period”. This period is variable. But during this period, the individual is infective.
 
Pathogenesis
Envelope glycoprotein of HIV binds with the surface molecule CD4 of ‘T’ lymphocytes, monocytes, macrophages, cutaneous Langerhan's cells, dendritic cells of all tissues.
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Fig. 1.133: HIV patient presented with tuberculous cold abscess with discharging sinus.
CD4 of lymphocytes—T helper cells induce and control the normal immune response.
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Figs 1.134A and B: Picture showing HIV kit and wearing of the HIV kit as a precaution while doing surgery for HIV infected individuals.
HIV suppresses immune response completely directly by suppressing ‘T’ cell, indirectly by suppressing ‘B’ cell. Finally it dismantles and destroys the immune system making the individual prone to opportunistic infections.
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Fig. 1.135: Severe infection of ear cartilage in a HIV infected patient.
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After HIV infection, antibodies develop to virus envelope and core proteins which persist throughout life.
 
General Features in HIV
  • Weight loss more than 10%.
  • Fever more than 1 month.
  • Diarrhoea more than 1 month.
  • Neuralgia, arthralgia, headache.
  • Lymphadenopathy.
  • Cutaneous rashes, dermatitis, fungal (Candida), bacterial, viral (herpes simplex 1 and 2) infection.
  • Dental infection, gingivitis, candidiasis of oral cavity and oesophagus.
  • Varicella zoster infection.
  • Opportunistic infections.
  • Poor healing after surgery, trauma, infection with more complications.
 
Tumours in HIV Infection
  • Kaposi's sarcoma—40% common.
  • Lymphomas (NHL common) (3–4%).
  • Cervical cancer.
  • CNS lymphomas.
  • Ano-genital squamous cell carcinoma.
  • Testicular tumours (Germ cell types).
  • Lung cancer.
  • GIT lymphomas and adenocarcinomas.
  • Squamous cell carcinoma of anal canal and cervix.
 
Pulmonary Problems in HIV Infection
  • Pneumonia.
  • Tuberculosis.
  • Fungal infections.
  • Pneumocystis carinii pneumonia.
  • Cytomegalovirus pneumonia.
 
GIT Problems in HIV Infection
  • GIT infections—bacterial, protozoal, viral.
  • Kaposi's sarcoma, lymphomas, adenocarcinomas.
  • Hepatitis (‘C’ virus), cholestasis.
  • Anorectal diseases.
  • Abdominal tuberculosis.
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    Fig. 1.136: Kaposi's sarcoma.
 
Neurological Problems in HIV Infection
  • Encephalitis, aseptic meningitis, myelitis.
  • Neuropathies with demyelination.
  • Opportunistic infections like Toxoplasma, Cryptococcus causing severe meningitis.
  • Primary CNS lymphomas.
  • CNS tuberculosis (Tuberculomas).
  • Visual problems.
 
Management
Investigations
  • Tests for HIV.
  • Tests for specific and opportunistic infections.
  • Tests relevant for associated tumours.
Treatment
  1. Antiviral therapy:
    • 70Nucleoside reverse transcriptase inhibitor (NRTI): Zidovudine, didanosine, abacavir, lamivudine, stavudine.
    • Non-nucleoside reverse transcriptase inhibitor (NNRTI): Nevirapine, delavirdine.
    • Protease inhibitors: Ritonavir, indinavir, amprenavir.
  2. Treatment of opportunistic infections.
  3. Treatment of tumours.
  4. Immunotherapy:
    • Alpha and gamma interferons.
    • Interleukins.
  5. Bone marrow transplantation.
  6. Anti-CD3 or IL-2 after HAART (Highly Active Anti-Retroviral Therapy).
  7. Psychotherapy.
  8. Counselling of HIV patients and their families.
  9. Life-expectancy after initial HIV infection is 8-10 years.
Prevention
Continues to be our best weapon in combating the menace of HIV infection.
  • Safe sex. Condom usage reduces the risk of transmission.
  • Health education.
  • Use of disposable needles to prevent infections.
HIV, hospital and surgeon
  • Isolation per se of HIV patient is not required.
  • Proper care should be taken to prevent transmission of the virus.
  • Open wounds, disposal of excreta, fluids, discharge, pus and other infective materials should be taken care of properly.
  • Risk of HIV infection through needle prick is very less (0.03%).
    Following measures should be taken while managing HIV patients:
  • Wearing double gloves.
  • Wearing proper spectacles (as HIV can get transmitted through eyes directly).
  • Wearing proper head mask, theatre shoes, apron.
  • Measures to prevent spread of infection from patient to patient in the hospital.
  • Disposal of needles through a sharp disposing container.
Disinfection
  • Autoclave is ideal.
  • Boiling.
  • Sodium hypochlorite solution.
  • 2% glutaraldehyde solution.
71E. Swellings
CHAPTER OUTLINE
  • ❖ Lipoma
  • ❖ Cysts
  • ❖ Dermoids
  • ❖ Sebaceous cyst
  • ❖ Glomus Tumour
  • ❖ Papilloma
  • ❖ Warts
  • ❖ Fibroma
  • ❖ Bursae
  • ❖ Semimembranosus Bursa
  • ❖ Morrant Baker's Cyst
  • ❖ Lymph Cyst
  • ❖ Lymphangioma
  • ❖ Calcinosis Cutis
  • ❖ Neuroma
  • ❖ Neurofibroma
  • ❖ Neurilemmoma
  • ❖ Ganglion
  • ❖ Chordoma
  • ❖ Epignathus
 
Swelling means obvious enlargement of a part of the body due to various causes like congenital, inflammatory or neoplastic. Mass denotes the lesion with difficulty to define the extent – mass abdomen; lump denotes defined lesion within the organ or causing the alteration in the gross nature/shape of the part or organ like – lump in the breast.
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Fig. 1.137: Swelling scalp; could be sebaceous cyst.
 
LIPOMA
  • It is a benign neoplasm arising from yellow fat. Often it can be hyperplasia or combination of neoplasm and hyperplasia.
  • A lipoma is composed of mature adipocytes and uniform nuclei that are identical to those seen in normal adult fat. The fat in lipoma is considered unavailable for general metabolism.
  • It is the most common benign tumour (karyotype 12q change). Prevalence is 2.1 per 100 people.
  • It is called as universal tumour (ubiquitous tumour) as it can occur anywhere in the body except brain.
  • It can be localised (encapsulated) or diffuse (nonencapsulated).
    • Localised lipoma is encapsulated with yellowish orange colour.
    • Diffuse lipomas are not encapsulated and not localised. It is common in palm, sole, head, neck. It is seen in subcutaneous and intermuscular tissues. It is difficult to remove surgically. Recurrence is high after incomplete removal.
  • Lipoma can be superficial or deep.
    • Superficial lipomas are more common; common in subcutaneous plane. It is common in back, neck, proximal extremities and abdomen. It is commonly less than 5 cm; but can attain large size. There is no gender predisposition.
    • Deep lipomas are commonly intramuscular, but often may be intermuscular; often both intra- and intermuscular (infiltrating lipoma). They are common in lower limbs (45%), trunk (17%), shoulder and upper limb. They attain large size compared to superficial lipomas. They are more common in men.
  • Lipoma can be single or multiple.
    • Single lipoma is common. It is usually superficial in subcutaneous plane but can be deep also.
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      Figs 1.138A and B: Large lipoma in the nape of neck.
    • 72Multiple lipomas are 15% common; common in males (6:1). Common in back, shoulder and upper arm; can be symmetrical. It can be associated with many syndromes like multiple endocrine neoplasia (MEN), Cowden's, Frohlich, Proteus, Bannayan-Zonana syndromes.
    • Multiple lipomatosis represents a diffuse overgrowth of mature adipose tissue; involves subcutaneous and muscular planes extensively; common in shoulder and pelvic girdles. It is common in younger age group. 30% of them are familial; Adiposa dolorosa (Dercum's disease) is a multiple lipomatosis mainly seen in females (30:1—female to male ratio); there is tender fat deposition especially in the trunk and girdles; it is common in epileptic and psychiatric patients.
  • Benign tumour arising from brown fat is called as hibernoma (reddish brown), which has got serpentine vascular elements.
  • Lipoma with fibrous component is called as fibrolipoma (most frequent nonlipomatous component in lipoma is fibrous tissue). Fibrolipoma is nonseptal.
  • Lipoma with telangiectasis is called as naevolipoma.
  • Neurolipoma (with nerve tissue and is painful), angiolipoma (with vascular element), myolipoma, chondroid lipoma, spindle cell lipoma, pleomorphic lipoma – are different types depending on the type of nonadipose component associated.
  • Lipoblastoma is a benign tumour of immature fat occurring in infant boys in subcutaneous tissue of extremity.
  • Benign lipomatous lesions may occur focally in a joint or tendon sheath or with diffuse villonodular proliferation in the synovium—lipoma arborescens. Synovectomy may be needed in this patient.
  • Malignant transformation of lipoma is non-existent. Liposarcoma does not arise from mature fat cells but from primitive mesenchymal cells.
 
Sites
 
Clinical Features
  • Localised swelling, which is lobular (surface), nontender.
  • Often fluctuant like feel but actually not (because fat in body temperature remains soft). It is usually nontransilluminant.
  • Mobile, with edges slipping between the palpating fingers (slip sign).
  • Skin is free.
  • Lipomas may be pedunculated at times.
  • It is rare in children.
  • Pain in lipoma may be due to neural element or compression to nerves or adjacent structures. Angiolipomas being highly vascular is commonly tender.
  • Trunk is the most common site; nape of neck and limbs are next common.
  • Clinically lipoma can be single, multiple or diffuse.
Note:
A diagnostic criterion used by some clinicians for superficial lipomas is hardening of swelling after application of ice. This test is of less important.
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Figs 1.139A and B: Diffuse lipoma on the plantar aspect of foot and back.
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Fig. 1.140: Slip sign of lipoma.
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Fig. 1.141: Large lipoma in the back over scapula.
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Fig. 1.142: Pedunculated lipoma. It is common in axillary region. Lobular surface with narrow pedicle is typical. Often ulceration can occur in the surface due to repeated friction. It often mimics papilloma.
 
Differential diagnosis
  • Neurofibroma – it moves horizontally but not longitudinally along the line of the nerve. Neurofibroma is firmer.
  • Cystic swellings like dermoid, sebaceous cyst.
  • Liposarcoma – all lipomas are benign. Large lipoma should be differentiated from liposarcoma.
  • Other soft tissue tumours.
 
Investigations
  • Ultrasound or CT or MR imaging is done in deep or large or intracavitary lipomas.
  • FNAC or incision biopsy is needed in large or deep or intracavitary lipomas to confirm it as benign.
 
Complications
  • Myxomatous changes—occurs in retroperitoneal lipoma.
  • Saponification.
  • Calcification—11% mineralization.
  • Submucosal lipoma can cause intussusception and so intestinal obstruction.
Note:
It is now considered that all sarcomas are of de novo in origin to begin with at mitochondrial level; so benign soft tissue tumour turning into sarcoma is not existing (except of neural origin like neurofibroma).
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Figs 1.143A and B: Large lipoma in buttock region.
 
Treatment
  • Excision.
  • Small lipoma is excised under local anaesthesia and larger one under general anaesthesia.
  • Recurrence is 11%
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Fig. 1.144: Gross feature of specimen of lipoma.
 
CYSTS
Cyst is a collection of fluid in a sac lined by epithelium or endothelium. Word meaning of cyst isbladder” (Greek) (Greek word ‘KUSTIS’ means bladder).
 
True Cyst
  • Cyst wall is lined by epithelium or endothelium.
  • If infection occurs, cyst wall also will be lined by granulation tissue.
  • Fluid is usually serous or mucoid derived from the secretion of the lining.
 
False Cyst
  • It does not have epithelial lining.
  • Fluid collection occurs as a result of exudation or degeneration.
Example:
  • Pseudocyst of pancreas.
  • Wall of cystic swelling in tuberculous peritonitis.
  • Cystic degeneration of tumour.
  • After haemorrhage, in a haematoma, RBC's are lysed, gets absorbed and fluid remains as a false cyst.
    Apoplectic cyst” is formed in brain as a result of ischaemia, causing collection of fluid.
 
Classification
  1. Congenital cyst
    • Dermoids: Sequestration dermoid.
    • Tubulodermoids: Thyroglossal cyst, postanal dermoid, ependymal cyst, urachal cyst.
    • Cysts of embryonic remnants: Cysts from paramesonephric duct and mesonephric duct, cysts of urachus and vitellointestinal duct.
  2. Acquired cysts
    • Retention cysts: They are accumulation of secretions of a gland due to obstruction of the duct, e.g. sebaceous cyst, Bartholin's cyst, cyst of parotid, breast, epididymis.
    • Distention cyst: Lymph cyst, ovarian cyst, colloid goitre.
    • Exudation cyst: Bursa, hydrocoele, pancreatic pseudocyst.
  3. Cystic tumours: Dermoid cyst of ovary, cystadenomas.
  4. Traumatic cyst: Due to trauma, haematoma occurs usually in thigh, loin, shin. It eventually gets lined by endothelium containing brown coloured fluid with cholesterol crystals.
  5. Degenerative cyst: Due to cystic degeneration of a solid tumour (due to necrosis of tumour).
  6. Parasitic cyst: Hydatid cyst, trichiniasis, cysticercosis.
 
Clinical Features of a Cyst
  • Hemispherical swelling which is smooth, fluctuant, nontender, well-localised.
  • Some cysts are transilluminant.
  • Presentation varies depending on its anatomical location and pathology.
  • Cyst can be single or multiple. Sebaceous cysts are often multiple.
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Figs 1.145A and B: Traumatic cyst thigh with false cyst wall with clot inside.
 
Effects of a Cyst
  • Compression of adjacent structures (CBD): Choledochal cyst compressing over the CBD.
  • Infection.
  • Sinus formation.
  • Haemorrhage.
  • Torsion, e.g. ovarian cyst.
  • Calcification, e.g. hydatid cyst, cysticercosis.
  • Cachexia: In malignant ovarian cyst patient goes for severe cachexia.
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Figs 1.146A and B: Brilliantly transilluminant swellings—possibly lymph cyst.
 
DERMOIDS
 
Types
 
1. Sequestration Dermoids
  • It occurs at the line of embryonic fusion, due to inclusion of epithelium beneath the surface which later gets sequestered forming a cystic swelling in the deeper plane.
  • It is congenital type.
  • Dermoids occurring in the skull may extend into the cranial cavity.
  • When it occurs as an external angular dermoid, it extends into the orbital cavity.
  • It can extend into any cavity in relation to its anatomical location (e.g. thorax, abdomen).
Types of angular dermoid
  1. External angular dermoid:
    It is a sequestration dermoid situated over the external angular process of the frontal bone. Outer extremity of the eyebrow extends over some part of the swelling. This typical feature differentiates it from the swelling arising from the lacrimal gland. It may extend into the orbital cavity also (Frontozygomatic suture).
  2. Internal angular dermoid:
    It is a sequestration dermoid cyst in central position near the root of the nose. It occurs in frontonasal suture line. It is rare. It mimics swelling from lacrimal sac or mucocele of frontal sinus. Mucocele of frontal sinus is due to blockage of frontonasal duct.
  • Dermoid cyst contains putty like desquamated material, hair follicle, sebaceous and sweat glands. It is lined by both dermal and epidermal components.
  • Dermoid cyst in skull region has different anatomical types as it often may extend into cranial cavity.
    • Cyst which is located entirely outside the skull bone over suture line but without bone indentation.
    • Cyst located outside the skull bone but with a bone defect underneath. Bone defect may be either on outer table of skull or through both tables of skull with attachment to dura.
    • Cyst lying partly outside and partly inside the skull with a connecting stalk between the two like a dumb bell.
    • Cyst is entirely within the skull bone between skull and dura. It is very rare but known.
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Fig. 1.147: Sequestration dermoid in skull—anatomical types.
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Figs 1.148A and B: Types of angular dermoid. (A) External angular dermoid. (B) Internal angular dermoid (midline).
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Fig. 1.149: Postauricular dermoid in different patients.
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Figs 1.150A and B: Dermoid in the midline—suprasternal space of Burns/sternum. It may extend into deeper plane and so it needs CT chest and evaluation.
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Fig. 1.151: External angular dermoid, right sided.
Clinical features
  • Painless swelling in the line of embryonic fusion.
  • Presents in the second or third decade onwards.
  • Smooth, soft, nontender, fluctuant (Paget's test positive, i.e. swelling is fixed with two fingers and summit is indented to get yielding sensation due to fluid).
  • Nontransilluminating.
  • Free skin, often adherent into the deeper plane.
  • There will be resorption and indentation of the bone beneath.
  • Impulse on coughing may be present only if there is intracranial extension.
Differential diagnosis
  • Sebaceous cyst.
  • Lipoma.
Investigations
  • X-ray—skull or part.
  • CT scan head or part.
Treatment
  • Excision is done under general anaesthesia. Often formal neurosurgical approach is required by raising cranial osteocutaneous flaps.
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Fig. 1.152: Dermoid in the ear. It arises due to sequestration at the fusion line of the one of the six developmental ear tubercles (Each ear develops from six ear tubercles).
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2. Tubulodermoids
It arises from the embryonic tubular structures; it is due to accumulation of secretions of the lining of the unobliterated portion of congenital ectodermal tube / duct.
Thyroglossal cyst—It is due to persistent thyroglossal duct during development of the thyroid gland.
Ependymal cyst—They originate from the sequestration of the neuroectodermal cells. They are benign neuroepithelial cysts lined by ependymal cells. They are most commonly located deep in the parenchyma. Ependymal cysts have been postulated to be the entity responsible for the interhemispheric cysts with the Dandy walker cyst and agenesis of the corpus callosum. Large cyst can cause obstructive hydrocephalous.
Post-anal dermoid—It develops from post-anal gut, i.e remnant of neuroenteric canal probably as a teratoma; located in front of the sacrum and coccyx. It is symptomless unless attains a large size or infected or causes pressure symptoms. Rectal examination reveals the cyst. It is treated by complete excision. Coccyx may need to be removed to have an easy access.
Urachal cyst—It arises from the remnant of the urachus; presents as swelling in the midline at lower abdomen as extraperitoneal mass. It can get infected, or rupture into umbilicus or peritoneal cavity or calculi can form or adenocarcinoma can develop in the cyst.
 
3. Implantation Dermoid
  • Due to minor pricks or trauma, epidermis gets buried into the deeper subcutaneous tissue which causes reaction and cyst formation (trauma is forgotten often). It is an acquired cyst.
  • It is common in fingers (common in tailors, gardeners), toes and feet.
features
  • Swelling is painless, observed after minor trauma, slowly progressing in fingers or toes.
  • It is smooth, soft, mobile, tensely cystic, non-transilluminating and is often adherent to skin.
  • It contains only squamous epithelium, without hair follicle/sweat or sebaceous glands.
  • Complications are infection, rupture and pressure effect over digital nerves.
  • Differential diagnosis: Lipoma, Bursa.
  • Treatment: Excision—under local anaesthesia.
 
4. Teratomatous Dermoid
  • It arises from all germinal layers ecto-, meso- and endoderms.
  • It occurs in ovary, testis, retroperitoneum, mediastinum.
  • It contains hair, teeth, cartilage, sebum and muscle.
  • It can be benign or malignant.
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Figs 1.153A and B: Implantation dermoid finger and thumb—classical site.
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Figs 1.154A and B: Implantation dermoids in the hand and foot.
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Fig. 1.155: Dermoid cyst ovary right sided.
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Fig. 1.156: Cut section of dermoid cyst ovary showing sebum.
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Fig. 1.157: Twisted gangrenous cyst ovary.
 
SEBACEOUS CYST (Wen, Epidermoid Cyst)
  • It is a retention cyst. It is due to blockage of the duct of sebaceous gland, causing a cystic swelling. Sebaceous glands are situated in dermis which secretes sebum through sebaceous duct which opens either directly to skin surface or in to a hair follicle.
  • It is common in face, scalp, scrotum.
  • It is not seen in palms and soles as there are no sebaceous glands.
  • Sebaceous cyst contains yellowish white cheesy material with fat and epithelium. It has putty like consistency, with a parasite in the wall of the sebaceous cyst—Demodex folliculorum. It is lined by only epidermal layer of squamous epithelium.
 
Clinical Features
  • Painless swelling which is smooth, soft, nontender, freely mobile, adherent to skin especially over the summit, fluctuant (positive Paget's test), nontransilluminating with punctum over the summit.
  • It moulds on finger indentation.
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Figs 1.158A and B: Small sebaceous cysts in face and back with typical punctum over the summit.
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Figs 1.159A and B: Large sebaceous cyst in the face and scalp. Note the hair loss on the surface.
Sequestration dermoid
Sebaceous cyst
  • Occurs in the line of fusion
  • Occurs anywhere except palm and sole
  • Skin is not adherent (free)
  • Skin is adherent over summit
  • Extends often into deeper plane or cavities through suture line
  • Subcutaneous plane—do not extend to deeper plane
  • Punctum is absent
  • Punctum is present—70% cases
  • Bone resorption and indentation is common
  • Freely mobile without bone resorption
  • With restricted mobility
  • Superficial swelling, mobile
  • Needs proper evaluation with X-ray/CT scan
  • Excision is done under general anaesthesia
  • Excision is done under local anaesthesia
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Fig. 1.160: Infected sebaceous cyst face.
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Fig. 1.161A:
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Figs 1.161A and B: Sebaceous cyst showing moulding sign.
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Fig. 1.162: Strawberry scrotum—multiple sebaceous cysts on the scrotum.
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  • Punctum is present over the summit in 70% of cases because here sebaceous duct opens directly into the skin which gets blocked. Punctum is depressed black coloured spot over the summit of the sebaceous cyst. Because of the denuded squamous epithelium (keratin), it is black in colour. In 30% cases, sebaceous duct opens into the hair follicle and so punctum is not seen.
    (Fordyce's disease is heterotopic sebaceous glands in mucosa of the lip and oral cavity).
  • Hair loss over the surface is common due to constant pressure over the roots of the hair follicles.
  • Unpleasant odour of sebum content is typical.
 
Complications
  • Infection and abscess formation.
  • Surface gets ulcerated leading to formation of a painful, fungating mass with discharge called as—Cock's peculiar tumour—often resembles epithelioma. It is a misnomer as it is not a tumour. It is a chronic granuloma on an ulcerated surface of a sebaceous cyst.
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    Fig. 1.163: Sebaceous horn scalp.
  • Sebaceous horn results from hardening of slowly discharged sebum through the punctum. (Horn is one which has greater length than its base diameter. Cutaneous horn is keratin deposition).
Note:
  • Multiple sebaceous cysts may be associated with syndromes like Gardner's syndrome.
  • Sebaceous cyst in the scrotum is usually multiple, firm and often calcified without any punctum. It is often treated by partial or total scrotectomy. Scrotum with multiple sebaceous cysts is strawberry scrotum.
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Fig. 1.164: Sebaceous horn face.
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Fig. 1.165: Multiple sebaceous cysts back.
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Figs 1.166A and B: Cock's peculiar tumour over scalp and ear.
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Fig. 1.167: Incision for sebaceous cyst is elliptical which includes punctum.
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Fig. 1.168A:
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Figs 1.168A and B: Elliptical incision and removal of sebaceous cyst.
 
Treatment
  • Excision including skin adjacent to punctum using elliptical incision—dissection method.
  • Incision and avulsion of cyst wall.
  • If abscess is formed, then drainage initially and later excision is done.
  • If capsule is not removed properly the cyst will recur.
 
GLOMUS TUMOUR
  • It is also called as glomangioma.
  • It arises from the cutaneous glomus composed of a tortuous arteriole which communicates directly into the venule (Sucquet-Hoyer canal) and these vessels being surrounded by network of small nerves making this lesion very painful. This communication is called as Sucquet-Hoyer canal.
  • Tumour consists of a mixture of blood spaces, nonmedullated nerve tissue, muscle fibres derived from the wall of the arteriole, with large cuboidal glomus cells—angiomyoneuroma.
  • They are often seen in limbs and common in nail-beds near the finger tips, as purple red swelling.
  • It is 2–3 mm in size.
  • It does not turn into malignancy.
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Fig. 1.169: Glomus tumour in finger tip—subungual region.
 
Features
  • Severe burning sensation and pain, out of proportionate to the size. The most common site is nail-bed.
  • Even the slightest pressure will give rise to severe pain. Dilated vessels compress over nerves.
  • It is compressible and pain is more when the limb is exposed to sudden changes in temperature (cold stimulus).
  • On increasing the pressure in the arm above systolic, pain disappears.
  • It looks like a reddish blue spot which does not blanch on percussion.
  • Subungual type may not be visible but only to cause episodic digital severe pain.
  • It is usually single, but rarely multiplicity is observed as familial.
  • Differential Diagnosis
  • Pyogenic granuloma—bleeds on touch.
  • Subungual melanoma—painless pigmented lesion.
  • Treatment: Excision cures the condition.
 
PAPILLOMA
  • It is warty swelling from the skin or often from the mucous membrane.
  • It has got a central axis of connective tissue, blood vessels and lymphatics.
 
True Papilloma
  • It is a benign tumour with localised overgrowth of all layers of the skin. It is commonly pedunculated but rarely can be sessile.
  • It contains sweat glands, sebaceous glands and hair follicles.
    zoom view
    Fig. 1.170: Pedunculated papilloma with its pedicle.
  • Pedunculated papilloma is villous with a central axis of connective tissues, blood vessels and lymphatics.
  • Papilloma can be cutaneous or mucosal. Cutaneous can be squamous or basal cell type. Squamous cell papilloma can be soft which is seen in eyelids in elderly; or can be congenital which can be sessile or pedunculated; single or multiple. Squamous papilloma also occurs in oral cavity. Basal cell papilloma is oily semitransparent brownish raised seborrhoeic keratotic lesion in skin around trunk of elderly.
    Papilloma may be single.
    multiple.
    Papilloma may be pigmented.
    nonpigmented.
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  • True papilloma may turn into squamous cell carcinoma occasionally. There will be sudden increase in size, bleeding or ulceration.
    zoom view
    Fig. 1.171: Papilloma right waist (sessile). Note the warty surface.
  • Papilloma can occur in the breast called as duct papilloma which is the most common cause of bloody discharge from the nipple.
  • Papilloma can occur in mucous membrane like in oral cavity, urinary bladder (transitional papilloma), in the rectum (columnar), in the larynx, in the gallbladder (cuboidal).
    zoom view
    Fig. 1.172: Papilloma tongue.
 
Infective Papilloma
Infective papilloma is a warty lesion due to infection, e.g. condyloma acuminata.
 
Differential Diagnosis
Amelanotic melanoma, pedunculated lipoma, carcinoma.
 
Treatment
  • True papilloma is excised with its base along with surrounding 1 cm skin margin.
  • Infective warts can be treated by excision or CO2 snow or diathermy coagulation.
Note:
Fibroepithelial papilloma also called as skin tags/achrochordon is very common benign skin lesion of usually 5 mm diameter in size; common in adults; common in neck, axilla, thigh and groin. It is a vascularised keratinised squamous epithelium, can cause local irritation and insignificant bleeding. If it causes cosmetic problem it is removed by laser/cautery or excision.
 
WARTS
  • They are usually multiple hyperkeratotic skin patches with finger like projections, common in children and adolescents.
  • They are common in finger tips, face, axilla and sole of the feet. It may be familial but often stimulated by virus.
  • They are dry, overgrown projections from the skin of finger often painful, tender and disfiguring. Repeated rubbing may cause infection. It can spread to other fingers and other parts of the body. Kiss lesions can occur.
  • Warts attain their size in few weeks and then persist for many months to years. They may regress spontaneously also.
  • Plantar wart (Verruca plantaris) is wart in the sole. Speciality of this is it gets pushed into the sole of the foot due to walking. It is common in ball and heel of the foot. It is pearly white in color with brownish haemorrhagic flecks. It is often covered by apparently normal skin because wart is buried into the skin. It looks like a circular pit. It is grey white finger/filiform like strands in the center of the lesion and is soft. Plantar warts can be multiple. It is painful and very tender on pressing (more than callosity or corns). A defined clear lump may not be felt.
  • Butcher's wart/pathologist's wart/verrucas necrogenica is due to entry of Mycobacterium tuberculosis through broken skin which are common in milkmaids. It presents as bluish red warty lesion from which fluid oozes out on pressure between projections. It is common over dorsum of hand. Lesion is surrounded by pustules.
  • Senile warts and venereal warts are other types. Venereal warts are same as infective papilloma.
  • Differential diagnoses are true papilloma, callosities, neurofibromas.
  • Treatment is excision. Salicylic acid, podophyllin cream applications are also used. Laser ablation of warts is commonly advocated.
 
FIBROMA
It is a benign tumour arising from fibrous tissue. It is capsulated.
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Fig. 1.173: Fibroma hand.
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Classification of True Fibroma
  1. Soft fibroma—contains immature fibrous tissue. Common in face, presents as soft brown swelling.
  2. Hard fibroma—contains well-formed fibrous tissue.
 
Treatment
Treatment of true fibroma is excision.
Note:
  • True fibroma is rare and cannot be diagnosed clinically. It is mostly combined with mesodermal tissues like nerve sheath (neurofibroma), fat (fibrolipoma), muscle (fibromyoma).
  • An entity called aggressive fibromatosis is known to occur as unencapsulated proliferation of fibrous tissue, common in abdominal and chest wall. It is considered presently as locally malignant. It does not spread through lymphatics or through blood. But recurrence is common.
  • Desmoid tumour is a variant of aggressive fibromatosis, seen in females, often associated with Gardner's syndrome (Desmos = tendon, eidos = appearance). Refer chapter Abdominal Wall and Umbilicus.
  • Recurrent fibroid of Paget's is a rare type of fibrosarcoma occurring in a scar tissue after many years.
 
BURSAE
Bursa is a sac like cavity containing fluid within, which in normal location prevents friction between tendon and bone.
  • Minor injuries and pressure leads into bursitis, which will present as a swelling at the site.
  • Inflammation of this bursa due to friction causes bursitis, which commonly presents as swelling, pain, and restricted movements.
  • Bursa secretes synovia like clear fluid in a cavity lined by flat endothelium. It reduces the friction at the site between tendon and bone. Normally fluid content is little to cause a swelling. Minor trauma or infection causes sudden increase in fluid secretion of the bursa making it to enlarge and clinically palpable as pathological bursitis. Bursa is common around knee, elbow, heel and hip.
  • Long-standing bursitis leads into thickening of its wall often with calcification making it feel hard with indurated surface. Lining of bursa may become rough or fluid may contain loose fibrinous particles to create grating sensation (crepitus) on the surface.
  • Often overlying skin becomes thick, cracked and horny due to repeated friction and inflammation.
  • Bursa may get adherent to deeper tissue as well as overlying skin to make it immobile. Bursa is usually well-localised, smooth, fluctuant, nontender swelling. Often it can be bilateral—in knee or elbow.
  • Joint related should be examined. Bursa may be communicating with the adjacent joint.
  • Gout or rheumatoid arthritis can cause bursa. For example, olecranon bursa can develop in gout patient.
  • Bursa should be differentiated from cold abscess, soft tissue tumour, aneurysm, synovial tumour (sarcoma) at different locations.
 
Complications of Bursa
  • Infection of bursa can occur due to trauma to overlying skin or through blood.
  • Mechanical disturbances and discomfort.
 
Management
  • US of the anatomical site, X-ray of the part or MRI are very useful.
  • Avoiding friction and other aggravating factors may control many bursae.
  • Aspiration and steroid injection may be useful.
  • Bursa which is felt indurated with thick wall or calcified or infected or attained large size or which interferes with joint movement or daily activities needs surgical excision. Subcutaneous bursa can be excised under local anaesthesia; large or deeper bursa requires general anaesthesia for excision.
 
Different Types
It can be anatomical or adventitious.
 
Anatomical
  • Anatomical bursae are located normally in a particular anatomical site with a purpose of reducing friction. They are commonly deep and adjacent to a bone or joint.
  • They become pathological and clinically significant when it presents with bursitis.
  • They are soft, cystic, well localised, nontransilluminating swelling at known anatomical site.
    • Subhyoid bursa: An horizontally oval swelling situated below the hyoid bone and in front of the thyrohyoid membrane.
    • Subacromial bursa: In front and lateral to humeral head in relation to supraspinatus tendon between acromion and greater tuberosity of humerus.
    • Bicipitoradial bursa.
    • Olecranon bursa (Student's elbow, Miner's elbow): It is subcutaneous bursa in relation to olecranon which becomes distended due to prolonged periods of leaning over elbow. Gout may involve this bursa.
    • Psoas bursa: A tensely cystic swelling situated beneath and below the inguinal ligament, in the lateral aspect of the femoral triangle. But it will not extend above the inguinal ligament in to the iliac region (unlike in psoas abscess which extends above and is cross fluctuant). Psoas bursa lies between the psoas tendon and lesser trochanter. When it is enlarged, it causes diffuse swelling over outer part of femoral triangle lateral to femoral vessels. When hip is moved swelling becomes painful. It also should be differentiated from femoral hernia.
    • Prepatellar bursa (Housemaid's knee/miner's beat knee): It lies subcutaneously in front of lower half of patella and upper half of patellar tendon (upper part) undergoes inflammation in people who do much kneeling. Joint is normal here.
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Fig. 1.174: Prepatellar bursa.
  • Subcutaneous infrapatellar bursa occurs between skin and lower part of the tibial tuberosity and ligamentum patellae. It is called as Clergyman's knee. ‘Clergyman’ is Christian priest who kneels down during prayer.
  • Suprapatellar bursitis is deep to patella and vastus intermedius, in front of lower end of femur. It communicates with knee joint.
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Fig. 1.175: Bursa near elbow joint.
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Fig. 1.176: Prepatellar (Housemaid's knee) and infrapatellar bursae (Clergyman's knee).
  • Brodie's bursa lies deep to medial head of gastrocnemius.
  • Semimembranosus bursa
  • Bursa anserina—under the tendons of Guy ropes (sartorius, gracilis and semitendinosus tendons—Goose's foot).
  • Retrocalcaneum bursa —between calcaneum and tendo- Achilis.
 
Adventitious Bursa
  • Adventitious bursa occurs in an unusual place/site due to friction/pressure between two layers of tissue. Once it becomes chronic it may get adherent to overlying skin or tissue underneath.
  • It may get infected, wall gets calcified, and fluid may become thick. It is well-localised, cystic usually nontender swelling. It becomes painful and tender if infected.
  • Lining of bursa may become rough or fluid may contain loose fibrinous particles to create grating sensation/crepitus on the surface.
    zoom view
    Fig. 1.177: Location of olecranon bursa (Student's elbow).
    zoom view
    Fig. 1.178: Adventitious bursa over lateral aspect of foot—a common site.
    zoom view
    Fig. 1.179: Common site of adventitious bursa (Bunion).
  • Examples
    • Bunion is adventitious bursa in patient with hallux valgus occurring between head of first metatarsal and skin.
    • Tailor's bursa occurs between lateral malleolus and skin.
    • Porter's bursa occurs between skin over shoulder and clavicle.
    • Weaver's bursa occurs between gluteus maximus, ischial tuberosity and skin.
    • 85Retro-Achillis bursitis occurs between skin and Achilles tendon.
    • Subcalcaneal bursitis occurs between calcaneum and heel in long distance runners.
    • Billing gate hump appears over 7th cervical spine deep to overlying skin in people carrying weight over it. Billing gate is a large fish market in London.
  • Condition should be differentiated from soft tissue tumour, sebaceous cyst, ganglion (depending on the location of bursa).
  • Management:
    • X-ray of the part and FNAC of swelling should be done.
    • Later it is excised usually under local anaesthesia.
 
SEMIMEMBRANOSUS BURSA
It is a cystic swelling in the upper medial aspect of the popilteal fossa under the semimembranosus tendon. It is said to be due to friction under the tendon causing bursitis.
 
Features
  • It is located between semimembranosus tendon and femoral condyle above the knee joint line.
  • It is common in young adult; in both sexes. It is most common swelling of the popliteal fossa.
  • It is nontender, cystic/tensely cystic (firm) swelling located above and on medial aspect of the popliteal fossa, fluctuant, noncompressible, often transilluminating, often with a fluid thrill. When it enlarges it comes out of semimembranosus tendon to become subcutaneous.
  • Content of bursa does not communicate with knee joint. So fluid cannot be reduced into the joint cavity; but often appears flaccid on flexion of knee or by firm pressure probably due to displacement of fluid into deeper recesses of the bursa. The swelling becomes tense when knee is extended.
  • Knee joint is normal.
  • Differential Diagnosis
    • Baker's cyst, popliteal aneurysm.
  • Management
    • Ultrasound of popilteal fossa shows the cystic swelling under semimembranosus tendon.
    • X-ray knee joint is normal.
    • Excision is done under general anaesthesia using tourniquet in prone position. Complete excision of the sac is needed to prevent recurrence.
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Fig. 1.180: Semimembranosus bursa typical location.
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Figs 1.181A and B: Semimembranosus bursa—typical location. On flexion it only becomes flaccid but does not disappear.
 
MORRANT BAKER'S CYST
It is a cystic swelling containing gel like fluid in the lower midline of the popliteal fossa. It occurs due to herniation of the synovial membrane of the knee joint as a result of chronic arthritis.
  • It is pulsion/pressure diverticulum of the synovial membrane towards surface under the gastrocnemius through an opening in the joint capsule. It is below the joint line.
 
Clinical Features
  • It is common in middle-aged individuals.
  • It is smooth, soft and cystic, nontransilluminant, often tender swelling located below (the joint line) and in midline of the popliteal fossa.
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Fig. 1.182: Morrant Baker's cyst—typical location.
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  • On flexion swelling disappears and on extension swelling increases in size.
  • Pain and tenderness are present in knee joint with effusion showing positive patellar tap.
  • The knee joint movements are painful and restricted.
  • Baker's cyst may rupture sometimes causing severe sudden pain and swelling in the calf mimicking deep vein thrombosis.
zoom view
Figs 1.183A and B: Baker's cyst. It is below the joint line.
 
Differential diagnosis for Baker's cyst
  • Semimembranosus bursa.
  • Thrombosed popliteal aneurysm (often bilateral).
 
Management
  • X-ray of joint shows arthritic changes.
  • MRI is needed.
  • Arthritis is treated and Baker's cyst is excised under general anaesthesia in prone position.
 
LYMPH CYST (LYMPHATIC CYST)
  • It is an acquired type of distension cyst wherein lymphatics form a localised swelling with a capsule around it.
  • It usually occurs in subcutaneous plane, which is smooth, soft, nontender, mobile, and brilliantly transilluminant. It is usually not adherent to the skin.
  • Common sites are neck and limbs.
  • It can get infected and form an abscess.
  • Differential diagnosis: Cold abscess, dermoid cyst.
  • Treatment: Excision.
 
LYMPHANGIOMA
It is congenital localised clusters of dilated lymph sacs in the skin and subcutaneous tissue that has failed to join the normal lymph system during development period.
 
Types
 
Capillary Lymphangioma
  • It is simple type which can be present at birth but noticeable skin vesicles often develop in few years.
  • It is common at the junction of body to limbs-like near shoulder, axilla, groin or buttock.
  • Skin vesicles contain clear watery or yellow fluid. Bleeding within the vesicle may turn it into brown or black. Its features includes multiple, indistinct white/brown/black coloured vesicles of 0.5 to 4 mm size at typical locations in children involving around 5–20 cm area of skin in the particular location.
  • If it is less than 5 cm in size it is called as lymphangioma circumscriptum.
  • If it is more than 5 cm in size it is called as lymphangioma diffusum.
  • If it is with reticulated ridges, it is called as lymphoedema ab igne.
  • Area is soft, spongy, often fluctuant with fluid thrill and translucency. It is not compressible. Vesicles will not fade on pressure.
  • Often lesion may get infected to make it painful and tender.
  • Condition will not block the lymph drainage in normal lymphatics and skin oedema is absent.
  • Regional lymph nodes are not enlarged.
 
Cavernous Lymphangioma
  • It is soft, lobulated, fluctuant, brilliantly transilluminant larger lymphatic swelling with often multiple communicating lymphatic cysts.
  • It often extends into deeper plane like muscle. It is common in face, mouth, lips (macrocheilia), tongue (macroglossia).
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Fig. 1.184: Lymphangioma circumscripta(Courtesy: Dr Balasaraswathy, DVD, DNB, Consultant Dermatologist, Mangaluru)
 
Cystic Hygroma
It is collection of clustered sequestered lymph sacs (occurring during developmental period in utero) presenting in newborn as large swelling which is soft, smooth, fluctuant, brilliantly transilluminant, and compressible (For detail refer chapter 5, Neck).
 
CALCINOSIS CUTIS
  • It is a type of calcification (dystrophic) in or under the skin. Usually presents as a circumscribed lesion in the skin.
  • Commonly seen in females. Common site is in the waist (Fig. 1.188)
  • Usually bilateral.
  • It is said to be due to friction causing degeneration of skin and immediate deeper structure with increased local alkalinity of the tissue causes precipitation of the calcium leading to solid, hard, swelling in the skin. Cut section shows hard, yellowish material.
  • It may mimic calcified lipoma or neurofibroma.
  • Treatment is excision and closure of defect often with local flaps.
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Fig. 1.185: Calcinosis cutis near waist is a common site. It is common in females.
 
NEUROMA
Two types of neuromas are found.
  • False neuroma.
  • True neuroma.
 
False Neuroma
  • It occurs due to injury to the nerve either after trauma or amputation which presents as a tender swelling.
  • It arises from the connective tissue of nerve sheath.
  • It contains fibrous tissue with coiled nerve fibres.
  • It can be end neuroma, commonly seen in amputation stump as a tender localised firm swelling often adherent to the stump scar. It can cause neuralgia in the stump. It prevents the proper usage of prosthesis. So during amputation, nerve should be pulled down and cut so as to make cut end to retract more proximally, which prevents the formation of neuroma.
  • It can be lateral (side) neuroma which is observed after partial nerve injury, usually after trauma. It presents as a tender, firm swelling along the line of the peripheral nerve.
zoom view
Figs 1.186A and B: Types of false neuromas: (A) End neuroma: (B) Lateral neuroma.
 
True Neuroma
  • It is a rare tumour.
  • It occurs in connection with sympathetic system, spinal cord.
 
Types
Ganglioneuroma
  • It contains ganglion cells and nerve fibres.
  • It occurs in connection with sympathetic chain. So it is observed in neck (parapharyngeal mass), thorax, retroperitoneum, adrenal medulla.
  • It is relatively benign and symptomless and often attains a large size.
  • Early complete excision can give a cure.
Neuroblastoma
  • It is poorly differentiated, aggressive, embryonic type of tumour.
  • It is seen in infants and children.
  • It spreads through blood but can go for spontaneous remission occasionally.
Myelinic Neuroma
  • It contains only nerve fibres.
  • Ganglion cells are absent.
  • It occurs in spinal cord or pia mater.
 
NEUROFIBROMA
  • It is a benign tumour arising from connective tissue of the nerve containing ectodermal, neural and mesodermal connective tissue components.
  • It can be single or multiple. Neurofibromas may be associated with pheochromocytomas, hypertension and few syndromes.
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Figs 1.187A and B: Multiple neurofibroma.
 
Sites
  • Cranial.
  • Spinal. Neurofibroma is the most common intradural extramedullary spinal tumour.
  • Peripheral.
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Fig. 1.188: Patient with multiple neurofibromatosis underwent laparotomy showing serosal neurofibroma.
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Figs 1.189A and B: Plexiform neurofibroma in the (A) Face and neck; and (B) Buttock.
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Fig. 1.190: Plexiform neurofibromatosis involving trigeminal (5th cranial) nerve.
 
Types
  • Nodular neurofibroma:
    • It presents as single smooth, firm, tender (often) swelling which moves horizontally or perpendicular to the direction of the nerve, not in the direction of the nerve.
    • There is pain and hyperaesthesia in the distribution of the nerve.
  • Plexiform neurofibroma:
    • It commonly occurs along the distribution of 5th cranial nerve in the skin of face. It often occurs in the cutaneous distribution of the peripheral nerve.
    • It attains enormous size with thickening of the skin which hangs downwards. It causes erosion into the bone, orbit and deeper structure.
    • It may also undergo myxomatous degeneration. It causes cosmetic problem.
    • Paraesthesia along the distribution of the trigeminal nerve (commonly ophthalmic division) is common.
    • Pachy dermatocele —a variant of plexiform neurofibroma where neck is involved. There is thickening and oedema of skin, pigmentation, thromobosed veins with enormous proliferation of subcutaneous nerve fibers causing folded pendulous hanging thickened skin with tissues. It is common along trigeminal (5th cranial) nerve; rarely is it seen in limbs and scalp skin.
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Fig. 1.191: Multiple neurofibromatosis with café-au-lait spots in the skin.
  • Generalised neurofibromatosis (von Recklinghausen's disease): (1:4000 births)
    • It is an inherited autosomal dominant disease wherein there will be multiple neurofibromas in the body—chromo-some 17. It is called as type 1 in which more than 50% will be familial. Type 1, more commonly, called as von Recklinghausen's disease. Type 2 is acoustic neurofibromatosis (mutation of chromosome 22). All layers of nerve with Schwann cells and fibroblasts show tumour proliferation.
    • It may be cranial, spinal or peripheral.
    • 89It is associated with pigmented spots (coffee coloured) in the skin, commonly seen on the back, abdomen, thigh (café au lait spots). More than 5 in number, with each 1.5 cm or more in size is significant. Café-au-lait signifies common neuroectodermal origin of nerve sheath cells and melanocytes.
    • Axillary/groin freckles and Lisch nodules, pigmented iris, hamartoma may be present.
    • Neurological disturbance is uncommon.
    • It may be associated with MEN type IIb (Multiple neurofibromas of eyelids, lips, and face; medullary carcinoma of thyroid; pheochromocytoma, hyperparathyroidism), primary brain tumours and bone cysts.
  • Elephantiatic neurofibromatosis:
    • It is of congenital origin. It involves limbs.
    • Skin of the limb is greatly thickened, dry and coarse.
  • Cutaneous neurofibromatosis:
    • They are small, multiple, firm/hard nodules arising from terminal ends of dermal nerves. Overlying skin is normal without any changes. It commonly occurs all over the body. It can be pedunculated or sessile. It can occur in scalp to result in a turban tumour.
 
Clinical Features
  • Mild pain or painless swelling usually in subcutaneous or cutaneous plane with tingling, numbness and paraesthesia along the distribution of nerve.
  • Round/oval/fusiform swelling along the peripheral/cutaneous nerves which moves perpendicular to the direction of the nerve but not along the longitudinal direction of nerve fibre with smooth surface and firm consistency. It is nontender or mild tenderness may be present. Skin is free unless it is of cutaneous type. Cutaneous type is often soft.
 
Complications
  • Cystic degeneration.
  • Haemorrhage into the tissues.
  • Spinal and cranial neurofibromas can cause neurological deficits.
  • Erosion into deeper planes, bone, orbit.
  • Muscle atrophy.
  • Spinal dumbbell tumour can cause compression of spinal cord and paralysis of the limb.
  • Sarcomatous changes: Common in generalised type (5%). When it occurs it shows rapid enlargement, warmness, more vascularity with dilated veins. Secondaries in lungs can occur through blood spread.
Note:
  • The most common spinal tumour is neurofibroma.
  • von Recklinghausen disease of primary hyperparathyroidism is different as it is due to raised PTH level causing osteitis fibrosa cystica.
  • Familial type of neurofibroma may be associated with scoliosis.
  • Café-au-lait spots are also seen in McCune Albright syndrome.
 
Treatment
  • Excision.
 
NEURILEMMOMA (SCHWANNOMA)
It is arising from Schwann (neurilemmal cells) cells. They are lobulated, encapsulated, soft, whitish grey in appearance. They displace the nerve from which they arise and can be removed. They are common in acoustic nerve (cerebellopontine angle) but also can occur in a peripheral nerve. Occasionally, they are multiple. Calcification is common. It is ectodermal in origin.
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Fig. 1.192: Lingual schwannoma (Courtesy: Dr Harish Rao, Professor in Surgery, KMC, Mangaluru).
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Fig. 1.193A:
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Figs 1.193A and B: Neurilemmoma—gross look and cut section.
Two types:
Anthony A— Two rows of spindle cells with central acellular area (Verocay bodies).
Anthony B— Acellular myloid areas.
Presentation is pain along the distribution of the nerve, hyperaesthesia and tenderness and as, soft or firm, lobulated, well localised mobile swelling.
 
Treatment
  • Excision—easier without causing neurological damage.
Note:
Recurrent schwannoma could be malignant.
 
GANGLION
It is a cystic swelling occurring in relation to tendon sheath or synovial sheath or joint capsule. It contains clear gel like fluid.
zoom view
Figs 1.194A and B: Ganglion over the dorsum of the wrist— typical location. It can occur over the flexor aspect also. It can be transilluminant also.
 
Pathogenesis
  • Cystic degeneration of the tendon sheath.
  • Leakage of synovial fluid through joint capsule.
  • There are small islets of microspaces in synovial sheath which often fuse together or one of them gets enlarged to form ganglion.
 
Clinical Features
  • Well-localised swelling which is smooth, soft, cystic, or tensely cystic, (Paget's test is +ve), nontender, transilluminant. It is mobile but mobility is restricted when tendon is contracted against resistance.
  • Occasionally it is communicating with joint capsule.
  • Often pain, tenderness and restricted joint movement may be the presentation (but rare).
 
Differential Diagnosis
  • Lipoma.
  • Lymph cyst.
  • Sebaceous cyst.
  • Small ganglion often mistaken for sesamoid bone or exostoses.
  • Bursa.
 
Treatment
  • Asymptomatic ganglion is better left alone because of high recurrence rate.
  • Excision. Usually done under local anaesthesia (lignocaine plain 2%). Patient should be explained of high recurrence rate (30%). After excision always it should be sent for histopathology. Firm crepe bandage application for 4 weeks is better in these patients.
  • Aspiration and sclerosant injection may be useful.
(In olden days people used to rupture the ganglion using bible book).
 
CHORDOMA
Tumour arising from the remnants of notochord.
It is seen in:
  • Sacrococcygeal region.
  • Sphenoid sinus region.
  • Around the foramen magnum.
  • It invades into the surrounding structure like nerves.
  • Resection is difficult.
  • Radioresistant.
 
EPIGNATHUS
This is a type of growth anomaly seen in neonates wherein growth from the base of skull protrudes through the mouth.
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Fig. 1.195: Epignathus.
Note:
  • Enucleation is removal of the swelling within the tissue of origin with normal part of tissue of origin is being retained, e.g. enucleation of prostate in benign prostatic hyperplasia (BPH).
  • Excision is removal of tissue/tumour entirely with its capsule.
  • Wide excision is removal of tumour with surrounding tissue margin adequately for clearance.
  • Compartment excision is removal of tumour/diseased tissue with all adjacent soft tissues in one compartment except neurovascular bundle. It is done in limbs for soft tissue sarcoma as a curative but limb saving procedure.
  • Radical excision/radical block dissection is removal of tumour widely with adjacent soft tissues with lymph node dissection.
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Fig. 1.196: Different incisions used in surgical approaches to remove swelling.
92F. Electrolyte and Nutrition
CHAPTER OUTLINE
  • ❖ Normal Physiology
  • ❖ Water Loss
  • ❖ Water Excess
  • ❖ ECF Loss
  • ❖ ECF Excess
  • ❖ Hyponatraemia
  • ❖ Hypernatraemia
  • ❖ Hypokalaemia
  • ❖ Hyperkalaemia
  • ❖ Hypermagnesaemia
  • ❖ Hypomagnesaemia
  • ❖ Acid-base Balance
  • ❖ Metabolic Alkalosis
  • ❖ Respiratory Alkalosis
  • ❖ Metabolic Acidosis
  • ❖ Respiratory Acidosis
  • ❖ Anion Gap
  • ❖ Fluid Therapy
  • ❖ Colloids
  • ❖ Nutrition
  • ❖ Gastrostomy
  • ❖ Jejunostomy
  • ❖ Total Parenteral Nutrition
  • ❖ Refeeding Syndrome
  • ❖ Obesity and Morbid Obesity
 
NORMAL PHYSIOLOGY
Total body water is 60% of body weight in males, 50% of body weight in females, i.e. 30 litres.
  • Intracellular water—20 litres (2/3).
  • Extracellular water—10 litres (1/3).
    • Plasma (1/4) (2.5 litres).
    • Interstitial fluid (7.5 litres).
Ion
ICF
ECF and plasma
Sodium
10 mmol/L
140 mmol/L
Potassium
150 mmol/L
4.5 mmol/L
Chloride
Trace only
105 mmol/L
ECF volume and osmolality regulation is controlled by three hormones. Aldosterone, ADH, atrial natriuretic hormone.
 
WATER LOSS (VOLUME LOSS)
It is decrease in the whole body fluid volume which includes both ECF and ICF. It is usually ECF loss which is more important and assessed. It can be isotonic volume depletion with both salt and water loss leading into hypovolaemia, or only water loss with only minimal loss of electrolytes leading into dehydration.
 
Causes and Features
  • Isotonic volume depletion occurs due to diarrhoea, vomiting, and excess diuresis. Here normal or decreased sodium is observed. Fluid loss is only of ECF and so early intravascular volume reduction occurs. This causes hypotension and decreased tissue perfusion. Features are—dry tongue, rapid pulse, cold clammy extremities, sunken eyes, hypotension, oliguria, raised blood urea, decreased urinary sodium. Hypovolaemia can be mild (< 2l fluid loss); moderate (2–3 L fluid loss); severe (>3 L fluid loss).
  • Only pure water loss occurs due to poor fluid intake and diabetes insipidus. It causes dehydration with proportionate decrease in total body water (2/3rd ICF, 1/3rd ECF). As ECF including intravascular fluid loss is less, hypotension is less. Features here are—severe thirst, confusion and convulsions due to hypernatraemia; blood pressure is relatively normal. Dehydration can be mild (weight loss 5%); moderate (10%); severe (15%).
 
Management
  • Evaluation is done by doing serum sodium, urinary sodium, and blood urea.
  • Isotonic volume depletion is corrected by 0.9% normal saline.
  • Pure water depletion is corrected by more water intake/ intravenous 5% dextrose.
  • Monitoring fluid therapy by skin and tongue examination, weight gain, pulse, blood pressure, CVP, PCWP.
 
WATER EXCESS (ECF VOLUME EXCESS)
It can be divided into water and salt excess or predominantly water excess called as water intoxication.
Water and salt excess occurs in CCF, cirrhosis, nephrotic syndrome, hypoproteinaemia, renal failure, excessive saline infusion.
Water intoxication occurs in TURP, excess infusion of 5% dextrose only, SIADH secretion, psychogenic polydypsia. It is managed by stopping fluid infusion or procedure (TURP); fluid restriction, and treating the cause.
 
Causes
  • Excessive amount of intravenous dextrose (5%).
  • During colorectal bowel wash for preparation of large bowel for surgery, if water is used instead of saline, especially in children.
  • In TURP (Transurethral resection of prostate) when excess irrigating fluid water or glycine is used (commonly used).
  • In syndrome of inappropriate antidiuretic hormone (SIADH) which is commonly associated with lobar pneumonia, empyema, oat cell carcinoma and head injury.
93
 
Investigations
  • Haematocrit and sodium level (will show fall in level).
  • Low potassium. Low blood urea.
 
Treatment
  • Water and salt restriction and observation.
  • Monitoring in ICU.
  • Management of fluid and electrolyte balance.
  • Infusion of hypotonic sodium chloride.
    Administration of diuretics and hypertonic saline should be avoided, as it may cause rapid changes in serum sodium and water level which will lead to neuronal demyelination and fatal outcome.
 
ECF LOSS
  • Here only ECF loss is present with normal ICF.
  • It is seen in vomiting, diarrhoea, intestinal obstruction.
  • Treatment is infusion of normal saline.
 
ECF EXCESS
  • Only ECF excess without an ICF excess.
  • Excessive infusion of saline with impaired excretion.
  • Raised JVP (earliest and best clinical sign), cardiac failure and peripheral oedema.
  • Treatment is fluid restriction and diuretics like frusemide.
 
HYPONATRAEMIA
Sodium level less than 130 mEq/l. Hyponatraemia is said to be severe if serum sodium becomes lesser than 100 mEq/l in acute type; and lesser than 115 mEq/l in chronic type.
It can be due to water overload (dilutional) or sodium loss.
 
Types of Hyponatraemia
  • Acute—presents as neurological manifestations.
  • Chronic—causes pontine myelinolysis. It presents as behavioural changes, progressive weakness, and cranial nerve palsies.
Types also may be:
  • Hypervolaemic hyponatraemia wherein rapid absorption of fluid occurs into intravascular compartment leading into pulmonary and cerebral oedema. It is due to decreased osmolality causing movement of ECF into the cells. Serum sodium level lesser than 100 mmol/l is called as severe hyponatraemia, causes convulsions. Here urinary sodium will be less than 15 mmol/l. Acute hyponatraemia is corrected by fluid restriction, hypertonic saline, loop diuretics like frusemide. Monitoring the serum sodium level of the patient is essential. Sodium should be corrected up to above the level of 125 mmol/l. Correction should be slow and gradual at a rate of 2 mEq/l/h with up to 20 mEq/l correction in 24 hours with 4th hourly assessment of serum sodium. Overcorrection of sodium should not be done. Rapid correction can lead into irreversible myelin lysis of pontine.
  • Hypovolaemic hyponatraemia: It is due to hypovolaemia by diarrhoea, vomiting, wherein urine sodium level is less than 20 mmol/l; due to diuresis or renal causes wherein urine sodium level is more than 20 mmol/l or it may be due to correction of hypovolaemia using hypotonic fluid like 5% dextrose. Condition can be treated well using isotonic normal saline.
  • Normovolaemic hyponatraemia: It may be due to renal failure or syndrome of inappropriate ADH secretion (SIADH). In mild asymptomatic patients it is corrected by fluid restriction (1 l/day will raise the serum Na). Vasopressin antagonist demeclocycline which increases the diluting ability of kidney is used in severe cases.
  • Pseudohyponatraemia: Plasma osmolality is mainly achieved by serum sodium; but small proportion, i.e. 25% of osmolality is due to other solutes like glucose, lipids, plasma proteins, urea which will not move easily between intracellular and extracellular spaces. When concentration of these molecules raise due to some pathology, proportionately relative concentration of sodium will drop causing pseudohyponatraemia. Here condition causing related to specific solutes mentioned above is treated, than hyponatraemia.
 
Causes
  • Intestinal obstruction.
  • Intestinal fistulas—biliary, duodenal, gastric, pancreatic.
  • Gastric outlet obstruction with severe vomiting.
  • Ryle's tube aspiration.
  • Severe diarrhoea due to viral cause, in colitis, colorectal polyps.
  • Syndrome of inappropriate antidiuretic hormone (SIADH).
  • Immediately after surgery and trauma, sodium depletion occurs.
  • Stroke.
 
Investigations
  • Serum electrolytes. Urinary sodium is low.
  • Sodium deficit is calculated by: (125 – present serum sodium) × body weight in kg × 0.6.
 
Treatment
  • Intravenous infusion of normal saline as a slow and gradual correction at a rate of 2 mEq/L/hour in acute cases and < 1 mEq/L/hour in chronic cases. Correction should not exceed more than 20 mEq/L/day in acute cases and more than 10 mEq/L/day in chronic cases. Hypertonic saline of 1.6% or 3% also can be used in severe cases. 0.9% normal saline contains 154 mEq of NaCl; 3% saline contains 500 mEq of NaCl.
  • The cause is treated.
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HYPERNATRAEMIA
Serum sodium level > 150 mEq/L. Excess infusion of normal saline causes overload in circulating salt and water. It is usually due to water deficit.
 
Causes
  • Renal dysfunction.
  • Cardiac failure.
  • Drug induced like NSAID, corticosteroids.
    It may be either primary sodium excess or primary potassium excess or primary water deficit.
 
Types of Hypernatraemia
  • Euvolemic (pure water loss): It is due to failure of water intake like in comatous patients, bedridden people, post-operative patients and in patients with high fever leading into extrarenal loss of water. It can occur in diabetes insipidus or chronic renal failure as renal loss of water.
  • Hypovolaemic (among loss of water and sodium, more water is lost than sodium): It is due to vomiting, diarrhoea, more undue sweating (extrarenal); osmotic diuresis by glucose/mannitol (renal).
  • Hypervolaemic (both sodium and water gain but sodium gain is more than water gain) as seen in more salt intake, excess steroids, sodium bicarbonate/hypertonic saline infusion (salt gain).
 
Clinical Features
  • Pitting oedema.
  • Puffiness of face.
  • Increased urination.
  • Often dilated jugular veins.
  • Features of pulmonary oedema.
 
Investigation
  • Serum electrolytes, plasma and urine osmolality, renal function tests, haematocrit.
 
Management
  • Restriction of saline and sodium. Treatment of pulmonary oedema.
  • Hypernatraemia should be corrected slowly as follows:
    • Initial infusion of normal saline, then infusion of half strength saline (0.45%) and later with 5% dextrose, i.e. gradual controlled correction is done. Otherwise cerebral oedema and hyperglycaemia can develop.
    • Oral and nasogastric administration of water/fluids.
 
HYPOKALAEMIA
 
Sudden Hypokalaemia
Serum potassium level less than 3.5 mEq/l.
It occurs in patients in diabetic coma treated by insulin and saline infusion.
 
Gradual Hypokalaemia
 
Causes
  • Diarrhoea of any causes, villous tumour of the rectum, ulcerative colitis.
  • After trauma or surgery.
  • Pyloric stenosis with gastric outlet obstruction.
  • Duodenal fistula, ileostomy.
  • After ureterosigmoidostomy.
  • Insulin therapy.
  • Poisoning.
  • Drugs like beta agonists.
  • Familial periodic paralysis.
 
Clinical Features
  • Slurred speech.
  • Muscular hypotonia—physical sign.
  • Depressed reflexes.
  • Paralytic ileus.
  • Weakness of respiratory muscles.
  • Cardiac arrhythmias.
  • Inability to produce concentrated urine and so causes nocturia and polyuria.
    ECG shows prolonged QT interval, depression of the ST segment and inversion of T wave, prominent U wave.
    Often hypokalaemia is associated with alkalosis.
    Serum potassium will be decreased.
 
Treatment
  • Oral potassium 2 g 6th hourly, 15 ml potassium chloride syrup (20 mmol of K).
  • IV KCl 40 mmol/litre given in 5% dextrose or normal saline slowly, often under ECG monitoring [Total dose is 40 mmol (0.2 mmol /kg/hour). Maximum dose per hour is 20 mmol].
  • Hypokalaemic alkalosis which occurs in pyloric stenosis should be treated carefully by IV potassium as there will be severe potassium loss.
 
HYPERKALAEMIA
Normal range of potassium is 4.0 to 4.5 mEq/l.
Hyperkalaemia manifests when potassium exceeds 6 mEq/l.
 
Causes
  • Renal failure.
  • Rapid infusion of potassium.
  • Transfusion of stored blood.
  • Diabetic ketoacidosis.
  • Adrenal insufficiency.
  • Potassium sparing diuretics, cyclosporine, beta blockers.
  • Metabolic acidosis.
  • 95Insulin deficiency.
  • Tissue destruction, burns, trauma, tumour necrosis, crush injury.
  • In vitro haemolysis, thrombocytosis, tourniquet application, exercise—pseudohyperkalaemia.
  • Familial hyperkalaemic periodic paralysis.
    Potassium excess is a dangerous condition which can cause sudden cardiac arrest.
 
Investigations
High serum potassium level. Peak ‘T’ wave in an ECG.
 
Treatment
  • IV administration of 50 ml of 50% glucose with 10 units of soluble insulin, slowly.
  • Infusion of 10% calcium gluconate (as cardioprotection) intravenously.
  • Calcium chloride is given in severe cases as calcium in this form is released immediately without hepatic metabolism.
  • Diuresis using frusemide injection.
  • Haemodialysis when required—very useful.
  • Continuous ECG monitoring is a must.
  • Polyesterene sulphonate ion exchange resin 30 g/hour in 50 ml of 70% sorbitol as an enema.
  • Salbutamol nebulisation or intravenously 0.5 mg in 4 ml of saline/Albuterol nebulisation.
  • IV sodium bicarbonate—shifts potassium in to cells. 7.5%, with 50–100 ml intravenously in 10 minutes.
 
HYPERMAGNESAEMIA
It is rare. Serum magnesium > 2.5 mEq/l.
Normal serum magnesium is 1.5–2.5 mEq/l and intra-cellular magnesium which is more (2nd higher) is 26 mEq/l. Magnesium is mainly deposited in bone (60%). It is a cofactor for many enzymes necessary in phosphorylation of glucose in the cell and ATP utilisation in muscle fiber. Daily required dietary intake of magnesium is 0.4 gram. It is reabsorbed well in proximal renal tubule.
 
Causes
  • Advanced renal failure treated with magnesium containing antacids, diabetic ketoacidosis.
  • Intentionally produced hypermagnesaemia while treating preeclampsia.
 
Clinical Features
  • Loss of tendon reflexes (most common).
  • Neuromuscular depression.
  • Flaccid quadriplegia.
  • Respiratory paralysis.
  • Somnolence.
  • Hypotension.
 
HYPOMAGNESAEMIA
  • Serum magnesium <1.5 mEq/l.
 
Causes
  • Malnutrition, alcohol.
  • Large GI fluid loss.
  • Patients on total parenteral nutrition.
 
Clinical Features
  • Hyperreflexia.
  • Muscle spasm.
  • Paraesthesia.
  • Tetany.
  • It mimics hypocalcaemia. It is often associated with hypokalaemia and hypocalcaemia.
 
Treatment
Two gram (16 mEq) of magnesium sulphate slow intravenously, in 10 minutes. Later maintenance dose of 1 mEq/kg/day as slow continuous infusion is given/oral magnesium is needed.
 
ACID-BASE BALANCE
Normal pH (– log 10 of H+) is 7.36–7.44.
Note:
When H+ increases pH decreases.
An acid is a substance that dissociates water to release hydrogen ion. A base is a substance that takes hydrogen ion. A buffer is a combination of weak acid and conjugate base. These buffers maintain the H+ concentration in blood within fine limits. Natural buffers are extracellular or intracellular. Bicarbonate/carbonic acid buffer, phosphate buffer and plasma proteins are extracellular natural buffers. Haemoglobin and other proteins are intracellular buffers. Bicarbonate/carbonic acid buffer is most important as carbonic acid levels are regulated by lungs which eliminates excess of it as CO2. Bicarbonate part is separately controlled by kidney.
Acidosis is pH of blood less than 7.35. Alkalosis is pH more than 7.45.
 
Henderson Equation (Used to Assess Hydrogen Ion Concentration)
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OR
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Here constant K is 800 (for H2CO3 / HCO3 buffer).
Carbonic acid (H2CO3) is solubility coefficient of CO2 in blood (α) multiplied by partial pressure of CO2 (PCO2). α is 0.03 ml/mmHg/100 ml of blood; PCO2 is 40 mmHg. H2CO3 = αPCO2 = 0.03 × 40 = 1.2 ml. Normal blood bicarbonate/HCO3 level is 24 mmol/L. so H+ is 800 × 1.2 divided by 24 = 40 mmol/L.
 
Henderson-Hasselbalch Equation (Used to Assess pH)
It is used to find out pH of the blood using logarithm. Negative logarithm of constant K (800 for carbonic buffer) is called as pKa. It is 6.1 for H2CO3/HCO3 buffer system.
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METABOLIC ALKALOSIS
Primary base excess, i.e. HCO3. A standard bicarbonate above 27 mmol/litre.
 
Causes
  • Repeated vomiting due to any cause. Commonly seen in cases of pyloric stenosis. Here hypokalaemic alkalosis occurs which is an important aspect for managing the patient.
  • Excess alkali ingestion, e.g. antacids.
  • Cortisol excess either due to over administration or Cushing's syndrome.
 
Clinical Features
  • Cheyne stokes breathing with period of apnoea of 5–30 seconds.
  • Tetany due to alkalosis. More often latent tetany which is revealed by Trousseau's sign.
 
Investigations
Serum electrolytes, arterial blood gas analysis.
 
Treatment
  • Normal saline or double strength normal saline IV infusion, with slow IV potassium chloride 40 mmol/litre in saline, slowly under ECG monitoring.
  • pH more than 7.7 causes life-threatening alkalosis which requires rapid correction by infusing dilute hydrochloric acid or ammonium chloride, however, with care and monitoring.
 
RESPIRATORY ALKALOSIS
Arterial PCO2 is below normal.
 
Causes
  • Hyperventilation during anaesthesia, due to head injury/severe pain.
  • High altitude.
  • Hyperpyrexia.
  • Encephalitis, hypothalamic tumours, drugs like salicylates, due to cirrhosis of liver.
  • Hysteria.
 
Features and Management
  • Headache, tingling, circumoral anaesthesia, tightness in chest, tetany, arrhythmias are the features.
  • Low PaCO2, low HCO3, high alkaline pH are typical. Serum HCO3 will not fall below 15 mEq/L.
  • It can be acute or chronic.
  • It is managed by oxygen therapy, treating the cause, acetazolamide in high altitude.
  • Respiratory suppression due to alkalosis is treated by CO2.
 
METABOLIC ACIDOSIS
It is an excess acid or base deficit. A standard bicarbonate below 21 mmol/litre.
 
Causes
Increase in fixed acid:
  • Diabetic ketoacidosis.
  • Starvation.
  • Hypoxia.
  • Renal insufficiency.
  • Cardiac arrest.
  • Excessive exercise.
  • Intestinal strangulation. Here anion gap is increased.
Loss of base:
  • Diarrhoea.
  • Ulcerative colitis.
  • Gastrocolic fistula.
  • Intestinal fistula.
  • Ureterosigmoidostomy causes hyperchloraemic hypokalaemic acidosis. Here anion gap is normal.
 
Features
  • Rapid, deep, noisy breathing (air-hunger)—Kussmaul's breathing.
  • Cold clammy skin, tachycardia, right heart strain, altered level of consciousness.
  • Cardiac arrhythmias, hypotension.
  • Anorexia, muscle weakness, vomiting.
  • pH below 7.2 is dangerous and life-threatening.
  • Capillary stasis.
  • Urine is strongly acidic.
  • Low standard HCO3 level.
  • Base deficit.
  • 97It is evaluated by doing arterial blood gas analysis (ABG) which shows low HCO3, low pH; anion gap; urinary anion gap (UAG). Normal UAG is zero or positive. In metabolic acidosis due to GI cause, UAG becomes negative due to increased NH4Cl excretion; if it is due to renal cause, UAG will be positive.
 
Treatment
  • Correction of hypoxia.
  • 50 mmol of 8.4% sodium bicarbonate infusion IV.
    Sodium bicarbonate required in mEq/L = Body weight in kg × Base deficit × 0.3.
  • Correction of electrolytes.
  • Specific treatment for lactic acidosis (type A [shock / respiratory/CO/cyanide/anaemia]; type B [diabetes/hepatic/toxins/drugs])—only careful use of NaHCO3 in severe cases, dichloracetate which stimulates pyruate dehydrogenase to reduce lactate.
  • Specific therapies for diabetic ketoacidosis, alcoholic acidosis, aspirin poisoning, renal causes.
 
RESPIRATORY ACIDOSIS
It is a feature of respiratory failure with high arterial PCO2 causing fall in pH.
 
Causes
  • During and after anaesthesia.
  • Chronic bronchitis.
  • Emphysema.
  • Thoracic diseases.
  • Upper abdominal surgeries and diseases.
  • Respiratory airway obstruction.
  • Myasthenia gravis.
  • Poliomyelitis.
  • Stroke, infection, obesity, hypoventilation.
 
Features and Treatment
  • Features of hypercapnia like dyspnoea, confusion, psychosis, hallucinations, sleep disturbances, tremor, jerks, and personality changes. CNS manifestations are more severe in respiratory acidosis than in metabolic acidosis as lipid soluble CO2 crosses blood-brain barrier easily than HCO3.
  • Acute respiratory acidosis is managed by oxygen therapy, ventilator support. Oxygen therapy should not be used in chronic hypercapnoea unless it is really indicated as hypoxia stimulated respiration may be suppressed. Alkali therapy also is not usually used unless acidosis is very severe (below 7.15) or there is severe bronchospasm.
 
ANION GAP
  • It is calculated estimation of the undetermined or unmeasured anions in the blood.
  • It is (Na+ + K+) — (HCO3¯ + Cl¯).
  • Normal anion gap is 10-16 mmol/litre.
  • Anion gap is charge difference between unmeasured anion and cation. Important unmeasured anions are anionic protein, phosphate, sulphate, organic acids. Unmeasured cations are calcium and magnesium. Albumin is the main component of anion gap. When albumin decreases by one g/dl then anion gap decreases by 2 mEq/L.
Increased anion gap is seen in
Normal anion gap is seen in
  • Metabolic acidosis due to ketoacidosis
  • Diarrhoea
  • Lactic acidosis
  • GIT fistulae
  • Poisoning
  • Hyperchloraemic acidosis
  • Renal failure
 
FLUID THERAPY
Osmolality of a solution is assessed by the amount of solute dissolved in a solvent like water measured in weight (kg).
Osmolarity of a solution is assessed by the amount of solute dissolved in a solvent like water measured in volume (litre).
Normal plasma Osmolality is 285 mOsm/kg (275–295).
Osmolality is calculated by two methods
  1. Osmolality of plasma =
    zoom view
    It is based on the fact that solution of 1 mOsmol/kg freezes at – 1.86°C; whereas normal plasma freezes at – 0.54°C.
  2. Osmolality of plasma =
    zoom view
It is based on the concentrations of major solutes in plasma. So sodium concentration contributes mainly to the osmolality.
Colloidal osmotic pressure is difference in plasma osmotic pressure and interstitial fluid pressure which is normally 25 mm Hg, which is mainly by plasma albumin concentration. Plasma proteins do not go out of capillary wall into the interstitium.
 
Principles of Fluid Therapy
 
Indications
  • For rapid restoration of fluid and electrolytes in dehydration due to vomiting, diarrhoea, shock due to haemorrhage or sepsis or burns.
  • Total parenteral nutrition.
  • Anaphylaxis, cardiac arrest, hypoxia.
  • Post-gastrointestinal surgeries.
  • For maintenance, replacement of loss or as a special fluid.
 
Advantage
Controlled, accurate and adjustable, rapid and predictable.
98
 
Problems in Fluid Therapy
  • Needs hospitalisation; costly; needs asepsis.
  • Fluid overload; pulmonary oedema and cardiac failure; infection.
  • Thrombophlebitis; haematoma; cellulitis in local area.
  • Pyrogenic reaction; air embolism; bacteraemia.
  • Discomfort; poor patient acceptance.
Daily requirement of sodium is 100 mEq; potassium is 60 mEq; calcium is 5 mEq; magnesium 1 mEq.
One litre of normal isotonic saline contains 154 mEq of sodium.
Ringer's lactate is the most physiological fluid (crystalloid) containing sodium—130 mEq/lt; potassium—4 mEq/lt; chloride—109 mEq/lt; lactate (bicarbonate)—28 mEq/lt; and calcium—3 mEq/lt. It should be avoided in liver failure patients. As it does not contain glucose it can be used in diabetics.
Other crystalloid fluids—normal saline, dextrose saline, 5% dextrose, isolyte P, isolyte G, isolyte M.
Colloids are of large molecules which shift the fluid from interstitial compartment to intravascular compartment and are used as plasma expanders. Haemaccel, hetastarch, pentastarch, dextran 40/70 are colloids.
Special purpose fluids are sodium bicarbonate 7.5% and 8.4% used in metabolic acidosis, forced diuresis, hyperkalaemia; mannitol 10/20% used as an osmotic diuretic agent; hypertonic saline 1.6%, 3%, 5% and 7.5% used in hyponatraemia of different severity; albumin 4.5% as plasma expander; albumin 20% in severe hypoalbuminaemia.
 
Calculation of Drop Rate of IV Fluids
1 ml =16 drops in usual drip set. For microdrip set one ml = 60 drops.
  1. Quantity of fluid required in liters per day × 10 = Drop rate/minute. 2.5 litres is usually used quantity of fluid/day. So 2.5 × 10 = 25 drops/minute.
  2. Fluid volume in ml to be infused in one hour divided by four = Number of drops/minute. Example: 100 ml/hour means 25 drops/minute.
  3. Number of microdrop/minute = Volume in ml/hour (50 microdrop/minute = 50 ml/hour).
Note:
  • Weight loss more than 10% of individual's weight in 6 months is called as significant weight loss.
  • Body mass index (BMI) is body weight in kilograms divided by height in meters squared. BMI less than 18.5 signifies nutritional impairment and below 15 signifies severe malnutrition.
  • Daily fluid loss from kidneys is 1500 ml; from lungs is 400 ml; from skin is 800 ml; from stool is 60–150 ml.
  • Energy requirement per day is 20–30 kcal/kg, i.e. around 2000 kcal/day total.
  • Glucose requirement is 200 g per day; fat requirement is 200 g per week; nitrogen (protein) requirement is 0.15 g/kg per day. Nitrogen need increases to 0.25 g/kg/day in hypercatabolic status.
  • Transit time is rapid in jejunum; three times slower in ileum; still slower in colon.
  • Fluid absorption capacity is 40% in jejunum; 70% in ileum; 90% in colon.
  • Electrolyte and vitamin B12 absorption and enterohepatic circulation occurs in ileum and so ileum is more important than jejunum.
 
Crystalloids
Crystalloids are aqueous solutions of mineral salts or other water soluble molecules. They are used mainly to improve the volume and electrolyte supplementation.
 
Crystalloids commonly used
Type
Content
Indications
Contraindications and problems
5% Dextrose
One litre contains 50 gram of glucose. It is hypotonic; pH is 4.5; provides 170 kcal/L
Used in pre- and post-operative fluid therapy; 5% and 10% dextrose is used as protector of liver in obstructive jaundice, pre-operative preparation in biliopancreatic surgeries, clear toxic substances. It is useful in correction of hypernatraemia due to pure water loss like diabetes insipidus, excess use of electrolytes; 5% dextrose is infused with frusemide.
Cerebral oedema as it is hypotonic; cranial surgeries; stroke; hypovolaemic shock as it may cause hyperglycaemia and osmotic diuresis; hyponatraemia; water intoxication; it should not be used for rapid correction of hypernatraemia; diabetes and hyperglycaemia.
Note: Intravenous administration of dextrose can cause low potassium, magnesium and phosphate; and causes thrombophlebitis.
Normal saline (isotonic saline— 0.9% NaCl/ NS).
3% normal saline (hypertonic) contains 513 mEq/litre of sodium; is used in hyponatraemia due to SIADH or water intoxication or severe hyponatraemia
One litre contains 154 mEq each of sodium and chloride.
  • It mainly exists in ECF to maintain osmolality; it increases the intravascular volume and is so very useful to stabilize the blood pressure in hypovolaemia.
  • It is used in diarrhoea, vomiting, excessive sweating; in treatment of alkalosis; in hyponatraemia; diabetic ketoacidosis; hypercalcaemia; brain surgery and injuries.
  • It is used in giving wash to body cavities like peritoneum or any wounds (warm NS).
  • It is avoided in hypertension, pre-eclampsia, elderly, dehydration with hypokalaemia.
  • Large volume infusion may cause sodium retention and hyperchloraemia.99
  • Many drugs are given using NS as vehicle.
  • It is safer in renal failure as it does not contain potassium.
Dextrose (5%) with normal saline (0.9 NaCI), (DNS)
One litre contains 50 grams of glucose, 154 mEq each of sodium and chloride; pH 4.2; osmolarity 585 mOsm/litre.
It corrects hypovolaemia and hyponatraemia. It is used alkalosis due to vomiting and nasogastric aspiration.
It is not used in cardiac and renal failure. Used in shock but not used in severe hypovolaemic shock.
Dextrose with 0.45% normal saline
One litre contains 50 grams of glucose; 77 mEq each of sodium and chloride.
It is commonly used in fluid therapy; treatment of severe hypernatraemia as it corrects it gently; to avoid cerebral oedema. It is used in maintenance therapy and in post-operative period.
It is not used in hyponatraemia, and in diarrhoea and vomiting.
Ringer's lactate (Hartmann's/ balanced salt) solution
One litre contains 130 mEq sodium (as sodium lactate); 109 mEq of chloride; 4 mEq potassium; 28 mEq of bicarbonate; 3 mEq of calcium. It is devoid of glucose.
  • It is used in corrections of severe hypovolaemia as it expands intravascular volume rapidly.
  • It is useful in managing metabolic acidosis as lactate in liver is metabolized to bicarbonate.
  • It is useful fluid for therapy in postoperative period, burns, diarrhoea. It also corrects hypokalaemia. It maintains normal ECF fluid and electrolyte balance.
  • In diabetic ketoacidosis it provides glucose free fluid.
  • It can cause lactic acidosis, so contraindicated in hypoxia, severe shock, liver diseases, in vomiting and nasogastric aspiration, in metabolic alkalosis.
  • It cannot be used along with blood transfusion as calcium in Ringer lactate can bind with citrate of transfusing blood precipitating clotting of the donor blood. Blood products and RL cannot be infused simultaneously.
Isolyte M (Maintenance)
One litre contains 50 grams of glucose; 40 mEq sodium; 38 mEq chloride; 35 mEq potassium; 15 mEq phosphate; 20 mEq acetate.
  • It gives calories, water, electrolytes, pH. Rich potassium in it is useful in correcting the hypokalaemia provided renal function is good. It can correct acidosis also.
  • It is useful in diarrhoea, bilious vomiting.
It is not useful in correcting hyponatraemia as sodium concentration in it is low.
Isolyte G (Gastric)
  • One litre contains 50 grams of glucose, 63 mEq of sodium, 130 mEq of chloride, 17 mEq of potassium, 69 mEq of ammonium.
  • Gastric juice contains nearly similar contents of Isolyte G. In liver ammonium converts into urea and hydrogen ion. Hydrogen ion neutralizes alkalosis.
Gastric juice vomiting or continuous nasogastric aspiration which causes hypochloraemic, hypokalaemic, metabolic alkalosis which is corrected by Isolyte G.
Isolyte E (Extracellular replacement)
One litre contains 50 grams of glucose; 140 mEq of sodium; 103 mEq of chloride; 5 mEq of calcium; 10 mEq of potassium; 47 mEq of magnesium; 3 mEq of acetate; 8 mEq of citrate.
It is used mainly to replace extracellular fluid. It contains double the ECF concentrations of potassium and acetate (rest similar). It gives energy, water, magnesium, corrects acidosis.
It is not used in metabolic alkalosis due to vomiting, due to diuretics.
Isolyte P (Paediatric)
One litre contains 50 grams of glucose; 25 mEq of sodium; 22 mEq of chloride; 20 mEq of potassium; 3 mEq of magnesium; 23 mEq of acetate.
It is used in fluid therapy in paediatric age group.
It is not used in hyponatraemia, renal failure, hyperkalaemia, hypovolaemic shock.
100
 
Colloids
Colloids are of up to 20 u sized large molecules, which retain in the intravascular space for longer time and so raise the intravascular volume (3 times > than crystalloids). They improve cardiac output but not oxygen carrying capacity. Colloids should maintain oncotic pressure equal to that of plasma; should be stable and inert; non-toxic, non-antigenic, non-pyrogenic; should be easily sterilisable; should not interfere with blood grouping.
 
Colloids Commonly Used
Colloid
Content
Indications
Problems
Albumin (Heat treated human albumin)
It maintains 75% of plasma oncotic pressure. It is the vehicle to transport many low molecular substances including drugs.
  • 5% human albumin (50 grams/L) has colloid osmotic pressure of 20 mm of Hg (that of plasma pressure); its effects last for 18 hours. It increases the volume 1:1.
  • 25% human albumin (250 grams/L) has got colloid osmotic pressure of 70 mm Hg; expands the intravascular volume 5 times more by shifting the fluid from extravascular (interstitial) space to intravascular space; should not be used in hypovolaemia.
  • It is used - when rapid plasma volume expansion is needed like burns in correcting hypovolaemia sometimes; in plasmapheresis as exchange fluid.
  • 500 ml of 5% albumin is infused at a rate of 2 ml per minute.
  • It is contraindicated in cardiac failure, anaemia.
  • It can cause allergic reactions, nausea, febrile reactions.
Dextran
Bacteria (Leuconostoc mesenteroides and Streptococcus mutans) incubated in sucrose media producing complex branched glucan polymers as dextrans.
  • Dextran is first discovered by Louis Pasteur in wine.
  • It is used to expand intravascular volume.
  • Dextran 70 has got molecular weight of 70,000. Its excretion through kidney is poorer and so remains in the blood for weeks. It is used as 6% solution.
  • Dextran 40 has got molecular weight of 40, 000. It is used as 10% solution; its action is faster but shorter than dextan 70 due to faster excretion through kidney compared to dextran 70.
  • It is used as volume expander in hypovolaemia. It increases the blood sugar also.
  • It is also used as antithrombotic agent. Dextran is a plasminogen activator; inhibits erythrocyte aggregation and platelet adhesiveness.
  • It improves microcirculation and blood flow.
  • Dextran 40 is commonly used.
  • It causes electrolyte disturbances and hyponatraemia.
  • It causes acute renal failure by direct toxicity to glomerulus and tubules and by intraluminal hyperviscosity.
  • It should be used carefully in diabetic patients.
  • It can cause pulmonary and or cerebral oedema also due hyperosmolarity.
  • It can cause anaphylaxis (being a potent antigenic).
  • It can interfere with blood grouping and cross matching.
  • It prolongs the bleeding time and so may precipitate bleeding.
Haemaccel
500 ml bottle with active ingredient polygeline.
  • 1000 ml of hamaccel contains polypeptides of degraded gelatin (origin—bovine bone; cross linked via urea bridges), 35 grams (equivalent of 6.3 gram of nitrogen).
  • It also contains sodium and chloride of 145 mmol (0.85 gram); calcium 6.25 mmol (0.25 gram); potassium 5.1 mmol (0.20 gram); traces of phosphate, sulphate and anionic polypeptides. Its molecular weight is 30,000 with 1.7 viscosity.
  • Hamaccel should be stored in 2–25°C.
  • Haemaccel does not induce antibody formation.
  • It is used as a rapid volume replacement in circulatory collapse like shock, burns and trauma. It is infused rapidly at a rate of 125 drops/minute. H2 blocker like cimetidine or ranitidine should be given along with haemaccel as it releases histamine.
  • It improves the plasma volume rapidly and remains like that for 5 hours.
  • It will not interfere with coagulation, blood grouping and cross matching.
  • It is used also in heart lung machine.
  • Haemaccel can be mixed with other IV fluids and drugs.
  • Haemaccel can be infused up to 2000 ml.
Rapid histamine release and anaphylactoid reaction.
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Hetastarch (hydroxyethyl starch)
It is nonionic starch derivative, which is ethoxylated amylopectins which is a plasma volume expander.
  • It is a synthetic colloid available as 6% solution in 0.9% normal saline (30 gram hetastarch in 500 ml of isotonic saline). It is administered IV only using infusion pump; 20 ml / kg / hour; it is stored in room temperature. It is enzymatically degraded and causes rise in serum amylase level.
  • Total dose per day should be 1500 ml only.
  • It is used in hypovolaemia— shock, burns, trauma.
  • It is also used in leukapheresis.
  • It is nonantigenic; does not interfere with blood grouping.
  • It shows greater plasma volume expansion for longer period compared to 5% albumin.
  • Anaphylactoid reactions can occur.
  • Renal impairment should be observed.
  • It has no O2 carrying capacity; so should not allow haematocrit to fall below 30%.
  • Impairment of coagulation is possible.
Pentastarch
It is a subgroup of hetastarch with five hydroxyethyl groups with 50% esterification. It is a low molecular weight derivative; it is more effective plasma volume expander.
It is available as 3%, 6% and 10% in normal saline.
  • It is used in hypovolaemia.
  • It is useful in cardiac surgeries.
 
NUTRITION
 
Principles of Nutrition
  • Avoiding of malnutrition is the basic goal in nutrition therapy as malnutrition increases the morbidity and mortality of the disease process and prevents or delays the recovery. Malnutrition increases the chance of sepsis, prevents wound healing, increases the respiratory complications, and decreases the efficacy and tolerance to radiotherapy or chemotherapy.
  • Whenever possible enteral route of nutrition should be used ideally. If that is not possible then parenteral nutrition is used.
  • Overfeeding should be avoided as it leads into hyperglycaemia, hepatic steatosis, raised BUN, and excess CO2 production.
  • Timing and type of nutrition is also important.
  • Nutrition therapy reduces protein wasting.
  • Immunomodulators like glutamine, arginine and omega 3 fatty acids are also very useful. Glutamine is a nonessential amino acid synthesized in skeletal muscle. It is essential for cell proliferation during tissue repair. Glutamine helps GI mucosal cell proliferation, maintains mucosal integrity, improves immune function and prevents translocation of bacteria. It is useful in inflammatory bowel disease, short gut syndrome, burns, major trauma, and sepsis. Glutamine is used commonly by enteral route even though IV preparations are now available (but it is very unstable in solutions).
Caloric requirement:
  • Neonatal 100 kcal/kg/day.
  • Adult 40 kcal/kg/day.
  • Adult with catabolism 60 kcal/kg/day.
It is given as:
  • Carbohydrates 50%.
  • Fat 30–40%.
  • Protein 10–15%.
Caloric values:
  • Carbohydrate 4 kcal/g.
  • Protein 4 kcal/g.
  • Fat 9 kcal/g.
 
Indications for Nutritional Support
  1. Preoperative nutritional depletion.
  2. Postoperative complications: Sepsis, ileus, fistula.
  3. Intestinal fistula: High type wherein output is more than 500 ml/day. It may be duodenal, biliary, pancreatic, intestinal.
  4. Pancreatitis, malabsorption, ulcerative colitis, pyloric stenosis.
  5. Anorexia nervosa and intractable vomiting.
  6. Trauma—multiple fractures, fasciomaxillary injuries, head and neck injuries.
  7. Burns.
  8. Malignant disease.
  9. Renal and liver failure.
  10. Massive bowel resection causing short bowel syndrome.
Nutritional requirements: Carbohydrates, fat, proteins, vitamins (includes fat-soluble vitamins also), minerals, trace elements.
 
Methods of Feeding
Enteral:
  1. Gastrointestinal tract is the best route to provide nutrition.
  2. Enteral feeding can be delivered by bolus, by gravity or using mechanical pump.
    • By mouth: Requires:
      • Common sense,
      • Cleanliness,
      • Compassion.
    • 102By nasogastric tube: Confirmation of the tube in the stomach is made by injecting 5 ml of air down the tube and listening through a stethoscope for its bubbling entry into the stomach. Feeding rate is 30–50 ml/hours. 5 hours night time gap is given to allow gastric pH to return to normal.
  1. By enterostomy:
    • Gastrostomy.
    • Jejunostomy.
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Fig. 1.197: Nasogastric tube passed should be confirmed in place using stethoscope. Tube is used for feeding purpose.
Different preparations and formulas are available for enteral feeding. Soluble fibre containing diets along with nutrients are better to prevent diarrhoea.
 
Advantages of Enteral Nutrition
  • Enteral nutrition preserves mucosal protein, digestive enzymes, IgA secretion; prevents mucosal atrophy and bacterial translocation.
  • It is more physiological as nutrients pass through liver, the first filter to process and store. Gallstone formation is prevented (unlike long-term TPN) by stimulating gall-bladder motility.
  • It has got less serious complications. It is cost-effective.
  • It supplies glutamine and short chained fatty acids to gut.
 
Contraindications of Enteral Nutrition
  • Intestinal obstruction, GI bleed, paralytic ileus, severe diarrhoea, high output fistula.
  • Low cardiac output, haemodynamically unstable patient.
  • If safe access to enteral feeding is not present.
  • Anticipated complications if thought to be present should be avoided.
 
GASTROSTOMY
It is done if feeding is required for more than one month.
 
Types
Based on duration of use:
  • Temporary.
  • Permanent.
Based on lining:
  • Mucus lined (permanent).
  • Serosal lined (temporary).
Based on technique:
  1. Stamm temporary gastrostomy: After opening the abdomen, anterior wall of the stomach is opened. Feeding tube (Malecot's catheter) is placed in position. Two layers of purse string sutures are put around the tube. Wound is closed.
    zoom view
    Fig. 1.198: Gastrostomy tube in place for enteral feeding.
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    zoom view
    Figs 1.199A and B: Percutaneous endoscopic gastrostomy (PEG). Guidewire passed through a trocar in the abdominal wall into the stomach is pulled out across the oesophagus and mouth under visualisation using gastroscope. Gastrostomy catheter (tube) is passed along the guidewire and pushed downwards across mouth and oesophagus to reach the stomach. It is further pushed along the abdominal wall through the trocar. Gastrostomy tube is pulled out through abdominal wall and fixed. Trocar is removed. Placement of tip of gastrostomy tube can be confirmed by doing gastroscope.
  2. Kader-Senn temporary gastrostomy.
  3. Percutaneous endoscopic gastrostomy (popular)—now becoming common method.
  4. Janeway's mucus lined permanent gastrostomy by creating tunnel in stomach wall.
 
Contraindications
  • Previous gastric surgeries.
  • Intestinal obstruction.
  • Gastric outlet obstruction.
 
JEJUNOSTOMY
Jejunostomy for enteral nutrition is becoming more popular because of:
  • Its comfort,
  • Easy to do,
  • Can be kept for long time,
  • Lesser complication than gastrostomy.
Indications are same as gastrostomy.
 
Types
  1. Witzel jejunostomy: Site of placing jejunostomy is 30 cm from duodenojejunal junction.
  2. Needle jejunostomy using catheter of small gauge.
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Fig. 1.200: Needle jejunostomy.
 
TOTAL PARENTERAL NUTRITION (TPN)
All nutritional requirements are given only through intravenous route, not through gastrointestinal tract. It can be through a central catheter through the subclavian/internal jugular vein where the tip of venous catheter is at distal part of superior vena cava.
It can also be a peripheral (Peripheral parenteral nutrition/PPN) through a peripherally inserted central venous catheter (PICC) or through a formal peripheral venous line.
About 5% of hospital admissions require TPN.
 
Technique
  • Using a needle and guide wire a Subclavian vein catheter is passed just below the clavicle and fixed securely to the skin.
  • TPN is given through central vein and not through a peripheral vein.
  • Peripherally inserted central catheter (PICC) is also commonly used (PPN).
 
Goals, Factors and Assessment in TPN
  • To decrease adverse effects of catabolism; to increase protein synthesis, to reduce protein breakdown, to prevent weight loss.
  • To support ongoing metabolism.
  • To improve immune function, cardiac and respiratory function.
  • To maintain glycogen reserve in cardiac and respiratory muscles.
  • To maintain acid, base and electrolyte metabolism.
  • Age, premorbid state, muscle mass, weight, serum albumin should be assessed.
  • Underlying disease, its severity, therapies for the disease, GI function should be assessed.
  • Fluid requirement is assessed by—1500 ml for 20 kg weight + 20 ml/kg for additional weight.
  • Energy needed is calculated by calculating resting energy expenditure (REE).
    • By simple calculation: REE in kcal/day = 25 × weight in kg.
    • Harris Benedict equation: REE in men = 66 + (13.7 × weight in kg) + (5 × ht in cm) – (6.7 × age in years). In women = 655 + (9.6 × weight) + (1.8 × ht) – (4.7 × age). Activity/disease/thermal factors are also added.
    • Indirect calorimetry: It is more accurate method done using special instrument. REE: = (3.9 × VO2) + (1.1 × VCO2) – 61.
 
Components used in TPN/PPN
Carbohydrates: Dextrose is less costly (1 gram dextrose 3.4 kcal); can be used in 50–70% concentration during PN. It supplies calories, stimulates insulin release and glucose oxidation, prevents muscle protein breakdown, has got nitrogen sparing ability. Problems of carbohydrate/dextrose are—low calorie value compared to fat, requires large fluid volume to infuse, hyperglycaemia, causes more CO2 production, because of high osmolality it causes thrombophlebitis in 10% or above concentration. Rate of administration of dextrose is 5 mg/kg/min.
Fat: Fat gives high calorie (1 gram—9 kcal), essential fatty acids. It is given as emulsion containing long chain triglycerides. It contains soyabean/sunflower oil with egg yolk phospholipids (emulsifying factor), glycerin (isotonic). Fat has got low osmolality (260 mosm/L); it is available as 10%, 20%, 30% emulsions. Advantages of fat in PN are—high calorie, prevents hyperglycaemia, glucose and nitrogen sparing, less CO2 production, less insulin production; it prevents essential fatty acid deficiency (for this purpose 3 days a week dose is given), reduces thrombophlebitis. Problems of lipids in PN are—hypertriglyceridaemia, sepsis, fat embolism, fat overload, hepatic dysfunction, pancreatitis, delayed gastric emptying. Lipid emulsions are avoided in hyperlipidaemia, anaemia, acidosis, obesity. Lipid emulsion is a good culture media for bacteria and fungi; so care should be taken to prevent sepsis. Triglyceride level should be monitored weekly; if more than 400 mg%, infusion is discontinued. Mixture of long and medium chain fatty acids is better tolerated and efficient.
Amino acids: They are source of proteins. Calorie value of amino acid is 4 kcal/gram. 6.25 gram protein has 1 gram nitrogen. In PN 20% of energy comes from amino acids; rest from dextrose and fat. Daily protein need is 0.8–1.5 gram/kg. Protein supplement should be less in patients with CRF and hepatic encephalopathy. Its need is more in burns, trauma, enteropathy, sepsis. Protein supplement should not exceed 1.7 gram/kg/day; if so will cause raised urea production. Uses of amino acids in PN—in protein anabolism; prevents scatabolism. Proper monitoring by doing BUN or ammonia level is essential during amino acid therapy.
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Vitamins, electrolytes, trace elements and minerals: Electrolytes like sodium, potassium, magnesium, phosphate, calcium; fat-soluble vitamins like A, D, E, K; water-soluble vitamins; trace elements like chromium, copper, iodine, iron, manganese, selenium, zinc are all used in PN.
 
Complications
 
Technical
  1. Air embolism.
  2. Pneumothorax.
  3. Bleeding.
  4. Catheter displacement, sepsis, blockage.
  5. Infection, thrombosis.
 
Biochemical
  1. Electrolyte imbalance: Hyponatraemia, hypokalaemia, hypophosphataemia.
  2. Hyperosmolarity.
  3. Hyperglycaemia—common.
  4. Dehydration.
  5. Altered immunological and reticuloendothelial function.
  6. Azotaemia.
 
Others
  1. Dermatitis.
  2. Anaemia and increased capillary permeability.
  3. Cholestatic jaundice: It is common.
  4. Severe hepatic steatosis.
  5. Metabolic acidosis.
  6. Candida infection (candidiasis), staphylococcal infection (10–15%).
Anabolic steroid durabolin 25 mg IM weekly is given to improve nitrogen balance.
 
REFEEDING SYNDROME
  • Refeeding syndrome is occurrence of severe fluid and electrolyte imbalance in severely malnourished individual while starting the proper feeding enteral or parenteral nutrition. It is more common in TPN.
  • It causes hypomagnesaemia, hypocalcaemia and hypophosphataemia leading into myocardial dysfunction, respiratory changes, altered liver functions, altered level of consciousness, convulsions and often death.
  • Gradual feeding and correction of magnesium, phosphate and calcium and other electrolytes is important.
  • Condition is common in chronic starvation, severe anorexia and alcoholic patients.
 
OBESITY AND MORBID OBESITY
Obesity is weight more than 20% above the normal. Body mass index (BMI) is weight in kilogram divided by height in metres squared [wt in kg/(Ht in meters)2].
Morbid obesity is a condition wherein BMI is more than 40 kg/m2. It is often also defined as weight 100 lbs or more; or 100% over ideal body weight.
Weight more than double the expected weight to that age and height of the individual is also often called as morbid obesity. Body weight exceeding BMI 50 kg/m2 is called as superobesity.
 
Causes of obesity
  • Familial, hyperinsulinism, hyperadrenocorticism, hyogonadism.
  • Abnormal eating behaviour: Hormones which control eating are—ghrelin from stomach; insulin from pancreas; leptin from fat; PYY 3–36 from colon. Hypothalamus is the center in CNS which controls eating.
Nutritional status
BMI (kg/m2)
  • Underweight
  • <18.5
  • Normal
  • 18.5–24.9
  • Overweight (Preobesity)
  • 25.0–29.9
  • Obesity
  • >30
  • Class I
  • 30.0–34.9
  • Class II (Moderate)
  • 35.0–39.9
  • Class III (Severe / Morbid)
  • 40.0
  • Superobesity
  • >50
  • Super superobesity
  • >60
Obesity is more common in young women. Child of a normal weight parents has 10% chance to become obese. If both parents are obese then child has got 80% chances to develop obesity.
 
Problems with Morbid Obesity
Obstructive sleep apnoea, degenerative joint disease, back pain, hypertension, GERD, gallstones, type II diabetes, hyperlipidaemia, arrhythmias, venous diseases, DVT, skin diseases, urine incontinence, infertility, ventral hernias, obesity hypoventilation syndrome, polycystic ovarian disease, hirsutism, gynaecomastia, steatohepatosis, malignancies—are common problems. All these conditions are called as comorbidities.
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Infertility is common in married morbid obese women due to improper ovulation, polycystic ovary disease. Urinary incontinence is common in morbid obese women (stress incontinence and detrusor instability). Pregnancy in morbid obese patient is considered as high-risk pregnancy. Gestational diabetes, hypertension, are common. It is better these women to undergo bariatric surgery prior to pregnancy which definitely reduces the complications during pregnancy. Such individual after bariatric surgery needs more iron and vitamin supplements.
Evaluation of the patient—cardiac and respiratory assessment; lipid profile; blood glucose; renal and liver status assessment; anaesthesia risk assessment.
 
Medical Management
  • General: Diet, life style changes, exercise.
  • Drugs: (1) Orlistat is a selective inhibitor of gastric and pancreatic lipases that reduces the absorption of lipids from intestine. (2) Sibutramine is a noradrenaline and 5 HT reuptake inhibitor which act as appetite suppressor.
 
Surgical Treatment (Bariatric Surgery)
Bariatric surgery causes long-term durable weight loss. Patient's eating behaviour is reduced to slow ingestion of small boluses of food and or also reducing the absorptive surfaces.
 
Types of Bariatric Surgery
  1. Restrictive wherein caloric intake is reduced. Purely gastric restrictive procedures are vertical banded gastroplasty (VBG) and laparoscopic adjustable gastric banding (LAGB).
  2. Malabsorptive wherein absorption of calories and nutrients from food is reduced. Biliopancreatic diversion (BPD) and biliopancreatic diversion with duodenal switch (BPD-DS) are malabsorptive procedures.
  3. Combined wherein both methods are used. Roux-en-Y gastric bypass (RYGB) is both restrictive and malabsorptive types. Gastric bypass reduces GI polypeptide ghrelin level secreted from fundus of stomach and duodenum. Ghrelin acts on specific receptor in CNS—hypothalamus to initiate appetite. This stimulation is reduced to decrease appetite. In restrictive only procedure ghrelin level raises and so appetite stimulation is not controlled.
 
Indications for Bariatric Surgery
BMI more than 40 kg/m2 or BMI more than 35 kg/m2 with comorbidity is indication for bariatric surgery. American Association of Bariatric Surgery (ASBS) published indications and approved surgeries.
 
Contraindications
Patients who are unfit for general anaesthesia (cardiac/renal/respiratory/hepatic causes) or who are unable to adjust post-operative life styles or psychiatric patients are contraindications for bariatric surgery.
 
Preoperative Preparations and Evaluation
  • Complete cardiac, respiratory/renal/hepatic evaluation.
  • Lipid profile and blood glucose assessment.
  • Obstructive sleep apnoea in obese patient should be assessed using polysomnography and be treated.
  • Risk assessment for DVT should be done.
  • If GERD symptoms are present gastroscopy should be done.
  • USG abdomen to identify gallstones should be done; if gallstones present it is of usual practice to do cholecystectomy along with bariatric procedure.
  • Nutritional evaluation and dietician advice for preoperative and postoperative diet management.
  • Psychological screening is needed to all patients to counsel their postoperative care and diet.
  • Separate theatre table is needed for morbid obese patient. Equipments should be long and flexible. In laparoscopic surgery, special ports and instruments are needed.
 
DIFFERENT SURGERIES
 
Vertical Banded Gastroplasty (VBG); Mason (1982)
It is a purely restrictive type with creation of a calibrated stoma in the lesser curvature which is reinforced by an encircled mesh with a proximal gastric pouch. After laparotomy Ewald's stomach tube is passed per orally to place against lesser curve. A 2.5 cm circular window is created in the body of stomach near lesser curvature 8 cm below the angle of His. After this, four lines of linear vertical stapling are done from circular opening towards angle of His. This staple line ideally should be divided using another cutting linear stapler to reduce chances of dehiscence. This creates a 50 ml proximal gastric pouch. A 1.5 × 7 cm polypropylene mesh is placed around the lesser curve through circular opening and sutured to create a 5 cm collar stoma. It is not used at present; it is only of historical importance.
Complications of obesity
Obesity and surgery
Treatment for obesity
  • General: Difficulty in work, fatigue, depression, back pain, arthritis and gout
  • Cardiovascular: Hypertension, stroke, thrombophlebitis, pulmonary embolism
  • Pulmonary: Hypoventilation, poor respiratory effort
  • GIT: Hiatus hernia with reflux, changes in liver, pancreatitis, gallstones
  • Endocrine: Diabetes mellitus
  • Hernia and gallstones are more common in obese individual
  • Burst abdomen, incisional hernia are more common in obesity
  • Delay in recovering from anaesthesia
  • Infertility is more common
  • General: Dieting, exercise
  • Drugs: Orlistat, Sibutramine
  • Surgeries:
    • Restrictive
      • Vertical banded gastroplasty
      • Laparoscopic adjustable gastric banding (LAGB)
      • Jaw wiring
    • Malabsorptive
      • Biliopancreatic diversion (BPD)
      • Biliopancreatic diversion with duodenal switch (BPD-DS)
      • Jejunoileal bypass
    • Combined
    • Roux-en-Y gastric bypass (RYGB) open or laparoscopic
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zoom view
Fig. 1.201: Vertical banded gastroplasty (VBG).
VBG causes only medium term weight loss; its efficacy is less compared to other procedures. Complications of VBG are—stricture at stoma (20%), vomiting (30%), reflux (20%), staple line dehiscence (40%), conversion into other procedures. Mortality is 0.3%.
VBG is technically easier to do; it has got very less chances of long-term metabolic and nutritional deficiencies.
 
Laparoscopic Adjustable Gastric Banding (LAGB)
It is also a restrictive type (1992, Guy Bernard) to create a narrow stoma just below the OG junction. It is used in adolescents and elderly. It is contraindicated in hiatal and paraoesophageal hernias. It is done using laparoscopy.
Under general anaesthesia, with patient in reverse Trendelenburg position six laparoscopic ports are placed. Using pars flaccida method, retrogastric tunnel is created; a silicone band is passed through the tunnel to encircle the cardia just below the OG junction; tail of the band is buckled and locked. Stoma diameter is determined by inserting a calibration tube. Stomach over the band is imbricated using interrupted sutures except the buckle area. Silicone tube end is brought out through the abdominal wall to connect access port. It is used for band volume adjustment by injecting or withdrawing the saline.
Gastrograffin study is done on 1st postoperative day to assess band position and lumen patency. Patient is advised to have liquid diet for one month. Band adjustment is done under fluoroscopic guidance in 2 months. Adjustment is done to achieve weight loss at a rate of 2 kg/week. Efficacy of LAGB is 55%.
Complications of LAGB are—spleen/stomach injury; bleeding; band slippage (10%); band erosion (7.5%); tube related complications; vomiting; pouch dilatation; reflux. Conversion rate is 3%; mortality is less than 0.5%.
 
Jejunoileal Bypass
It was the first malabsorptive procedure done for obesity. Now this technique is not done due to high incidences of complications.
Proximal jejunum is divided and proximal cut end is anastomosed to distal ileum just proximal to ileocaecal valve to reduce the absorptive surface area of small bowel.
Complication rates were higher and so procedure is not practiced. Colon in these patients absorbs high level of oxalate causing nephrocalcinosis. Bypassed bowel promotes bacterial growth causing endotoxic-induced liver injury, cirrhosis, liver failure. Complications like protein, vtamin K, vtamin B12 deficiencies; gallstone formation; enteritis and diarrhoea; arthritis, osteoporosis are common.
 
Roux-en-Y Gastric Bypass
It is commonly done combined procedure. It can be done by open or laparoscopic method. Proximal stomach is dissected between 1st and 2nd branches of left gastric branches. Vagii nerves and nerves of Latarjet are retained carefully. Stomach is transected at this proximal site to create a proximal gastric pouch (15 ml if BMI is > 50; 30 ml if BMI is 40–50). It is usually carried out through linear stapler. Jejunum is transected 45 cm from ligament of Treitz. A side to side jejunojejunal anastomosis is done using stapler 75 cm distal to the distal cut end. Proximal Roux part of the distal jejunal cut part (75–150 cm, based on patient's preoperative weight) is brought out through the transverse mesocolon towards the created proximal gastric pouch and gastrojejunostomy is done to this proximal gastric pouch. Mesenteric defect is closed. Stomal integrity is checked on table by air distension and methylene blue infusion. Gastrograffin study is done in 24 hours to assess pouch size, stomal patency and distal obstruction. Oral food is started in 24 hours and patient is discharged in 4 days.
RYGB is more useful in weight loss compared to purely restrictive types. 5 years weight loss is 60–75%. It also prevents progression of noninsulin dependent diabetes mellitus, controls hypertension, sleep apnoea, hyperlipidaemia, asthma, arthritis, GERD.
Complications are— Roux obstruction, anastomotic leak, acute distal gastric dilatation, stomal stenosis, marginal ulcer, dumping syndrome, internal hernias, vitamin B12 deficiency, iron deficiency anaemia. Distal gastric dilatation needs emergency intervention which is usually due to jejunojejunal obstruction.
 
Laparoscopic RYGB (1994, Wittgrove, Clark, Trembly)
Technique is similar to open RYGB. Anastomoses are done using endoscopic stapler. GJ between gastric pouch and Roux jejunum is done either using linear stapler through laparoscopic port after making a gastrotomy in the pouch which is later sutured after staple firing; or using circular stapler anastomosis is done wherein anvil is initially passed transorally often under endoscopic guidance across the pouch into the 108Roux jejunum; or using hand sewing with absorbable sutures. Omentum is released from the colon and is covered over the GJ. Mesenteric defect and Patterson Brown defect are closed. A Bronlin antiobstructive stitch is placed between Roux and biliopancreatic limbs. Integrity of anastomosis is checked using insufflation of air, methylene blue. Complications are similar to open RYBG. Conversion rate is 9%. Advantages of LRYBG to open RYBG are—faster recovery, less post-operative pain, less wound related complications, less morbid one. Disadvantage of LRYBG is availability of facility, technical expertise, and steep learning curve.
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Fig. 1.202: Laparoscopic adjustable gastric banding (LAGB).
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Fig. 1.203: Jejunoileal bypass procedure (JIB).
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Fig. 1.204: Roux-en-Y gastric bypass procedure (RYBG).
Now technique is modified to antegastric, antecolic one which has become popular (Gagner).
 
Biliopancreatic Diversion (BPD) (Nicola Scopinaro, Italy)
It is done in patients who had failed restrictive procedure or who are superobese.
Distal subtotal gastrectomy is done with formation of proximal gastric pouch (of 400 ml in BMI 40–50; 200 ml in BMI >50). Ileum is transected 250 cm proximal to ileocaecal valve; distal ileal segment is brought up to anastomose into the proximal gastric pouch. Proximal biliopancreatic jejunoileal limb is anastomosed into distal ileal segment 50 cm proximal to ileocaecal valve as end to side stoma. Additionally cholecystectomy should be done.
Modification of BPD with duodenal switch (BPD-DS) has become more popular. Here sleeve gastrectomy along the greater curvature is done to create gastric reservoir (200 ml) along lesser curve. Duodenum just distal to first part is divided using stapler; proximal cut end is sutured to proximal upward pulled end of the distal ileal segment of earlier transected ileum, 250 cm from ileocaecal valve. Biliopancreaticoduodenal with proximal jejunoileal segment is later stapled to distal ileum 50 cm proximal to ileocaecal valve. Duodenal switch reduces the rate of marginal ulcer and dumping syndrome.
Results of BPD/BPD-DS are—excellent for weight reduction compared to restrictive procedures. But they need lifelong supplement of vitamins, fat-soluble vitamins, calcium, and iron. Technically BPD is easier to do when compared to BPD-DS.
Complications of BPD/BPD-DS are—anemia (30%); protein deficiency (20%); dumping syndrome; marginal ulcer (in BPD 10%; in BPD-DS it is 1%); osteoporosis; night blindness; biliopancreatic limb obstruction; staple line leak; staple line bleed; DVT; subphrenic abscess. Vitamin B12 deficiency is specific.
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Fig. 1.205: Biliopancreatic diversion procedure (BPD).
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Fig. 1.206: Biliopancreatic diversion with duodenal switch procedure (BPD-DS).
 
Ileal Interposition with Sleeve Gastrectomy
It is done mainly in type II diabetes. Often they are associated with obesity, dyslipidaemia, hypertension, nephropathy and neuropathy. Two types of ileal interposition with sleeve gastrectomy are done.
Type 1: Sleeve gastrectomy is done. 170 cm of ileum with mesentery is isolated 30 cm from ileocaecal junction. Jejunum is transected 50 cm from duodenojejunal flexure. Isolated 170 cm ileal segment is interposed 50 cm distal to DJ junction with end-to-end anastomosis on both ends.
Type 2: After doing sleeve gastrectomy, gastroduodenal junction is transected; cut proximal end of duodenum is closed. 170 cm ileal segment with mesentry is isolated and interposed between cut end of stomach and side of jejunum 50 cm distal to DJ flexure.
 
Cholecystolithiasis After Bariatric Surgery
Gallstone formation is common after bariatric surgery (50%). It is due to rapid weight loss. If gallstones are present at the time of bariatric surgery it is essential to do laparoscopic cholecystectomy during bariatric procedure. It is controversial about doing prophylactic cholecystectomy during bariatric surgery even though it is practiced in many places. Advantages are—it prevents future gallstone formation at the time of bariatric surgery (loss of access); it prevents difficulties in approaching CBD in case needed endoscopically due to surgery. Disadvantage is cholecystectomy adds additional 1 hour time for bariatric surgery increasing the risk of immediate complications. Patients who are not having gallstones at the time of bariatric surgery, should receive ursodeoxycholic acid 300 mg twice daily for 6-12 months of post-bariatric surgery period. Often stomach is anchored to abdominal wall as access part to biliary system for future need.
Note:
Many of these patients after bariatric surgery require plastic surgery for abdominal contour (panniculectomy, abdominoplasty) after weight reduction due to bariatric surgery.
110G. Shock
The first noteworthy characteristic of the blood in shock is a high capillary red count…. When haemorrhage as a complicating factor tending to reduce the blood count is considered, these high counts are striking. They indicate that in shock a concentration of the blood occurs, at least in the superficial capillaries.
—Walter Bradford Cannon, J Fraser, AN Hooper, 1918
CHAPTER OUTLINE
  • ❖ Shock
  • ❖ Stages of Shock
  • ❖ Effects of Shock
  • ❖ Clinical Features of Shock
  • ❖ Assessment, Investigations and Monitoring
  • ❖ Investigations in Shock
  • ❖ Central Venous Pressure
  • ❖ Pulmonary Capillary Wedge Pressure
  • ❖ Systemic Inflammatory Response Syndrome
  • ❖ Multiple Organ Dysfunction Syndrome
  • ❖ Oxygen Therapy
  • ❖ Topical O2 Therapy
  • ❖ Cardiac Arrest
 
SHOCK
Shock is a state of poor perfusion with impaired cellular metabolism manifesting with severe pathophysiological abnormalities. It is due to circulatory collapse and tissue hypoxia. Normal aerobic metabolism is not maintained due to hypoperfusion. Shock is meant by ‘inadequate perfusion’ to maintain normal organ function.
At cellular level hypoxia causes change of normal aerobic to anaerobic metabolism causing lactic acidosis. Intracellular potassium is released into circulation. Lysosomes from cells get released into blood causing cell lysis. Hypoxia and acidosis through complements release free oxygen radicals and cytokines which damage capillary endothelium. Eventually cardiovascular, respiratory, renal, endocrine and GIT will be affected presenting as systemic features.
Shock may be hypovolaemic, cardiogenic, obstructive, distributive or of endocrine variety.
 
Pathophysiology of Shock
Any cause of shock
Low cardiac output
Vasoconstriction occurs as a compensation to perfuse vital organs like brain, heart, kidneys, liver
Because of vasoconstriction and tachycardia
Dynamic circulation increases
Tachypnoea occurs to increase the oxygen saturation
Peripheral veins (capacitance vessels) constrict diverting blood from splanchnic system towards essential vital organs
111Decreased renal blood flow reduces the GFR and thereby the urine output
Renin angiotensin mechanism gets activated causing further vasoconstriction and aldosterone release
Causes salt and water retention
ADH is released
Further concentration of urine occurs
When shock persists cardiac output falls further
Hypotension and tachycardia occurs leading to poor perfusion of coronaries
Hypoxia—metabolic acidosis
Release of cardiac depressants
Cardiac (pump) failure
Hypoxia
Anaerobic metabolism
Lactic acidosis
Cell wall damage
Sodium and calcium enter the cell
Potassium leaks out of the cell
Causes hyperkalaemia, hyponatraemia and hypocalcaemia
Intracellular lysosomes break down releasing powerful enzymes which destroy own cell
SICK CELL SYNDROME
Platelets are activated forming small clots in many places
Disseminated intravascular coagulation (DIC) (Consumption coagulopathy)
Further bleeding.
 
STAGES OF SHOCK
Factors like infection, trauma, burns, haemorrhage, hypovolaemia
Hypoxia and its effects.
SIRS (Systemic inflammatory response syndrome) is due to vasodilatation, increased endothelial permeability, thrombosis, leucocyte migration and activation.
All these lead to altered cytokines level, abnormal NO (nitric oxide) synthesis, abnormal arachidonic acid metabolism, neutrophil activation, free radical production, altered complement activation, failure to have a localisation of inflammation. It is severe type of reversible shock.
Which will lead to established microvascular occlusion, cellular dysfunction, sick cell syndrome, DIC and PUMP failure.
MODS (Multiorgan dysfunction syndrome) (Irreversible shock)—of lungs, kidneys, liver, clotting system and brain.
Stages of shock
Stage 1
Stage of compensatory shock by neuroendocrine response to maintain the perfusion of the vital organs like brain, heart, kidney, liver.
Stage 2
Stage of decompensatory shock where there is progressive shock causing persistent shock with severe hypotension (with mean arterial pressure < 65 mmHg); oliguria, tachycardia.
Stage 3
Stage of irreversible shock with severe hypoxia and MODS.
Note:
  • Distributive shock is one in which there is vasodilatation, decreased vascular resistance, hypotension, altered micro-vascular perfusion with arteriovenous shunting, altered cellular oxygen metabolism. It is seen in septic shock, spinal trauma, adrenal crisis and anaphylaxis.
  • Obstructive shock occurs due to mechanical impediment of circulation due to pulmonary embolism, tension pneumothorax or cardiac tamponade.
 
EFFECTS OF SHOCK
Heart: Low perfusion → low venous return → decreased cardiac output → hypotension → tachycardia. Persistent shock causes hypoxia and release of myocardial depressants leading to further cardiac damage.
Lung: Interstitial oedema → decreased gaseous exchange → pulmonary arteriovenous shunting → tachypnoea → Adult/Acute respiratory distress syndrome (ARDS) and pulmonary oedema.
Metabolic: Shock leads to hypoxia, which activates anaerobic metabolism leading to lactic acidosis. Antidiuretic hormone (ADH) is released which increases the reabsorption of water from renal tubules. Other hormones released are ACTH, prostaglandins, histamine, bradykinin, and serotonin to compensate the effects of shock to increase the perfusion of vital organs like heart, brain and lungs.
Cellular changes occur in persistent shock due to release of lysosomal enzymes, which alters the cell membrane permeability causing cell death—sick cell syndrome.
112Sympathetic overactivity alters the microcirculation leading to capillary dysfunction.
Brain perfusion, when decreases the patient becomes drowsy. Brain is the last organ to get underperfused in shock.
Kidneys: GFR decreases and tubular reabsorption of salt and water increases for compensatory response. But in severe cases tubular necrosis sets in leading into irreversible damage.
Blood: Alteration in cellular components including platelets leads to Disseminated intravascular coagulation (DIC). It causes bleeding from all organs.
Gastrointestinal tract: Mucosal ischaemia develops causing bleeding from GIT with haematemesis and malaena. It is aggravated by DIC. Hepatic ischaemia leads into increased enzyme levels.
 
Types of Shock
 
1. Vasovagal shock
It is sudden dilatation of peripheral and splanchnic vessels causing reduced cardiac output and shock. Often it may be life-threatening due to hypoxia.
 
2. Neurogenic shock
  • It is usually due to spinal cord injury, which causes dilatation of splanchnic vessels.
    • This type can safely be treated with vasoconstrictor drugs to bring up the blood pressure. There will be bradycardia, hypotension, arrhythmias, and decreased cardiac output. Blood pressure control, oxygen delivery, maintenance of haemodynamics, airway, fluid therapy, intravenous methylprednisolone therapy should be done. Dopamine and or phenylephrine (α agonist) can be used.
 
3. Hypovolaemic shock—most common type
  • Haemorrhage, may be due to injury to the liver, spleen, bone fractures, haemothorax, vascular injury, severe bleeding on table during surgeries of thyroid, liver, portal vein or major vessels.
  • Vomiting, diarrhoea due to any cause.
  • Burns.
 
4. Cardiogenic shock
  • Cardiogenic shock is defined as circulatory failure causing diminished forward flow leading into tissue hypoxia in the setting of adequate intravascular volume with systolic blood pressure <90 mmHg for 30 minutes; cardiac index <2.2 L/minute/sq metre; raised PCWP (pulmonary capillary wedge pressure) >15 mmHg. It is commonly seen in acute MI with a mortality >50%.
  • Cardiogenic shock develops within 24 hours of MI. It occurs when 50% of left ventricular wall is damaged by infarction.
  • It leads to pulmonary oedema and severe hypoxia. Ischaemic necrosis of left ventricular wall causes failure of pump thereby decreasing stroke volume.
Diagnosis is established by ECG, echocardiography, arterial blood gas analysis, cardiac enzymes, PCWP and electrolyte estimation (hypokalaemia and hypomagnesaemia are common) are the essential investigations.
Management
  • Proper oxygenation with intubation, ventilator support, cardioversion, pacing, antiarrhythmic drugs, correction of electrolytes, avoiding fluid overload, prevention of pulmonary oedema as immediate measures.
  • Dobutamine (β1 receptor agonist) is used to raise cardiac output provided there is adequate preload and intravascular volume (it is peripheral vasodilator and reduces BP). Dopamine is preferred in patients with hypotension. But it may increase peripheral resistance and heart rate worsening cardiac ischaemia. Often both dopamine and dobutamine combination may be required.
  • Careful judicial use of epinephrine, norepinephrine, phosphodiesterase inhibitors (amrinone, milrinone) are often needed. Anticoagulants and aspirin are given. Thrombolytics can be used. β blockers, nitrates (nitroglycerine causes coronary arterial dilatation), ACE inhibitors are also used.
  • Intra-aortic balloon pump (IABP) may need to be introduced transfemorally as a mechanical circulatory support to raise cardiac output and coronary blood flow.
  • Relief of pain, preserving of remaining myocardium and its function, maintaining adequate preload, oxygenation, minimizing sympathetic stimulation, correction of electrolytes should be the priorities.
  • Percutaneous transluminal coronary angioplasty (PTCA) and coronary artery bypass graft (CABG) are the final choices.
 
5. Cardiac compression shock
  • It is probably due to pericardial tamponade of any cause or kinking of great vessels, massive pulmonary embolism, tension pneumothorax, air embolism causes obstructive shock with reduced preload to heart.
  • Acute massive pulmonary embolism from a thrombus or an air embolism (50 ml of air), obstructing more than 50% of pulmonary vasculature leads to severe shock and sudden death.
  • Tachycardia, hypotension, pulmonary oedema, raised JVP, gallop rhythm are the features.
 
6. Septic shock
  • Septic shock may be due to gram-positive organisms, gram negative organisms, fungi, viruses or protozoal origin.
  • 113Gram-negative septicaemia/gram-negative septic shock is called as endotoxic shock. It occurs due to gram-negative bacterial infections, commonly seen in strangulated intestines, peritonitis, gastrointestinal fistulas, biliary and urinary infections, pancreatitis, major surgical wounds, diabetic wounds and crush injuries.
Gram-positive septic shock
Gram-negative septic shock
  • Due to exotoxin by gram +ve bacteraemia like Clostridium tetani/welchii, staphylococci, streptococci pneumococci
  • Fluid loss, hypotension is common; with normal cardiac output
Gram negative bacteria cause endotoxaemia and its effects. Urinary/gastrointestinal/biliary and respiratory foci are common
Pathophysiology of septic shock
Toxins/endotoxins from organisms like E. Coli, Klebsiella, Pseudomonas, and Proteus
Inflammation, cellular activation of macrophages, neutrophils, monocytes
Release of cytokines, free radicals
Chemotaxis of cells, endothelial injury, altered coagulation cascade—SIRS
Reversible hyperdynamic warm stage of septic shock with fever, tachycardia, tachypnoea
Severe circulatory failure with MODS (failure of lungs, kidneys, liver, heart) with DIC
Hypodynamic, irreversible cold stage of septic shock.
  • Septic shock is typically a vasodilatory shock wherein there is peripheral vasodilatation causing hypotension which is resistant to vasopressors. This is due to toxin induced release of isoform of nitric oxide synthetase from the vessel wall which causes sustained prolonged release of high levels of nitric oxide.
  • Magnitude of infection is quantified as:
    1. Sepsis which shows fever, tachycardia, leucocytosis.
    2. Severe sepsis which shows low tissue perfusion with organ dysfunction (lactic acidosis, dysfunction of liver, kidney, lungs).
    3. Septic shock with systemic hypotension (BP < 90 mmHg in spite adequate fluid therapy), severe organ dysfunction (acute lung, kidney, liver injury), maldistribution of blood flow, shunting in microcirculation.
Stages of septic shock
  1. Hyperdynamic (warm) shock:
    This stage is reversible stage. Patient is still having inflammatory response and so presents with fever, tachycardia, and tachypnoea. Pyrogenic response is still intact. Patient should be treated properly at this stage. Based on blood culture, urine culture (depending on the focus of infection), higher antibiotics like third generation cephalosporins, aminoglycosides, metronidazole are started. The underlying cause is treated like draining the pus, laparotomy for peritonitis, etc. Ventilatory support with ICU monitoring may prevent the patient going for the next cold stage of sepsis.
  2. Hypodynamic hypovolaemic septic shock (cold septic shock):
    Here pyrogenic response is lost. Patient is in decompensated shock. It is an irreversible stage along with MODS (Multi-organ dysfunction syndrome) with anuria, respiratory failure (cyanosis), jaundice (liver failure), cardiac depression, pulmonary oedema, hypoxia, drowsiness, eventually coma and death occurs (Irreversible stage).
Treatment of septic shock
  • Correction of fluid and electrolyte by crystalloids, blood transfusion. Perfusion is very/most important.
  • Appropriate antibiotics—third generation cephalosporins/aminoglycosides.
  • Treat the cause or focus—drainage of an abscess; laparotomy for peritonitis; resection of gangrenous bowel; wound excision.
  • Pus/urine/discharge/bile/blood culture and sensitivity for antibiotics.
  • Critical care, oxygen, ventilator support, dobutamine/ dopamine/noradrenaline to maintain blood pressure and urine output.
  • Activated C protein prevents the release of inflammatory mediators and blocks the effects of these mediators on cellular function.
  • Monitoring the patient by pulse oximetry, cardiac status, urine output, arterial blood gas analysis.
  • Short-term (one or two doses) high dose steroid therapy to control and protect cells from effects of endotoxaemia. It improves cardiac, renal and lung functions. Single dose of methylprednisolone or dexamethasone which often may be repeated again after 4 hours is said to be effective in endotoxic shock.
 
7. Anaphylactic shock
Injections—penicillins, anaesthetics, stings, venom, shellfish may be having antigens which will combine with IgE of mast cells and basophils, releasing histamine and large amount of SRS-A (Slow releasing substance of anaphylaxis). They cause bronchospasm, laryngeal oedema, respiratory distress, hypotension and shock. Mortality is 10%.
Rashes all over the body are commonly observed.
114
 
CLINICAL FEATURES OF SHOCK (HYPOVOL AEMIC SHOCK)
  • In early stage—tachycardia, sweating, cold periphery, hypotension, restlessness, air hunger, tachypnoea, oliguria, collapsed veins.
  • In late stage—cyanosis, anuria, jaundice, drowsiness.
Clinically shock may be:
  • Compensated with mild tachycardia, normal blood pressure, urine output, normal respiration and mild lactic acidosis.
  • Mild shock with mild lactic acidosis, tachycardia, tachypnoea and anxiousness.
  • Moderate shock with significant lactic acidosis, decreased urine, tachycardia, tachypnoea, drowsiness, and mild hypotension.
  • Severe shock with severe lactic acidosis, anuria, tachypnoea with gasping, severe tachycardia, profound hypotension and unconsciousness.
Note:
  • Shock index is ratio of pulse rate to blood pressure; normal shock index is < 1. In shock it reverses.
  • Tachycardia, tachypnoea, oliguria, hypotension are typical features in shock.
 
ASSESSMENT, INVESTIGATIONS AND MONITORING
  • Regular monitoring with blood pressure, pulse, heart rate, respiratory rate, urine output measurement (hourly) should be done. Urine output should be more than 0.5 ml/kg/hour. Pulse oximetry should be used.
  • Central venous pressure (CVP—only have gross assessment), pulmonary capillary wedge pressure (PCWP—an accurate assessment of left ventricular function) monitoring should be done. ICU care is needed during monitor period. But both CVP and PCWP are not accurate method of assessing tissue perfusion.
  • Complete blood count, ESR, pH assessment, serum electrolyte estimation, chest x-ray (to rule out ARDS/pulmonary problems).
  • Pus/urine/blood/bile/sputum cultures depending on the focus and need in sepsis.
  • Serum lactate estimation is an important prognostic factor. Level >2 mEq/L suggest tissue ischaemia.
  • USG of part, CT/MRI of the location of the pathology of the septic focus should be done; often may require repetition of these imaging to assess progress.
  • Blood urea, serum creatinine, liver function tests, prothrombin time (PT), activated partial thromboplastin time (APTT), ECG monitoring are also should be done.
  • All these tests including platelet count and arterial blood gas analysis (ABG) should be repeated at regular intervals.
 
Treatment of Shock
  • Treat the cause, e.g. arrest haemorrhage, drain pus.
  • Fluid replacement:
    • Plasma, normal saline, Ringer's lactate, plasma expander (haemaccel) (maximum 1 litre can be given in 24 hours).
    • Initially crystalloids then colloids are given. Blood transfusion is done whenever required.
    • Fluid therapy is ideally done with crystalloids like normal saline, Ringer's lactate, Hartmann's solution. Blood loss should be corrected by blood transfusion only. Crystalloids and colloids do not have O2 carrying capacity. Hypotonic solutions like dextrose are poor volume expanders and so should not be used in shock.
    • Dynamic fluid response is studied by infusing 500 ml of fluid rapidly in 10 minutes. Responders show improvement; transient responders show improvement temporarily but revert back to original status probably due to still existing fluid/blood loss or still existing fluid shift from intravascular space; nonresponders will not respond as fluid loss is severe and persistently ongoing.
  • Inotropic agents: Dopamine, dobutamine, adrenaline infusions—mainly in distributive shock like septic shock.
  • Correction of acid-base balance: Acidosis is corrected by using 8.4% sodium bicarbonate intravenously.
  • Steroid is often life-saving. 500–1000 mg of hydrocortisone can be given. It improves the perfusion, reduces the capillary 115leakage and systemic inflammatory effects.
    zoom view
    Fig. 1.207: Trendelenburg position—head down position, used in patient in shock.
  • Antibiotics in patients with sepsis; proper control of blood sugar and ketosis in diabetic patients.
  • Catheterisation to measure urine output (30–50 ml/hour or >0.5 ml/kg/hour should be maintained).
  • Nasal oxygen to improve oxygenation or ventilator support with intensive care unit monitoring has to be done.
  • CVP line to perfuse adequately and to monitor fluid balance. TPN is given when required.
  • PCWP to monitor very critical patient.
  • Haemodialysis may be necessary when kidneys are not functioning.
  • Control pain-using morphine (4 mg IV).
  • Ventilator and ICU/critical care management.
  • Injection ranitidine IV or omeprazole IV or pantoprazole IV.
  • Activated C protein even though costly is beneficial as it prevents the release and action of inflammatory response.
  • MAST (military antishock trouser): Provides circumferential external pressure of 40 mmHg. It is wrapped around lower limbs and abdomen, and inflated with required pressure. It redistributes the existing blood and fluid towards centre. It should be deflated carefully and gradually.
 
Remember
  • Response to dynamic fluid therapy can be checked in patient in shock by perfusing 500 ml of fluid rapidly in 10 minutes and patient is checked as nonresponder/transient only initial responder or proper responder.
  • Vasopressor like dobutamine is used only in distributive shock like due to sepsis (not in hypovolaemic, haemorrhagic shock where there is low preload).
  • Intubation and ventilator may be needed in shock.
  • The patient is monitored with ECG, pulse oximetry, blood pressure/invasive blood pressure, CVP/ PCWP, urine output, pupillary reaction (dilated or not), serum electrolytes, arterial PO2 and PCO2 analysis.
 
CENTRAL VENOUS PRESSURE (CVP)
It is a method to measure the right atrial pressure by placing a venous catheter (20 cm) into the SVC (superior vena cava). Commonly for CVP monitoring, a venous catheter is passed through internal jugular vein or infraclavicular subclavian vein to the SVC (used for TPN purpose). Occasionally a long catheter (60 cm) can be passed through basilic vein (not commonly done). Under radiological guidance, initially a needle is passed 3 cm above the medial end of the clavicle, in the hollow between the two heads of sternomastoid muscles, directing towards the suprasternal notch into the right internal jugular vein. Then through a guide wire, a venous catheter is passed into the SVC through right internal jugular vein, which can also be confirmed by changes in flow during inspiration and expiration.
Catheter is connected to saline manometer, taking manubriosternal angle (angle of Louis) as zero point.
Normal value is 2–10 cm of saline.
If less than 2 cm, more fluid is infused.
If more than 10 cm, fluid infusion should be restricted.
zoom view
Fig. 1.208: CVP cannula. Note the location of tip of CVP line in the SVC (or can be in the right atrium).
zoom view
Fig. 1.209: CVP line for monitoring and perfusing the patient in shock.
116
 
PULMONARY CAPILLARY WEDGE PRESSURE (PCWP)
It is a better indicator of circulating blood volume and left ventricular function.
Catheter used is Swan Ganz triple channel pulmonary artery balloon catheter.
 
Procedure
Under strict aseptic precaution, using cannula and guide wire, catheter is passed through internal jugular vein, into the right atrium. Balloon is inflated by 1.5 ml of air and then negotiated into pulmonary artery, until it reaches a small branch and wedges it. Pressure at this point is called as pulmonary capillary wedge pressure.
PCWP normally is 8–12 mmHg, considering mid axillary point as zero reference point.
After that, balloon is deflated to get pulmonary artery pressure which is normally 25 mmHg systolic and 10 mmHg diastolic.
PCWP catheter can be kept in situ only for 72 hours.
Differences between CV P and PCWP
CVP
PCWP
  1. Technically easier
  2. Normal pressure is 2—10 cm of saline
  3. Gives gross idea about fluid balance
  4. Left ventricular function is not assessed
  5. Not used to differentiate between right and left ventricular function
  6. Can be kept in situ as long as desired
  7. Catheter tip is in SVC
  8. Plain tip catheter
  9. Can be used for TPN, fluid infusion, etc.
  10. Complications are easy to tackle
  11. Not as sensitive and specific as PCWP
  1. Requires skilled experts
  2. 8—12 mmHg
  3. Better and specific
  4. Left ventricular function is very well-assessed
  5. Very well-differentiated
  6. Cannot be kept in situ for more than 72 hours
  7. Catheter tip is in pulmonary capillary with wedging
  8. 1.5 ml air filled balloon tip
  9. Can not be used for TPN, or fluid infusion
  10. Often difficult to tackle
  11. Sensitive and specific
zoom view
Fig. 1.210: Pulmonary capillary wedge pressure. Note the wedged balloon in the tip of the venous catheter in the pulmonary arteriole.
 
SYSTEMIC INFLAMMATORY RESPONSE SYNDROME (SIRS)
  • SIRS is systemic manifestations of inflammation due to variety of causes like infection, pancreatitis, polytrauma, burns, transfusion reaction, and malignancy. So it is often categorised as infectious cause SIRS or noninfectious cause SIRS. It causes either hyperthermia (>38°C) or hypothermia (<36°C); tachycardia (pulse >90/minute); tachypnoea (>20/minute); total white cell count >12,000/cu mm, or count <4000/cu mm.
  • It is final common pathway in shock due to any cause (trauma, sepsis, endotoxaemia, burns) where there is failure of inflammatory localisation with vasodilatation, increased endothelial permeability with damage, thrombosis, leucocyte migration and activation.
  • It is associated with release of free radicals, abnormal arachidonic acid release, cytokine release, neutrophil sequestration, abnormal NO synthesis, complement activation, DIC.
  • 117It is a part of severely decompensated reversible shock which eventually leads to MODS (Multiorgan dysfunction syndrome), a state of irreversible shock wherein patient is anuric, drowsy, cold and terminally ill.
  • SIRS carries poor prognosis.
 
MULTIPLE ORGAN DYSFUNCTION SYNDROME (MODS)
  • It is progressively becoming irreversible injury of all tissues like kidney, lungs, liver, GIT. Lungs and liver are commonly involved (70%). Next organs to be involved are kidney and GIT. Order of involvement of organs in MODS is—lungs → right ventricular failure → liver → kidney. But mortality is higher if kidney and lungs are involved.
  • It occurs in critically ill patient after severe trauma, burns, acute pancreatitis, bleeding and sepsis.
  • It is more common in elderly, diabetic, smokers, alcoholics, cirrhosis, malnutrition, patients under steroids and cytotoxic drugs, and uraemia.
  • Multiple features related to multiple organ dysfunctions are typical. Oliguria, jaundice, hypotension, drowsiness, respiratory distress are common.
  • Platelet microaggregation, acute pulmonary hypertension, ARDS, DIC, circulatory failure with reduced total oxygen utilization in spite of adequate oxygen supply, impaired defense mechanism are the pathogenetic features.
  • Respiratory, renal, hepatic, circulatory, coagulative and cardiac failure occurs as an end stage MODS.
  • Primary MODS is due to a well defined cause like pulmonary contusion, rhabdomyolysis, multiple transfusions.
  • Secondary MODS occurs as a result of host response in SIRS.
  • Management of MODS is critical care in ICU with ventilator support, haemodialysis, transfusions, antibiotics, proper nutrition in the form of TPN or enteral. MODS stage has got high mortality.
 
OXYGEN THERAPY
 
Indications
  1. Chest injuries, any severe haemorrhage.
  2. Gas gangrene with toxic haemolysis.
  3. Coal gas poisoning.
  4. Over morphinisation.
  5. Pulmonary embolism and fat embolism.
  6. Spontaneous pneumothorax, pulmonary oedema, cardiac infarction, pneumonia, cor pulmonale.
  7. Cardiogenic shock and acute bronchitis.
    27% oxygen is delivered through ventimask (disposable polythene mask) at a rate of 4–6 litres per minute. Oxygen is also given along with positive pressure ventilation.
 
HYPERBARIC OXYGEN
It is administration of oxygen 1 or 2 atmospheres above the atmospheric pressure in a compression chamber. It increases the arterial oxygen saturation so that oxygen perfusion of tissues will be increased.
 
Indications
  1. Carbon monoxide poisoning.
  2. Tetanus, gas gangrene infections.
  3. Bedsores, frostbites, necrotising fasciitis.
  4. Drenching in paralytic ileus to reduce the nitrogen gas in distended bowel.
  5. As a radiosensitizer in the treatment of cancer.
 
Complications
  • Cerebral gas embolism.
  • Rupture of tympanic membrane.
  • Visual defects.
  • O2 toxicity.
  • CO2 narcosis.
  • Respiratory depression.
 
Contraindications
  • Asthma/emphysema.
  • High fever.
  • Chronic sinusitis.
  • Viral infection.
  • Pregnancy.
 
TOPICAL O2 THERAPY
H2O2 to release nascent oxygen in ulcers and abscess.
 
CARDIAC ARREST
It is the cessation of the heart. Heart stops contracting.
Causes: All causes for shock.
 
Critical Period
Once heart and lungs stop, brain death occurs in 3 minutes.
  1. External cardiac compression (massage): Patient is laid flat on a hard surface (never on soft surface). Manual compression is exerted over the lower sternum using both hands one over other without bending the elbow at a rate of 60 to 70 per minute. Rib cage damage during procedure can be very well ignored (Heel of right hand is placed over the sternum 8 cm above xiphoid process and left hand is placed over it).
  2. 118Another person at the same time should give mouth to mouth breathing at a rate of 20 to 30 per minute after clearing the airway by removing froth and dentures. A bag with mask can be used to ventilate using air or oxygen.
  3. Endotracheal intubation and ventilator support.
  4. Injection of 1:10,000 adrenaline and 10% calcium chloride intravenously.
  5. Sodium bicarbonate 8.4% injection, hydrocortisone injection.
  6. Defibrillator, if there is ventricular fibrillation.
  7. Analysis of blood gas (PCO2 and PO2), and serum electrolytes assessment at repeated intervals.
  8. Urinary catheterization, Ryle's tube insertion.
  9. Monitoring the patient with BP, pulse, respiration, and temperature chart.
zoom view
Fig. 1.211: Technique of external cardiac massage.
zoom view
Fig. 1.212: Technique of mouth-to-mouth respiration. Note patient's nose should be held closed with right hand of the doctor/assistant and with left hand lower jaw should be pushed forward.
Once patient recovers, the cause and sequelae has to be managed properly.
 
Internal Open Cardiac Massage
This method is used when cardiac arrest occurs in the operation theatre during surgery, acute tamponade, and acute bilateral pneumothorax.
Left side thorax is opened through a lengthy incision along 4th or 5th intercostal space. Initially heart with intact pericardium is rhythmically compressed and relaxed using left hand against sternum. Mean while costal cartilages above and below are cut with a knife to have a better exposure. Pericardium is opened in front of the phrenic nerve. Direct cardiac massage is undertaken until heart regains its function and later shifted to ventilatory support and critical care.
zoom view
Fig. 1.213: Left thoracotomy for open internal cardiac massage.
 
Defibrillation Technique (Cardioversion)
Apply gelly to the site of electrodes. One electrode at the base of heart to the right of the sternum other over the estimated area of the apex of the heart. Ensure that nobody is in contact with the patient. Activate the defibrillator. Resume ventilation and ECG monitor immediately. After that, monitor continuously, correct the acidosis, catheterise and observe urine output. Arrange for ICU care.
zoom view
Fig. 1.214: Defibrillator used in case of cardiac arrest.
119H. Haemorrhage and Blood Transfusion
There are canals (or vessels) in it (the heart) to (every) member. Now if the priests of Sekhmet or any physician put his hands (or) his fingers (upon the head, upon the back of the) head, upon the two hands, upon the pulse, upon the two feet, (he) measures the heart, because its vessels are in the back of the head and in the pulse; and because its (pulsation is in) every vessel of every member.
—(Anonymous), Circa 2500 BC
CHAPTER OUTLINE
  • ❖ Haemorrhage
  • ❖ Blood Transfusion
  • ❖ Blood Substitutes
  • ❖ Massive Blood Transfusion
  • ❖ Autologous Blood Transfusion
  • ❖ Artificial Blood
  • ❖ Erythropoietin
  • ❖ Tourniquets
  • ❖ Disseminated Intravascular Coagulation
  • ❖ Mechanism of Blood Coagulation
 
HAEMORRHAGE
 
Classification
  1. Based on the source of bleeding:
    1. Arterial is bright red in colour, spurting like jet along with pulse of the patient.
    2. Venous is dark red, steady and continuous flow. Blood loss may be severe and rapid when bleeding is from femoral vein, jugular vein, other major veins, varicose veins, portal vein, oesophageal varices.
      Pulmonary arterial blood is dark red in colour and pulmonary venous blood is bright red in colour.
    3. Capillary: Here bleeding is rapid and bright red. It is often torrential due to continuous ooze.
  2. Based on the time of onset of bleeding in relation to any operative procedure:
    1. Primary: Occurs at the time of injury or operation.
    2. Reactionary: It occurs within 24 hours after surgery or after injury (commonly in 4–6 hours).
      Precipitating factors
      Common causes
      Coughing
      Thyroid surgery
      Vomiting
      Cholecystectomy
      Straining
      Major abdominal surgeries
      Rise of blood pressure
      Circumcision
      Restlessness
      Hydrocele surgery
      Venous refilling during recovery from anaesthesia
      Tonsillectomy
      Slipping of ligature
      Clot dislodgement
    3. Secondary: It usually occurs in 14 days after surgery.
      Factors
      Common causes
      Infection
      Erosion of carotid artery by cancer (secondaries in the neck)
      Pressure by
      drain or bone
      Haemorrhoidectomy
      Malignancy
      Inguinal block dissection
  3. Based on the type of haemorrhage:
    Revealed haemorrhage
    Concealed haemorrhage
    Initially concealed but later revealed
    It is visible external haemorrhage
    It constitutes
    Haematuria
    internal haemorrhage
    Haematemesis
    • Liver injury
    Melaena
    • Spleen injury
    • Fracture femur
    • Ruptured ectopic gestation
    • Cerebral haemorrhage
    • Haemothorax
  4. Based on the duration of haemorrhage:
    1. Acute haemorrhage: It is sudden, severe haemorrhage after trauma, surgery.
    2. Chronic haemorrhage: It is chronic repeated bleeding for a long period like in haemorrhoids, bleeding peptic ulcer, carcinoma caecum, etc. They present with chronic anaemia with hyperdynamic cardiac failure. They are 120in a state of chronic hypoxia. It is corrected by packed cell transfusion not by whole blood itself. Cause has to be treated accordingly.
    3. Acute on chronic haemorrage: It is more dangerous as the bleeding occurs in individuals who are already hypoxic, which may get worsened faster.
  5. Based on the possible intervention:
    1. Surgical haemorrhage—can be corrected by surgical intervention.
    2. Nonsurgical haemorrhageis diffuse ooze due to coagulation abnormalities and DIC.
 
Pathophysiology of Haemorrhage
Bleeding
Hypovolaemia
Low cardiac output
Tachycardia and shunting of blood from splanchnic vessels by venoconstriction so as to maintain perfusion of vital organs like brain, heart, lungs, kidneys
Hypoxia
Activation of cardiac depressants
Anaerobic metabolism and altered cell membrane function causing influx of more sodium and calcium inside the cell and potassium comes out of the cell
Hyponatraemic, hyperkalaemic, hypocalcaemic metabolic acidosis
Lysosomes of cell get lysed releasing powerful enzymes which is lethal to cell itself
SICK CELL SYNDROME
Platelets and coagulants are activated leading to formation of small clots DIC and further bleeding.
Progressive haemodilution leading to total circulatory failure.
Initially there is compensatory hypovolaemic shock and later there is decompensatory hypovolaemic shock which will lead to MODS and death.
DIC, acidosis and hypothermia are the major factors in worsening the situation in haemorrhage.
 
Clinical Features of Haemorrhage
  • Pallor, thirsty, cyanosis.
  • Tachycardia, tachypnoea.
    Classification of haemorrhagic shock (circulatory failure)
    Class
    Blood loss
    Features
    I
    Up to 15% (< 750 ml)
    Normal
    II
    Blood loss 15–30% (750–1500 ml)
    Palor, thirsty, tachycardia
    III
    Blood loss 30–40% (1500–2000 ml)
    Hypotension, tachycardia, oliguria, confusion
    IV
    Blood loss > 40% (> 2000 ml)
    Rapid pulse, low BP, anuria, unconsciousness, MODS
  • Air hunger.
  • Cold clammy skin due to vasoconstriction.
  • Dry face, dry mouth and goose skin appearance (due to contraction of arrector pilorum).
  • Rapid thready pulse, hypotension.
  • Oliguria.
  • Features related to specific causes.
Note: Tachycardia is not a reliable indicator of haemorrhage.
 
Measurement of Blood Loss
  • Clot size of a clenched fist is 500 ml.
  • Blood loss in a closed tibial fracture is 500–1500 ml; in a fracture femur is 500–2000 ml.
  • Weighing the swab before and after use is an important method of on-table assessment of blood loss.
 
Rains Factor
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Fig. 1.215: Mops used during major surgery should be kept in a rack so that quantity of bleeding during surgery can be assessed approximately.
121
  • Hb% and PCV estimation.
  • Blood volume estimation using radioiodine technique or micro-haematocrit method.
  • Measurement of CVP or PCWP.
  • Investigations specific for cause: U/S abdomen, Doppler and often angiogram in vascular injury, chest X-ray in haemothorax, CT scan in major injuries, CT scan head in head injuries.
 
Treatment
Stop the blood loss
Pressure; packing; position and rest; operative procedures.
Restoring the lost blood
Fresh whole blood transfusion; plasma expanders.
  • Restoration of blood loss: By blood transfusion, albumin 4.5%, SAG-M blood, saline, haemaccel (Gelatin), dextran, plasma infusions.
    Note: One unit of blood should raise 1 gm% of haemoglobin.
  • Catheterisation, foot end elevation, monitoring.
  • Oxygen support/intubation/ventilator and critical care.
  • Pressure, packing and head down (Trendelenburg) position to restore BP and blood supply of brain.
  • Wound exploration and proceeding, i.e. ligation of the small vessel, suturing the wound part, vessel suturing (anastomosis), excision of the tissues.
  • Absolute rest, analgesics, morphine 10–20 mg IM/IV to relieve pain, sedation.
  • ICT placing for haemothorax.
  • Laparotomy for liver or spleen or mesentery or bowel injuries, suturing, splenectomy.
  • Topical applications for local ooze—Oxycel, gauze soaked with adrenaline, bone wax for oozing from bone and other local haemostatic agents (collagen, thrombin).
  • In venous haemorrhage, elevation, ligation of vein or in case of large vein suturing of venous wall, pressure bandaging, packing will be helpful.
  • Tourniquet are often used in operation theatre for control of haemorrhage in limbs. But it is not advisable as a first aid measure.
  • TPN, CVP monitoring, electrolyte management are all equally important.
  • Steroid injection, antibiotics, ventilator support are often required.
Note:
Blood transfusion is required if Hb% is < 8 g%.
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Figs 216A and B:
122
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Figs 1.216A to C: Gel foam (gelatin sponge) is a good haemostatic agent on oozing surface like gallbladder bed after cholecystectomy.
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Fig. 1.217: Oxidised regenerated cellulose is very good local haemostatic agent; but it is much costlier than gelatin sopnge.
 
BLOOD TRANSFUSION
 
Indications
  • Acute blood loss following trauma, ≥15% of total body volume in otherwise healthy individuals (liver, spleen, kidney, GIT injuries, fractures, haemothorax, perineal injuries).
  • During major surgeries—abdominoperineal surgery, thoracic surgery, hepatobiliary surgery.
  • Following burns.
  • In septicaemia.
  • As a prophylactic measure prior to surgery.
  • Whole blood is given in acute blood loss.
  • Packed cells are given in chronic anaemia.
  • Blood fractions are given in ITP, haemophilias.
 
Donor Criteria
  • Donor should be fit without any serious diseases like HIV1 and HIV2 and hepatitis infections and malaria.
  • Weight of donor should be more than 45 kg.
 
Collection of Blood
  • Blood is collected in a sac containing 75 ml of CPD (Citrate phosphate dextrose) solution and stored in special refrigerators at 4 degree celcius. CPD blood lasts for 3 weeks.
  • Adenosine can be added to increase the storage life of the blood up to 5 weeks; it is called as CPDA solution.
  • In storage period, RBCs lose their ability to release oxygen in 7 days even though RBCs last for 3 weeks; so blood should be transfused within 7 days ideally. WBCs are destroyed in 2 days. Platelets and clotting factors are destroyed very early in 1–2 days.
After grouping and cross-matching, 540 ml of blood is transfused in 4 hours (40 drops per minute), using a filtered drip set.
One litre of blood contains 350 mg of iron. Normal excretion of iron is 1 mg/day. Iron overload can occur after many transfusions. Iron excretion can be increased by desferrioxamine infusion.
 
Blood Fractions
  1. Packed cells
    • It is obtained by centrifuging whole blood at 2000–2300 g for 15–20 minutes.
    • It is used in chronic anaemias, in old age, in children.
    • It minimises the cardiac overload due to transfusion.
    • It can be stored for 35 days at 1°–6°C.
    • One unit contains 300 ml with haematocrit about 70%. One unit raises Hb% by 1.0 gram.
  2. Plasma:
    • This is obtained in the same way as packed cells by centrifugation.
    • It is indicated in burns, hypoalbuminaemia, severe protein loss.
    • It can be fractionalised into different fragments:
      1. Human albumin 4.5% is obtained after repeated fractionations and can be stored for several months in liquid form at 4°C.
      2. Fresh frozen plasma (FFP): Fresh plasma obtained, is rapidly frozen and stored at –40°C. It contains all coagulant factors. 1 unit of FFP increases the clotting factors levels by 3%. It can be stored for 2 year. Rhesus D positive FFP can be transfused to Rhesus D negative female.
        Uses:
        • Severe liver disease with abnormal coagulation function.
        • Congenital clotting factor deficiency.
        • Deficiency following warfarin therapy, DIC, massive transfusion.
        • 123To maintain prothrombin time at normal level. Dose of FFP is 15 ml/kg.
      3. Cryoprecipitate: When fresh frozen plasma is allowed to thaw at 4°C, visible white supernatant layer develops and is called as cryoprecipitate which is rich in Factor VIII and fibrinogen. It is stored at minus 40°C and can be kept for 2 year. Cryoprecipitate is used to raise fibrinogen level at a dose to make plasma fibrinogen level 150 mg/dl. It is also used in inherited deficiency of Factor VIII, fibrinogen, Factor XIII, von Willebrand's disease.
        zoom view
        Fig. 1.218: Purified freeze dried human coagulation factor VIII is available for use in haemophilia patients.
      4. Fibrinogen is obtained by organic liquid fractionation of plasma and is stored in dried form. It is very useful in DIC and afibrinogenaemia. It has risk of transmitting hepatitis.
      5. Factor VIII and IX concentrate: They are freeze dried part from a large pooled plasma used in haemoplhilia and von Willebrand's disease.
  3. Platelet rich plasma: It is obtained by centrifugation of freshly donated blood at 150–200 g for 15–20 minutes. Platelet rich plasma contains 5.5 × 109/L platelets in 50 ml plasma. It can be random donor platelet or single donor platelet. Single donor platelet is prepared by plateletapheresis containing 3 × 109/L platelets in 200 ml of plasma. One single donor platelet is equal to 8 units of random donor platelet.
  4. Platelet concentrate: It is prepared by centrifugation of platelet rich plasma at 1200–1500 g for 15–20 minutes. Used in thrombocytopaenia and drug (aspirin, clopidogrel) induced haemorrhage. Platelet is transfused at a dose of 0.1 unit/kg, when platelet drops below 20,000/or episodes of bleeding. Platelet stored at 4°C should be used within 48 hours; when stored at room temperature can be used up to 5 days. One platelet concentrate can increase up to 10,000 platelet/cumm in one hour.
  5. Prothrombin complex concentrate (PCC) are derived from pooled plasma which contains factors II, IX and X; used in emergency reversal of warfarin therapy in uncontrolled haemorrhage.
 
SAG-M Blood
A proportion of donations will have plasma removed and will be replaced by crystalloid solution of SAG-M.
  • S — Sodium chloride.
  • A — Adenine.
  • G — Glucose anhydrate.
  • M — Mannitol.
Precautions
  • For every four units of SAG-M blood, one whole blood has to be given.
  • Later for every two units of SAG-M blood, one unit (400 ml) of 4.5% human albumin has to be given.
  • Coagulation status and platelet count should be checked regularly.
 
Complications of Blood Transfusions (Please also see table for entire list)
Febrile reactions: It is the most common complication due to impurities like pyrogens in the blood or in infusion set. Headaches, fever, chills and rigors, tachycardia, nausea are the features. Transfusion is temporarily stopped or the flow is slowed down with administration of antipyretic drug to reduce fever. Often transfusion of that unit needs to be discontinued.
Allergic reaction (3%): Utricaria and allergy to specific proteins in the donor's plasma can occur. Usually it is mild and is treated with steroid and antihistaminics. In severe utricaria that unit of blood is discarded; new washed RBC's and platelets are used.
Acute haemolytic reactions: It is the most dangerous complication. It is due to ABO incompatibility. Usually it is nonfatal but occasionally can be fatal. It is commonly due to technical error at different levels. It amounts for criminal negligence in court of law. Intravascular destruction causes haemoglobinemia, haemoglobinuria, acute renal failure and DIC. Dyspnoea, chest pain, sweating, fever with chills, tachycardia, hypotension, and cardiac arrest occurs in fatal type. Jaundice is a common feature in nonfatal type. Free haemoglobin level in blood will be above 5 mg/dl. Condition is treated as an emergency in critical care unit/ICU. Transfusion is stopped immediately; blood sample of recipient and transfusing blood is sent immediately for two laboratories for rechecking. Smoky urine of the patient is typical. Injection hydrocortisone/dexamethasone IV is given immediately. Fluid therapy, alkalization of blood is done using sodium lactate and sodium bicarbonate. Mannitol 20 gram in 100 ml is infused in 5 minutes; furosemide 120 mg is injected intravenously. Haemodialysis is needed if there is renal failure. Often ventilator support, defibrillator if cardiac arrest occurs is needed. Correction of acidosis, electrolytes is needed.
Transfusion-related acute lung injury: It is due to donor plasma antibody against HLA and leucocyte specific antigens of recipient. Occasionally it is due to recipient's antibody 124against donor's leucocytes. Features are—breathlessness, saturation drop, fever, hypotension which is observed 4 hours after transfusion. Chest x-ray shows bilateral diffuse infiltrate. They need ventilator support for short period with eventual rapid and complete recovery.
Transfusion-related graft versus host disease (TGVH): This very serious, very rare complication occurs due to recognition and reaction against host tissues by infused donor lymphocytes. It is common in immunosuppressed, lymphoma, leucaemic patients. Any type of blood products including leukocyte reduced blood can cause the condition. Features are—pancytopaenia, toxic epidermal necrosis, liver dysfunction with more than 90% mortality. It is difficult to treat.
Congestive cardiac failure (CCF): It occurs if especially large quantities of whole blood are transfused in chronic severe anaemia, pregnancy, elderly patients, in patients who have cardiac problems.
 
MASSIVE BLOOD TRANSFUSION
 
AUTOLOGOUS BLOOD TRANSFUSION
An healthy individual with no infection and haematocrit of ≥ 30% can predonate blood few weeks prior to any elective surgeries, which in turn, can be used at the time of surgery.
Autologous blood is used in orthopaedic, gynaecologic and urologic surgeries. Patient donates one unit of blood weekly; last one if at all being 72 hours before the date of surgery.
 
Recycled Blood
In major surgeries if there is significant blood loss, then patient's bled blood is carefully sucked out through a sterile system and is filtered and reused again to the patient. This will reduce the number of transfusions.
 
ARTIFICIAL BLOOD
  1. Perfluorocarbon (Fluosoleda; perfluoro decalin; Fluosol DA)—abiotic substitute as synthetic oxygen carrier. Its half life is 7 days. It is RBC substitute.
    • It has got high affinity for O2.
    • It is inert, colourless, odourless, dense, poorly soluble liquid.
    • It is biocompatible.
    • It is emulsified with albumin or lipids before infusion. Its emulsion alone injection can cause pulmonary embolism.
    • It can bind and release oxygen. But as it reduces the PPO2 quickly, it is a disadvantage. Patient ideally to be kept in hyperbaric place.
    • It is oily in nature hence has to be emulsified. It releases 1.3 ml of oxygen/100 ml. It should be kept frozen. It can cause anaphylaxis.
  2. Stroma-free haemoglobin—biomimetic haemoglobin based substitute. It has more affinity for oxygen as it does not contain 2, 3 DPG but has short half life. It is nephrotoxic.
  3. Chelates which reverse bound O2.
    • Intraoperative—salvage of blood: On table blood is collected, washed, filtered and transfused. Used in trauma.
125
 
ERYTHROPOIETIN
  • injection 1000–3500 units preoperatively also used to increase the RBC count.
  • It is used in CRF patients who are on haemodialysis. It is given twice weekly but it is costly.
 
TOURNIQUETS
Tourner means to turn (Greek). A tourniquet is used to cut off the blood supply to a limb temporarily so that a bloodless field is created while performing the surgery. Limb should be exsanguinated before applying/inflating the cuff of the tourniquet. It is done using a bandage or pressurized Rhys-Davis exsanguinator. A tourniquet is applied in mid-thigh above the knee joint in lower limb and in mid-biceps level above the elbow in upper limb. It should not be closer to joints. It is not applied over the forearm or leg. It is applied over layers of gauze or cotton, not over a bare skin. Pressure used in upper limb is 250 mmHg; lower limb is 300 mmHg (In children, it is 150 and 250 mmHg for upper and lower limbs respectively).
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Fig. 1.219: Esmarch rubber tourniquet.
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Fig. 1.220: Automatic gauged pressure tourniquet.
 
Uses
  • To attain bloodless field in limb surgeries—upper and lower limbs, orthopaedic surgeries, soft tissue tumours, amputations.
  • It is used (rubber tourniquet) to access veins for IV injections and IV sampling.
  • Tourniquet is used in diagnostic tests for varicose veins, purpura (ITP), carpal tunnel syndrome, tetany.
  • It is used as a first aid in bleeding conditions of limbs, snake bite (it is controversial).
  • Tourniquets are often used for small procedures in fingers and toes.
 
Types
  • Rubber tourniquet: Simple red rubber catheter is used for drawing blood, to have access to veins.
  • Martin's tourniquet made up of India rubber.
  • Pneumatic tourniquet: Used in limbs, will give the arterial pressure and also acts as a tourniquet (Sphygmomanometer cuff is simpler and easily available type).
  • Esmarch rubber elastic bandage tourniquet.
  • Conn pneumatic tourniquet is manually operated tourniquet where air is pumped up to the required pressure.
  • Specialised sophisticated tourniquets are available which gauge pressure and time accurately—automatic tourniquet.
126
Tourniquet time for upper limb is one hour and for lower limb is two hours.
 
Contraindications
  • In all peripheral vascular diseases and atherosclerosis.
  • Infection.
  • Deep venous thrombosis.
  • Crush injuries.
  • Sickle cell disease.
 
Complications
  • Crushing effect on muscles in thigh occurs leading to crush syndrome.
  • Tourniquet palsy in upper limb (radial nerve involvement)—neuropraxia.
  • Infection.
  • Improper application of tourniquet leads to more bleeding.
  • Forgetting the removal of tourniquet or taking more time to release may compromise the blood supply of the limb leading to severe ischaemia and gangrene. It occurs especially when tourniquet is used in finger or toe.
  • Skin blistering and necrosis.
 
DISSEMINATED INTRAVASCULAR COAGULATION
Disseminated intravascular coagulation (DIC) is a manifestation due to wide spread intravascular coagulation resulting in microthrombi formation, consumption of platelets and clotting factors and production of breakdown products eventually leading into severe bleeding and tissue ischaemia.
 
Causes
  • Major trauma causes DIC due to release of tissue thromboplastin. Burns, major surgery can also cause DIC.
  • Sepsis is the most common cause of DIC. Common sepsis causing DIC are gram-negative, meningococcal, malarial, histoplasmosis, aspergillosis, etc.
  • Acute pancreatitis can cause DIC by releasing proteolytic enzymes which activate prothrombin and factor X.
  • Septic abortion, abruption, retained dead foetus, amniotic fluid embolism are obstetric causes of DIC.
  • Carcinoma of pancreas, prostate, acute promyelocytic leucaemia often cause DIC.
  • Haemolysis, snake bite, liver dysfunction are other causes.
 
Types of DIC
  • Acute DIC presents with bleeding in gums, GIT, venepuncture site, haematuria, petechiae, oozing from surgical or traumatic wounds. Massive bleeding also can occur.
  • Chronic DIC is a low grade type with thrombotic features.
 
Investigations
  • In DIC—bleeding time, platelet counts are reduced. Thrombin time (TT), prothrombin time (PT) and activated partial thromboplastin time (APTT) are prolonged. Fibrinogen degradation product (FDP), D-dimer test are raised.
  • Complete haematocrit, investigations relevant to cause, renal function tests, LFT, electrolyte estimation, blood/discharge/pus/urine culture.
 
Treatment of DIC
  • Treatment of specific cause as per protocol. Correction of haemodynamic instability by fluid therapy, transfusion of packed cells or whole blood. Dopamine/dobutamine therapy.
  • Factor replacement—specific therapy for DIC—FFP, cryoprecipitate, platelet concentrate transfusions are essential. FFP is given at a dose of 15 ml/kg. Cryoprecipitate is used to raise fibrinogen level at a dose to make plasma fibrinogen level 150 mg/dl. Platelet is transfused at a dose of 0.1 unit/kg, when platelet drops below 20,000/or with episodes of bleeding.
  • Heparin use is often controversial. It is used mainly in chronic DIC, DIC with purpura, DIC of obstetric cause, cancer induced DIC, DIC due to acute antiphospholipid antibody syndrome.
  • EACA, tranexamic acid can be used but with questionable benefits.
 
MECHANISM OF BLOOD COAGULATION (HAEMOSTASIS)
Haemostasis is the spontaneous arrest of bleeding. When an injury occurs platelet adhesion occurs to injured vessel/capillary wall which activate the release of ADP (Adenosine diphosphate) which makes more platelet to aggregate (platelet aggregation). These activated platelets release thromboxane A2 which further increases the adhesion and aggregation of platelets. Circulating fibrinogen binds to an activated platelet receptors glycoprotein IIb and IIIa and fibrinogen gets converted into fibrin.
Coagulation cascade system:
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127
Clotting factors are proteins synthesised by the liver which with a series of cascade reaction activates clotting factors and achieves blood coagulation by a complex mechanism. Factor II, VII, IX and X are vitamin K dependent for their synthesis in liver (carboxylation of glutamic acid). In the process of coagulation each factor gets activated to an enzyme by partial proteolysis, which in turn, activates other needed coagulation factors. Eventually fibrinogen gets converted into soluble fibrin and later into insoluble fibrin.
Two types coagulation system are there:
  • Intrinsic pathway
  • Extrinsic pathway
In vitro coagulation occurs by intrinsic coagulation system. Cascade gets activated by vessel wall injury, shear stress of vessel or other factors. It activates the cascade to get final result.
 
Coagulation cascade system
Blood clotting factors
Factor No.
Common name
I
Fibrinogen
II
Prothrombin
III
Thromboplastin
IV
Ionic calcium
V
Hereditary labile factor, activator (AC) globulin, proaccelerin
VI
Accelerin, supposed to be active form of factor V
VII
Proconvertin; serum prothrombin—conversion accelerator (SPCA)
VIII
Antihemophilic factor (AHF)
IX
Plasma thromboplastin component (PTC; Christmas factor)
X
Stuart-Prower factor
XI
Plasma thromboplastin antecedent (PTA)
XII
Hageman factor
XIII
Fibrin stabilizing factor, fibrinase
XIV
Prekallikrein
XV
Kallikrein
XVI
Platelet factor
 
Hemophilia and von Willebrand's disease
They are the two most common inherited bleeding disorders due to deficiency of factor VIII.
Factor VIII has two components; smaller one—factor VIII C is needed for activation of factor X in intrinsic coagulation pathway; its deficiency leads to classic hemophilia. It is inherited as an X-linked recessive trait, thus it occurs in males and homozygous females. The larger component of factor VIII called von Willebrand's factor, facilitates the adhesion of platelets to subendothelial collagen, hence crucial for hemostasis, its absence leads to von Willebrand's disease.
Classic haemophilia is called haemophilia A is caused by deficiency of factor VIII C with X linked recessive trait. It occurs in males or homozygous females. Recurrent haemarthroses is a common presentation. Petechiae and echymoses are absent. Bleeding time is normal but coagulation time is prolonged. Treatment is replacement of factor VIII haemophilic factor. If not known patient may go for a life-threatening bleeding even after dental extraction.
Von Willebrand's disease is deficiency of larger component (99%) of the factor VIII-vWF. It is an autosomal dominant disease with normal bleeding time and normal platelet count. Common presentations are spontaneous bleeding from mucous membrane, excessive bleeding from wounds and severe menorrhagia. Haemarthroses is not common in von Willebrand's disease. Treatment is replacement of specific factors.
Haemophilia B also called as Christmas disease is due to factor IX deficiency is inherited as X linked autosomal recessive trait.
128I. Burns
The infusion of large quantities of fluid, mainly a salt solution, as many as 3–4 litres daily, has proved satisfactory. Sometimes a life is saved if not more than one-quarter of the body surface has received a third-degree burn…. I have given blood transfusions to two patients with severe burns, with recovery in one case and postponement of death in the other.
—Gustav Riehl, 1925
CHAPTER OUTLINE
  • ❖ Burns
  • ❖ Management of Burns
  • ❖ Eschar
  • ❖ Contracture in Burn Wound
  • ❖ Electrical Burns
  • ❖ Inhalation Injury
  • ❖ Chemical Burns
 
BURNS
 
Classification of Burns
 
Depending on the Percentage of Burns (Burn Severity Classification)
Mild (Minor):
  • Partial thickness burns <15% in adult or <10% in children.
  • Full thickness burns less than 2%.
  • Can be treated on outpatient basis.
Moderate:
  • Second degree of 15–25% burns (10–20% in children).
  • Third degree between 2–10% burns.
  • Burns which are not involving eyes, ears, face, hand, feet, perineum.
Major (severe):
  • Second degree burns more than 25% in adults, in children more than 20%.
  • All third degree burns of 10% or more.
  • Burns involving eyes, ears, feet, hands, perineum.
  • All inhalation and electrical burns.
  • Burns with fractures or major mechanical trauma.
 
I. Depending on thickness of skin involved
  1. First degree: Here the epidermis looks red and painful, no blisters, heals rapidly in 5–7 days by epithelialisation without scarring. It shows capillary filling.
    Rule of Nine (Wallace's rule of “9”) 1951
    Adults
    Children
    Infants
    Head and neck
    9%
    18%
    20%
    Front of chest and abdominal wall
    9 × 2 = 18%
    18%
    10 × 2 = 20%
    Back of chest and abdominal wall
    9 × 2 = 18%
    18%
    10 × 2 = 20%
    Lower limb
    18 × 2 = 36%
    13.5 × 2 = 27%
    10 × 2 = 20%
    Upper limb
    9 × 2 = 18%
    18%
    10 × 2 = 20%
    Perineum
    01%
    01%
    100%
    100%
    100%
    Note: It is head and lower limb percentage which differ in adults and children.
    129
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    Figs 1.221A and B: Percentage of burns in (A) Adults; (B) Children
    zoom view
    Fig. 1.222: First and second degree burn.
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    Fig. 1.223: Second degree burns with blisters.
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    Fig. 1.224: Extensive third degree burns with eschar.
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    Fig. 1.225: Extensive burns more than 50%.
    zoom view
    Fig. 1.226: Degrees of burns.
  2. Second degree: The affected area is mottled, red, painful, with blisters, heals by epithelialisation in 14–21 days.
    • Superficial second degree burn heals, causing pigmentation.
    • Deep second degree burn heals, causing scarring, and pigmentation. Sensation is present but no blanching.
  3. Third degree: The affected area is charred, parchment like, painless and insensitive, with thrombosis of superficial vessels. It requires grafting. Charred, denatured, insensitive, 130contracted full thickness burn is called as eschar. These wound must heal by re-epithelialisation from wound edge.
  4. Fourth degree: Involves the underlying tissues—muscles, bones.
 
II. Depending on thickness of skin involved
  1. Partial thickness burns: It is either first or second degree burn which is red and painful, often with blisters.
  2. Full thickness burns: It is third degree burns which is charred, insensitive, deep involving all layers of the skin.
 
Assessment of Burns
  • Wallace's rule of nine is used for early assessment—refer figure.
  • Using the Lund and Browder chart is better method for assessing the burns wound. Here each part of the body is individually assessed for involvement of burns.
  • Patient's entire hand area is 1%. Clean piece of paper is cut to the size of hand and through that percentage of burns is assessed. 44°C temperature takes 6 hours to cause deep burns. 65°C takes 45–60 seconds to cause deep full thickness burn.
Burn is a dynamic wound and so assessment should be repeated at regular intervals.
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Fig. 1.227: Third degree burns with charred skin, with thrombosed veins and eschar.
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Fig. 1.228: Face burns in an adult—severe third degree.
 
Clinical Features
  • History of burn.
  • Pain, burning, anxious status, tachycardia, tachypnoea, fluid loss.
  • In severe degrees features of shock.
Tolerable temperature to human skin is 40°C for brief period.
 
Pathophysiology
Heat causes coagulation necrosis of skin and subcutaneous tissue
Release of vasoactive peptides
Altered capillary permeability
Loss of fluid → Severe hypovolaemia
Decreased cardiac output → Decreased myocardial function
Decreased renal blood → Oliguria
flow (Renal failure)
Altered pulmonary resistance causing pulmonary oedema
Infection
Systemic inflammatory response syndrome (SIRS)
Multiorgan dysfunction syndrome (MODS).
There is increased capillary permeability, decreased plasma oncotic pressure causing loss of protein and fluid from intravascular space. Vasoconstriction occurs due to raised capillary hydrostatic pressure leading into cellular aggregation. Blockage of lymphatics causes poor clearance of fluid and proteins from interstitial spaces. Cell membrane function is impaired causing intracellular fluid accumulation. Activation and release of various complement factors, histamine, and prostaglandins results in myocardial dysfunction, oedema of tissues, reduced immunoglobulin synthesis. Catecholamine levels are raised drastically in patient with burn. There will be lipolysis, proteolysis, increased release of glutamine and alanine from skeletal muscles. Urea production is increased due to more proteolysis.
Massive oedema in the body is due to altered pressure gradient because of the injury to basement membrane.
zoom view
Fig. 1.229: Burn zones (Jackson's).
131
Cardiac dysfunction is due to:
  • Hypovolaemia.
  • Release of cardiac depressants.
  • Hormonal causes like catecholamines, vasopressin, angiotensins.
Renal changes are due to:
  • Release of ADH from posterior pituitary to cause maximum water reabsorption.
  • Release of aldosterone from adrenals to cause maximum sodium reabsorption.
  • Toxins released from the wound along with sepsis causes acute tubular necrosis.
  • Myoglobin released from muscles (in case of electric injury or often from eschar) is most injurious to kidneys.
Pulmonary changes are due to:
  • Altered ventilation-perfusion ratio.
  • Pulmonary oedema due to burn injury, fluid overload, inhalation injury.
  • ARDS.
  • Aspiration.
  • Septicaemia.
GIT changes are due to:
  • Acute gastric dilatation which occurs in 2–4 days.
  • Paralytic ileus, Curling's ulcer (due to decreased mucosal defence; not due to increased HCl).
  • Cholestasis and hepatic damage.
  • Acute acalculous cholecystitis, acute pancreatitis can occur.
Bowel mucosal ischaemia causes poor motility, reduced food digestion and absorption with increased translocation of bacteria causing peritoneal oedema, septicaemia and abdominal compartment syndrome.
 
Metabolic Changes
  • Hypermetabolic rate (BMR).
  • Negative nitrogen balance.
  • Electrolyte imbalance.
  • Deficiencies of vitamins and essential elements.
  • Metabolic acidosis due to hypoxia and lactic acid.
 
Sepsis in burn patient
  • Focus may be at the burn site, catheter site, cannula/CVP line site, or respiratory infection.
  • Low immunity, loss of proteins and immunoglobulins, loss of barrier causes sepsis. Opportunistic infection is also common.
  • Associated conditions like diabetes, HIV infection, old age, respiratory diseases worsen the sepsis in burn injury.
  • It may be local infection commonly by staphylococcus aureus in early period, pseudomonas, candida, aspergillus, herpes simplex virus in partial thickness nasolabial burns. It may be suppurative thrombophlebitis also.
  • Systemic infection like pneumonia, bacteraemia, septicaemia can occur.
  • Burns itself creates immunosuppression (cell-mediated immunity).
  • Sepsis is identified by fever, lethargy, leucocytosis, thrombocytopenia.
zoom view
Fig. 1.230: Burns over chest wall with eschar. Note the extent of involvement.
 
Effects of Burn Injury
  • Shock due to hypovolaemia.
  • Renal failure.
  • Pulmonary oedema, respiratory infection, adult respiratory distress syndrome (ARDS), respiratory failure.
  • Infection by Staphylococcus aureus, beta haemolytic Streptococcus, Pseudomonas, Klebsiella leads to bacteraemia, septicaemia. Fungal and viral infections of dangerous types can also occur.
    132
    zoom view
    Fig. 1.231: Deep burns face with eyelid involvement.
  • GIT: Hypovolaemia, ischaemia of mucosa, erosive gastritis—Curling's ulcer (seen in burns >35%).
  • Fluid and electrolyte imbalance.
  • Postburn immunosuppression predisposes to severe opportunistic infection.
  • Eschar formation and its problems like defective circulation, ischaemia when it is circumferential.
  • Electrical injuries often cause fractures, major internal organ injury, convulsions.
  • Development of contracture is a late problem. It leads to ectropion, microstomia, disability of different joints, defective hand functions, growth retardation causing shortening.
  • Inhalation burn causes pulmonary oedema, respiratory arrest, ARDS.
  • Chemical injury causes severe GIT disturbances like erosions, perforation, stricture oesophagus (alkali), pyloric stenosis (acid), mediastinal injury.
  • Other problems commonly seen are DVT, pulmonary embolism, urinary infection, bed-sores, severe malnutrition with catabolic status, respiratory infection.
  • Complications of burns contracture itself like hypertrophic scar, keloid formation.
  • Toxic shock syndrome: It is a life-threatening exotoxin mediated disease caused by Staphylococcus aureus. It is common in children, presents with rashes, myalgia, diarrhoea, vomiting, and multiorgan failure with high mortality.
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Figs 1.232A and B: Burns hand both palmar and dorsal aspect.
zoom view
Fig. 1.233: Deep burn in the scalp involving extensively.
 
MANAGEMENT OF BURNS
 
First Aid
  • Stop the burning process and keep the patient away from the burning area.
  • Cool the area with tap water by continuous irrigation for 20 minutes (not cold water as it can cause hypothermia).
133
 
Definitive Treatment
  • Admit the patient.
  • Maintain airway, breathing, circulation (ABC). Emergency endotracheal intubation may be required in early period itself; in such situation succinylcholine should not be used.
  • Assess the percentage, degree, and type of burn.
  • Keep the patient in a clean environment.
  • Sedation and proper analgesia.
  • Patient should be in burns unit (ideally air-conditioned) with barrier nursing, sterile clothes, bed sheets with all aseptic methods.
 
Fluid Resuscitation
Formulas to calculate the fluid replacement:
  1. Parkland regime: Commonly used:
    4 ml/% burn/kg body weight/24 hours.
    Maximum percentage considered is 50%.
    Half the volume is given in first 8 hours, rest given in 16 hours.
  2. Muir and Burclay regime: For colloid after 12–24 hours.
    3 Rations given in first 12 hours.
    2 Rations in second 12 hours.
    1 Ration in third 12 hours.
  3. Galveston regime (pediatric):
    5000 ml/m2 burned + 1500 ml/m2 total
  4. Modified Brooke formula:
    First 24 hours:
    RL: 4 ml/kg/% burns in 24 hours
    (first half in first 8 hours)
    Colloid—none.
    Second 24 hours:
    Crystalloids—to maintain urine output
    Colloids—0.3 ml to 0.5 ml/kg/burns in 24 hours.
    (Albumin in RL solution) (Albumin alone should be given with care if really indicated only).
  5. Evan's formula:
    In first 24 hours:
    Normal saline 1 ml/kg/% burns
    Colloids 1 ml/kg/% burns
    5% dextrose in water, 2000 ml in adult.
    In second 24 hours:
    Half of the volume used in first 24 hours.
Fluids used are Ringer lactate, Hartmann fluid, plasma. Ringer lactate is the fluid of choice. Blood is transfused in later period (after 48 hours).
First 24 hours only crystalloids should be given (Crystalloids are one which can pass through capillary wall like saline either hypo, iso or hypertonic, dextrose saline, ringer lactate).
Sodium is assessed by formula: 0.52 mmol × kg body weight × % body burns, given at a rate of 4.0 to 4.4 ml/kg/hour.
After 24 hours up to 30–48 hours, colloids should be given to compensate plasma loss (colloids are one which are retained in intravascular compartment). Plasma, haemaccel (gelatin), dextrans, hetastarch are used. Usually at a rate of 0.35–0.5 ml/kg/% burns is used in 24 hours.
  • Urinary catheterization to monitor output; 30–50 ml/hour should be the urine output.
  • Tetanus toxoid.
  • Monitoring the patient: Hourly pulse, BP, PO2, PCO2, electrolyte analysis, blood urea, nasal oxygen, often intubation is required.
  • IV ranitidine 50 mg 8th hourly.
  • Ryle's tube insertion initially for aspiration purpose later for feeding (Enteral feeding). For burns >15%.
  • Antibiotics: Penicillins, aminoglycosides, cephalosporins, metronidazole.
  • Culture of the discharge; total white cell count and platelet count at regular intervals are essential to identify the sepsis along with fever, tachycardia and tachypnoea.
  • In burns of oral cavity tracheostomy may be required to maintain the airway.
  • Total parenteral nutrition (TPN) is required for faster recovery, using carbohydrates, lipids, vitamins (through a CVP line).
  • Tracheostomy/intubation tube may be required in impending respiratory failure or upper airway block.
  • Intensive nursing care.
 
Local Management
  • Dressing at regular intervals under general anaesthesia using paraffin gauze, hydrocolloids, plastic films, vaseline impregnated gauze or fenestrated silicone sheet or biological dressings like amniotic membrane or synthetic biobrane.
  • Open method with application of silver sulfadiazine without any dressings, used commonly in burns of face, head and neck.
  • Closed method is with dressings done to soothen and to protect the wound, to reduce the pain, as an absorbent.
  • Tangential excision of burn wound with skin grafting can be done within 48 hours in patients with less than 25% burns. It is usually done in deep dermal burn wherein dead dermis is removed layer by layer until fresh bleeding occurs. Later skin grafting is done.
    Advantages of tangential excision: It reduces—the chance of secondary infection, the hospital stay, and formation of hypertrophic scar or contracture, the cost.
  • In burns of head and neck region, exposure treatment is advised.
  • Slough excision is done regularly.
134
Topical agent
Advantages
Problems
Silver sulfadiazine (1%)
  • Antiseptic (G +ve and G –ve)
  • Neutropenia, pseudoeschar
  • It diffuses poorly through the eschar
  • Soothening, good penetration,
  • Hydration and softening of eschar occurs
  • Causes hypertrophic granulation and so not used once wound is clean and eschar is separated
  • It does not cause pain
  • Causes wound maceration
  • It should be avoided in pregnancy, nursing mother and infants below 2 years of age
Sulfamylon (5%/11%)
  • Antipseudomonal, anticlostridial
  • Very irritant, painful
(Mafenide acetate)
  • Penetrates very well in to tissues
  • It is water soluble
  • It is good antipseudomonal agent
  • Causes acidosis, by inhibiting the carbonic anhydrase
Silver nitrate (0.5%)
  • Antiseptic, antipseudomonal.
  • Stains burnt area
Povidone iodine (5%)
  • Antiseptic (G +ve, G –ve)
  • Irritant and painful
  • Used on granulation tissue after eschar separation
  • Not used in partial burns
  • Used in perineum and buttocks to prevent maceration
Silver sulphadiazine and cerium nitrate
  • Boosts cell-mediated immunity and forms sterile eschar
  • After cleaning with povidone iodine solution silver sulfadiazine ointment is used. It is an antiseptic and soothening agent. It causes neutropenia.
    Other agents used are Sulfamylon (Mafenide acetate) and Silver nitrate.
    • Sulfamylon is antipseudomonal and anticlostridial agent. It penetrates well into the tissues but it is very irritant. It causes acidosis.
    • Silver nitrate causes staining of burnt area.
    • 0.025% sodium hypochlorite (Dakin's solution) is effective against Gram +ve organisms; 0.25% acetic acid is effective against Gram –ve organisms, but both mildly inhibit epithelialisation.
Regular culture and sensitivity for bacteria is required, to see for streptococcal growth which should be less than 1,00,000 (10 5) per gram of tissues.
 
Wound coverage
  • Once the area granulates well, in 3 weeks usually, split skin grafting is done (SSG, Thiersch graft).
  • For wider area MESH split skin graft is used.
  • If there is eschar, escharotomy is required to prevent compression of vessels.
  • In certain areas like face and ear, full thickness graft (Wolfe graft) or flap is required.
  • Cultured skin: Full thickness skin biopsy of patient's skin is done immediately after admission. By specialized culture technology sheets of skin can be manufactured in 3 weeks as cultured epithelial grafts. It can cover skin of almost entire body. It is usually useful in burns of > 80%. Take up of cultured graft is 60–75%. Limitations are—time taken to develop cultured graft; more vulnerability for mechanical trauma; costly; time taken to manufacture; scarring.
Synthetic dressings in burn wound
  • Vaseline impregnated gauze dressing prevents stiffness of eschar.
  • Hydrocolloid dressing (duoderm) helps moist environment, proper epithelialisation. It is useful in mixed deep burns. It is changed once in 3 days.
  • Opsite is less expensive, with less pain, creates moist barrier. But it does not have antimicrobial effect and it causes accumulation of exudates.
  • Biobrane is collagen coated silicone sheet which gets adherent to wound acting as barrier without any pain. But it does not have antimicrobial effect and it causes accumulation of exudates. It is used for 2nd degree burns.
  • Transcyte has similar features of biobrane. It contains growth factor derived from cultured fibroblasts which promotes wound healing.
  • Integra contains deeper collagen matrix as dermal substitute; outer silicone sheet as epidermal substitute. Inner collagen matrix acts as dermis whereas outer silicone sheet is removed 2 weeks after dressing and additional autograft should be placed. It provides complete wound cover. Scarring after healing is reduced significantly.
Biologic dressings for burn wound
It is used to cover the wound temporarily as a barrier and also to have some immunologic function. Eventually graft will slough. Later wound is covered with auto-skin graft. It is used for massive burn injuries more than 50%. Possible problem is transmission of viral diseases.
Xenograft is of pig skin. Allograft is of cadaver skin (homograft)—it gives all existing normal skin function for temporary period. It may leave a dermal equivalent in the wound later.
 
ESCHAR
  • It is charred, denatured, full thickness, deep burns with contracted dermis.
  • It is insensitive, with thrombosed superficial veins.
  • Circumferential eschar in the upper limb, lower limb, neck, thorax can cause more oedema which initially causes venous compression and later arterial compression causing ischaemia, gangrene of the distal part. So distal area should be monitored for circulation.
  • If required deep longitudinal full thickness incisions are made in different areas so as to prevent collection of oedema fluid and 135also to prevent compression over the vessels. This is called as escharotomy. Escharotomy causes large quantity of blood loss and so blood transfusion is needed while doing escharotomy. Incision should be of adequate length and depth during escharotomy. It should be placed in such a way so as to avoid injury to major neurovascular system. Release of muscle compartment is needed often in these patients.
  • Multiple incisions or incisions over the joints may be needed.
  • Early rapid separation of eschar indicates severe sepsis underneath.
  • Eventually eschar should be excised and the area is allowed to granulate and skin grafting should be done.
Pseudoeschar is thickened burnt skin due to repeated silver sulphadiazine application.
 
CONTRACTURE IN BURN WOUND
Contracture in burns can occur anywhere. It is more common wherein flexibility and mobility is present like along the joint, eyelids, cheeks, lips, neck, elbow, knee, etc. Contracture can be intrinsic by loss of tissue or extrinsic by pull during healing phase contraction. Contracture proceeds towards position of comfort until it meets or closely reaches opposite surface. There is clearly wound shortening. Disorganised over formation of compact collagen (3 times normal) causes hypertrophic scar leading further contracture.
Deficit of neck extension is graded, normal >110°; E1 95–110°; E2 is 85–95°; E3 is <85° with mentosternal synechia.
 
Complications of Burns Contracture
  • Ectropion of eyelid causing keratitis and corneal ulcer.
  • Disfigurement in face.
  • Narrowing of mouth microstomia.
  • Contracture in the neck causing restricted neck movements.
  • Disability and nonfunctioning of joints due to contracture.
  • Hypertrophic scar and keloid formation.
  • Repeated breaking of scar and infection, ulcer, cellulitis.
  • Pain and tenderness in the scar contracture.
  • Marjolin's ulcer:
    It is a very well-differentiated squamous cell carcinoma occurring in a scar ulcer due to repeated breakdown (unstable scar of long duration).
    • It is locally malignant.
    • As there are no lymphatics in the scar, so there is no spread to lymph nodes.
    • As there are no nerves in the scar it is painless.
    • It has raised and everted edge with induration.
    • Biopsy confirms the diagnosis.
Treatment: Treatment is either wide excision or amputation. It is curable.
Once it spreads out of the scar tissue it behaves like any other squamous cell carcinoma and so can spread to regional lymph nodes.
Radiotherapy is not given for Marjolin's ulcer.
 
Treatment for Contracture
  • Release of contracture surgically and use of skin graft or “Z” plasty or different flaps. Different flaps used are—transposition flaps, vertical or transverse; laterally based flap; bilobed flap; bipedicled flap; advancement flap; regional flap; random cutaneous flap (Epaulette flap, Charretera flap); fasciocutaneous/myocutaneous flap; tube flap; expanded skin flap; combined skin graft and flap; microvascular free flap.
  • Proper physiotherapy and rehabilitation is essential.
  • Pressure garments to prevent hypertrophic scars.
  • Management of itching in the scar using aloe vera, antihistamines and moisturizing creams.
 
Problems in managing burn contracture
  • Giving proper anaesthesia is challenging.
  • Scar excision can cause significant bleeding.
  • Identifying major structures in the area and safeguarding vascular and other structures is often worrisome.
  • Need for repeated surgeries as staged one.
  • Maintaining the position with skeletal traction, fixation, collar, POP cast, etc.
  • Psychological problems and needs counseling.
  • Prolonged hospital stay, cost factors.
zoom view
Fig. 1.234: Ectropion of upper eyelid due to burns.
136
zoom view
Figs 1.235A to C: Contracture at different parts of the body—chest, face and neck.
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Figs 1.236A to C: (A) Marjolin's ulcer developed over burns scar; (B) Severe contracture at knee joint causing deformity (C) Same patient with knee contracture undergoing release surgery.
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Figs 1.237A to C: (A) Infant had burns in head and neck region causing severe contracture; (B) Elbow contracture due to burns; (C) Keloid in the hand after burn injury.
 
ELECTRICAL BURNS
 
Types of Electrical Injury
  • Low tension injury: less than 1000 volts.
  • High tension injury: more than 1000 volts—may be due to current itself causing intense damage on the tissues up to 2000°C; flash injury due to electrical arc up to 4000°C; flame injury by catching of fire to the clothing and body; traumatic injury like fractures and internal organ injuries.
  • It is always a deep burn (always a major burn).
  • There is a wound of entry and wound of exit.
  • Patient may also have major internal organ injuries. GIT, thoracic injuries.
  • Often convulsions can develop.
  • Death may occur due to cardiac arrhythmias (instant death due to ventricular fibrillation).
  • Gas gangrene is common after electric injury.
  • Release of myoglobin can cause renal tubular damage and renal failure.
    137
    zoom view
    Figs 1.238A and B: High voltage electric burn wound of entry in the hand with extensive destruction. Some patient showing wound of exit in the buttock which is extensive and deep.
    zoom view
    Fig. 1.239: Wound of entry in an electric burn.
  • Acidosis is common and so often bicarbonate infusion is needed.
  • Patient should always be admitted and should be assessed by ECG, cardiac monitor, U/S abdomen, chest X-ray, sometimes even CT scan head, cardiac enzyme analysis.
  • Depending on the injury it is managed accordingly.
  • Fractures and dislocations are common in electrical injuries which is treated accordingly.
  • Mafenide acetate is better agent as it penetrates well and it is useful against clostridial infection.
  • Mannitol is used to prevent myoglobin induced renal failure.
  • Wound excision, amputation, surgery for internal organ injury, cardiac monitoring are essential part of the surgical management.
 
INHALATION INJURY
It occurs after major fire burns.
It is due to:
  • Inhalation of heat.
  • Noxious gases and incomplete products of combustion.
  • At the site of fire, oxygen concentration is less than 2% which can cause death in 45 seconds due to hypoxia.
  • Inhaled carbon monoxide binds with Hb immediately to form carboxyhaemoglobin causing severe anoxia and death.
Electrical burns
Types
Treatment
Complications
Monitoring and prevention
High voltage—can cause ventricular fibrillation, cardiac arrest, death. Extensive organ and surface injuries with fractures.
Low voltage—deep burn at the site of wound of entry.
Emergency resuscitation
Assessment of burn
Prevention of renal failure by hydration, dialysis, alkalisation of urine to clear myoglobin, mannitol therapy, IV sodium bicarbonate.
Extensive fasciotomy, debridement.
Infection control.
Reconstruction.
  • Neurological like epilepsy, haemiplegia, aphasia, memory loss, headache, transverse myelitis.
  • Cardiac—arrhythmias.
  • Vascular injuries—major vessels, bleeding.
  • Compartment syndromes.
  • Ischaemia, gangrene of limbs.
  • Contracture development.
  • Bronchopneumonia, pleural effusion.
  • Abdominal—ileus, erosive gastritis, Curling ulcer, injury to liver, pancreas, spleen, GIT, ARF.
  • Bone and joint injuries.
  • Cataract can occur in high voltage burn.
  • Severe potassium deficiency is common.
Monitoring:
ECG, echocardiography
Relevant investigations like X-ray, ultrasound, CT, electrolytes, urine analysis, LFT, renal function tests.
Prevention:
Care during electrical work and with electrical system.
Unused outlets should be sealed with plastic.
Electrical system should be away from water source.
138
  • CO has got 240 times more affinity for haemoglobin than oxygen. Carboxyhaemoglobin in blood more than 10% is dangerous; more than 60% is life-threatening.
  • Symptoms of carbon monoxide intoxication—headache, disorientation, visual changes, fatigue, vomiting, hallucinations, shock and cardiac arrest.
  • Smoke contains hydrocyanide which causes tissue hypoxia and profound acidosis.
  • Laryngeal oedema and laryngospasm.
  • Bronchial oedema and bronchospasm.
  • Formation of bronchial cast is typical which is due to oedema, lymph exudation, separation of ciliated epithelial cells from basement membrane. Inhaled gas causes supraglottic airway burn, laryngeal oedema, loss of respiratory epithelium, ARDS, CO poisoning, mechanical restriction of chest wall movement.
 
Later Problems
  • ARDS, pneumonia.
  • Atelectasis, pulmonary embolism.
  • Pulmonary oedema, pneumothorax.
 
Clinical Features
  • They have low oxygen saturation.
  • Charring of mouth, oropharynx with facial burns.
  • Carbon sputum.
  • Change in the voice, singed facial and nasal hair.
  • Decreased level of consciousness with stridor or dyspnoea.
  • Acute pulmonary insufficiency with asphyxia, CO poisoning, upper airway obstruction. After 3 to 5 days, ARDS and hypoxia develops. Bronchopneumonia with septicaemia occurs after 5 days.
 
Management
  • Replacing the patient from the site earliest.
  • Ventilator support for several weeks.
  • Antibiotics.
  • Bronchoscopy, at regular intervals to remove bronchial cast.
  • Tracheostomy whenever required.
  • Hyperbaric oxygen.
  • IV heparin to reduce bronchial cast. Heparin nebulisation (10,000 units in 3 ml saline 4th hourly) is also useful. N-acetylcysteine nebulisation—20% in 3 ml saline 4th hourly, bronchodilators like albuterol 2nd hourly is very useful. Hypertonic saline inhalation induces the effective coughing to remove casts. Racemic epinephrine is used to reduce mucosal oedema.
    Note:
    Steroids are not beneficial in inhalation burns.
  • Monitoring the patient with arterial blood gas analysis regularly.
 
CHEMICAL BURNS
  • In chemical burns, tissue destruction is more and progressive. It is always a deep burn.
  • Acid burn occurs in skin, soft tissues and GIT. In GIT, it is common in stomach either due to nitric acid or sulphuric acid which may lead to severe gastritis or pyloric stenosis. Other acids are formic acid, hydrofluoric acid. They cause metabolic acidosis, renal failure, ARDS, haemolysis. Acidaemia should be corrected by IV sodium bicarbonate.
  • Hydrofluoric acid is commonly used in industrial areas. It is strongest inorganic acid that can produce corrosion and dehydration. It chelates blood calcium causing hypocalcaemia and arrhythmias. It is managed with water irrigation, application of 2.5% calcium gluconate gel at 15 minutes interval, local intradermal and intra-arterial injection of 10% calcium gluconate. Continuous cardiac monitoring, IV calcium gluconate or calcium chloride administration is needed.
  • Alkali burns occur in oral cavity and oesophagus which leads to multiple oesophageal strictures. Sodium hydroxide, lime, potassium hydroxide and bleach are common alkalis involved. They cause saponification of fat, fluid loss, release of alkali proteinates and hydroxide ions which are toxic.
  • External chemical burns are always deep and cause extensive disfigurement with cosmetic problems.
  • Initial treatment is dilution with water (Hydrotherapy). It is done using 15–20 litres of running tap water.
  • Neutralisation with antidote should never be done at initial phase of treatment as it creates exothermic reaction which aggravates the tissue damage. Late neutralisation is done, if required by 0.2% acetic acid in alkali burns; sodium bicarbonate, calcium gluconate 10% gel, topical ziphrin solution in acid burns.
  • Treatment should always be with hospitalisation.
  • Mannitol diuresis, haemodialysis, calcium gluconate IV, pain relief, serum electrolyte management, TPN, ventilator support are systemic management required.
  • Late treatment is reconstruction of the face.
  • Oesophageal dilatation or colonic transposition is done for oesophageal stricture due to alkali burn.
  • Gastrojejunostomy is done for acid induced pyloric stenosis.
  • Tar burns are treated additionally with neosprin which contains Tween-80 emulsifier of tar.
  • Cement is calcium oxide alkali. Its burn is due to hydroxyl ion which is often deep. Treatment is removal of cloth, irrigation with water, keeping pH below 8. Often it may form eschar.
139J. Trauma
CHAPTER OUTLINE
  • ❖ Triage
  • ❖ Spinal Injury
  • ❖ Neck Injuries
  • ❖ Bullet Injuries
  • ❖ Blast Injuries
  • ❖ Penetrating Injuries
  • ❖ Abdominal Trauma
  • ❖ Blunt Trauma of Abdomen
  • ❖ Duodenal Injury
  • ❖ Pancreatic Injury
  • ❖ Small Bowel Injury
  • ❖ Colonic Injury
  • ❖ Liver Injury
  • ❖ Splenic Injury
  • ❖ Renal Injury
  • ❖ Urinary Bladder Injury
  • ❖ Abdominal Compartment Syndrome
  • ❖ Seat-belt Injuries
 
Trauma is a major public health problem in all countries. It causes death disability and both. 50% die immediately at the time of accident. 25% die in golden hour of trauma, i.e. first 4–6 hours of trauma. 25% may die late during treatment period due to sepsis and complications. Injuries may be penetrating, blunt, blast, chemical, electrical and other injuries.
zoom view
Fig. 1.240: Trauma causing large tissue defect exposing the bone.
 
TRIAGE
Triage means “To sort” in French.
Triage is a system to attend trauma patients, formulated by Committee of Trauma of the American College of Surgeons.
Advanced trauma life support (ATLS) is essential for first hour care of an injured patient.
Pre-hospital trauma life support (PHTLS) is to prevent deaths while injured patients are transported to the hospital.
 
Types of Triage System
  • Multiple casualties: Staff and facilities are sufficient but priority is given to life-threatening injuries.
  • Mass casualties: Staff and facilities are not sufficient to manage. Here those who are likely to have highest chance of survival are given priority.
 
Management
  • Initial evaluation of the patient.
  • Physiologic stabilisation.
  • Control of haemorrhage.
  • Management of thoracic and abdominal injury.
  • Management of cranial injury.
 
I. Primary Management
  • Airway management (blocked by food, vomitus, clot, fallen tongue).
  • Breathing.
  • Circulation.
  • Disability and level of consciousness assessment by Glasgow coma scale.
  • Exposure of the patient from head to toe for final assessment.
  • Fingers and tubes: Finger evaluation, Foley's catheterisation.
Goals
  • Identify life-threatening conditions.
  • Decide and implement appropriate treatment to the area of trauma.
  • First think to salvage the life, then think to salvage the limb.
  • Rapid assessment, rapid resuscitation, rapid stabilisation.
  • Optimum, complete care.
  • Transport efficiently to higher trauma centre.
 
II. Investigations
  • X-ray spine, chest, pelvis, extremities.
  • CT scan.
  • Blood group and cross-matching.
  • Arterial blood gas analysis.
  • Serum electrolytes.
  • U/S abdomen.
 
III. Secondary Survey
Re-evaluate the patient completely again.
 
IV. Definitive Care
(All discussed under individual topics.)
 
Mechanism of Trauma
  • Blunt trauma—direct or indirect blunt injury can occur. Seat belt reduces the blunt injury in vehicles.
  • Penetrating injury—severity depends on the extent of deeper injury.
  • Blast injury.
  • Crush injury—earthquake, industrial accidents, and train accidents—causes crush syndrome; compartment syndrome.
  • Burn injury.
  • Injury in alcohol patients.
zoom view
Fig. 1.241: Crush injury leg due to road traffic accident.
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Fig. 1.242: Ankle injury with open wound.
 
Revised Trauma Score (RTS)
It is a reliable physiological scoring system in trauma. Here Glasgow coma scale, systolic blood pressure, respiratory rate are used as parameters.
RTS = 0.9368 × GCS + 0.7326 × systolic BP + 0.2908 × Resp rate. RTS will come between 0–7.8. Value <4 needs critical care.
141
Glasgow coma scale
Blood pressure Systolic
Respiratory rate
Value
13–15
>89
10–19
4
9–12
76–89
>29
3
6–8
50–75
6–9
2
4–5
1–49
1–5
1
3
0
0
0
zoom view
Fig. 1.243: Degloving injury involving entire left lower limb, perineum, and left groin. Patient has lost scrotum and both testes. There were no internal injuries and vessels and nerves were intact. Patient underwent wound excision extensively and colostomy was done to promote healing of perineal wound and prevent contamination.
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Fig. 1.244: Class III dog bite on face in a boy.
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Fig. 1.245: Degloving of scalp with bone periosteum exposing the skull bone. Outer table was actually dead and required bone removal and graft after healthy granulation tissue was formed.
 
CONCEPTS IN TRAUMA MANAGEMENT
  • Concept of 'golden hour' to treat the trauma patient is important.
  • Multidisciplinary approach.
  • Planning, setting up, organizing, team work.
  • Assess respiratory system; circulation; bleeding areas—as priority.
  • Assess also whether patient is haemodynamically stable or unstable.
  • Arrange fluids, blood, catheters, ventilator, etc.
  • Further definitive therapy depending on severity and site of injury.
 
Damage Control Surgery
  • Resuscitation and early therapy in operation theatre itself.
  • Minimum but essential surgery to control bleeding and prevent contamination.
  • Secondary definitive surgery at a later period to have final control.
  • Damage control surgery is done when there is inability to control bleeding, complex abdominal injuries like of liver or pancreas, major vascular injuries with or without bowel injuries, retrohepatic IVC injury which is not accessible; decline in physiological reserve like temperature, pH, prothrombin time, serum lactate, systolic blood pressure less than 90 mmHg for 60 minutes; if operating time expected is more than one hour, inability to close the wound or whenever reopening the cavity is needed.
  • Principles of damage control surgery apply to injuries of the abdomen, thorax and extremities equally.
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Fig. 1.246: Hand injury involving all fingers.
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Fig. 1.247A:
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Figs 1.247A and B: A person has bitten this patient during a fight and removed the central part of lower lip. It was repaired primarily by Y repair. Remember human bites are most dangerous.
 
SPINAL INJURY
  • Assess the type, extent and severity of the injury.
  • Careful first aid and transfer to prevent further damage to the spinal cord.
  • Assess the sensory loss or motor loss properly.
  • Assess fractures clinically, by X-ray, CT scan (for fracture) and MRI (for spinal cord injuries).
  • Central cord syndrome is common and is due to hyperflexion or hyperextension of the neck in an injured patient causing ischaemia of spinal column due to interfering of spinal artery blood flow.
  • Brown-sequard syndrome: It is due to partial transection of the cord causing ipsilateral motor function loss and contralateral sensory function loss.
  • High dose of steroid is very useful to prevent further damage.
  • Rest, traction to neck.
  • Decompression of spinal canal surgically by removing bone, disc, haematoma is useful.
  • Spinal stabilisation.
 
NECK INJURIES
 
Indications for Neck Exploration in Injuries
  • Expanding haematoma.
  • Uncontrolled external haemorrhage.
  • Decreased carotid pulse.
  • Stridor, hoarseness, dysphonia, haemoptysis.
  • Severe dysphagia, odynophagia.
  • Blood in oropharynx.
 
Treatment
  • The neck is explored with adequate incision under general anaesthesia.
  • The injured structure like vessels, oesophagus, trachea, muscles are sutured.
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    Fig. 1.248: Neck trauma zones.
  • Antibiotics.
  • Blood transfusion is given as required.
  • Ryle's tube for 5–7 days.
Other injuries like head, thorax, abdomen, maxillofacial area are discussed in respective chapters.
 
BULLET INJURIES
Bullet injury has wound of entry and wound of exit. Extent of damage is not related to the external wounds. It is related to the travel of bullet inside and extent of blast or cavitation effect inside caused by the bullet. It causes burn damage.
It can damage vessels, organs like liver, spleen, kidneys, bowel, lungs, heart, cranial structures, soft tissues, bones and joints.
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Fig. 1.249: Multiple pellets over elbow region after gunshot.
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Management
  • The wounds are explored properly under general anaesthesia.
  • All dead tissues and dead muscles are excised.
  • Skin is generously and adequately incised.
  • Injured nerves are cleaned and silk marker stitches are placed to identify for later secondary suturing (Nerve should not be sutured primarily in bullet injury).
  • All foreign bodies are removed.
  • Tendon repair should not be done primarily.
  • Wound should not be closed. It should be left open.
  • Adequate blood transfusion and antibiotics coverage should be given.
  • Major artery or vein are sutured. Vein graft can be used. But synthetic graft should never be used.
  • Thorough inspection, irrigation and debridement of injured joints is done.
  • Immobilisation is done.
  • Tetanus toxoid, antitetanus globulin (3000 units IM), antigas gangrene serum is given.
  • Second look surgeries at a later period is done once patient has been stabilised.
  • Delayed primary closure in 4–7 days or secondary closure in 14 days is done.
  • Depending on extent of defect, skin grafting or flaps are used.
  • Laparotomy, thoracotomy, craniotomy are done depending on the site of the injury.
 
BLAST INJURIES
Here extent of damage is much more than bullet injuries.
It creates complex blast wave which contains blast pressure wave and mass movement of air.
This explosion pressure wave is more than 1000 pounds per square inch. This pressure wave has got incident pressure and reflected pressure. Both will cause severe damage.
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Fig. 1.250: Degloving injury buttock. It needs colostomy to protect the wound from sepsis. Later once skin coverage is done colostomy is closed.
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Figs 1.251A and B: Crush injury foot with retained skin from plantar aspect was rotated forward(Courtesy: Dr Mayur Rai, orthopaedician, KMC, Mangaluru).
 
Organs Affected
  • Ear drums, lungs.
  • GIT, brain.
  • Skeletal system.
Individual becomes deaf after blast and so rescue work may be delayed.
 
Management
  • Critical trauma care.
  • Management of shock and triage primary management.
  • Urgent surgeries like laparotomy, thoracotomy, craniotomy.
  • Massive blood transfusion.
  • Antibiotics.
  • Ventilator support.
  • Management of specific organs like eye, ear.
 
PENETRATING INJURIES
  • It can occur in abdomen, thorax, cranial cavity.
  • It causes haemorrhage, damage to internal organs like liver, bowel vessels, lung, pericardium and heart, brain.
  • It is life-threatening and immediate surgical intervention is the only treatment. Patient requires adequate amount of blood transfusion, antibiotics, shock management.
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Fig. 1.252: Penetrating injury. Pole missed all the major vessels. Miraculously the patient survived, after a marathon surgery to tell her tale to her children.
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Fig. 1.253: Stab wound on the back communicating into the thoracic cavity. Wound was explored and sutured, with an ICT inserted into the thoracic cavity.
 
ABDOMINAL TRAUMA
It can be:
  • Blunt trauma
  • Stab injury
  • Abdominal wall injury
Abdominal trauma is a major surgical emergency which most surgeons face. It is often associated with head injuries, chest, pelvic and bone injuries. Often patient is unconscious causing difficulty in diagnosing the condition. Often more importance is given to other system injuries like of head, thorax and bones whereas abdominal injury is not addressed properly causing life-threatening consequences. When patient is conscious, history related abdominal trauma is useful. Abrasion over the abdominal skin suggests the possibility of internal injury (London's sign). Distension, tenderness, rebound tenderness, fullness and dullness in the flank when present one should presume internal injury. Tachycardia, hypotension, shock may be evident when there is significant haemoperitoneum. Injuries may be organ injury like of liver, spleen, kidney, pancreas, etc. or bowel injury or retroperitoneal injury which is often under diagnosed or missed. Major vessel injury like of inferior vena cava, mesenteric vessels can cause real threat to life unless it is identified and managed early. 25% of entire trauma patients need surgical exploration of the abdomen.
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Fig. 1.254: Traumatic haemoperitoneum.
Abdominal trauma can be blunt or stab/penetrating or abdominal wall injuries. Spleen is the most common organ involved in blunt trauma. Often in blunt trauma first part of the jejunum or ileocaecal junction gives way (blow out effect) due to traction often causing complete transection of bowel horizontally close to the junction. It is due to force of the mobile part of the bowel over the fixed part. Liver is the most common organ involved in penetrating injuries.
Injuries of the abdomen may be closed injuries, compression injuries and penetrating injuries. Penetrating injuries may be low velocity injury like stab injuries or high velocity injury like gunshot injuries. Penetration of blunt weapon causes less deep trauma than sharp weapon (sickle, knife). In sickle injury tip and sharp edge moves in curved pattern and so it is often difficult to predict the depth, track and organs injured.
Routinely followed indications for exploration in abdominal trauma are—hypotension without any other cause; bleeding through wound; continuous bleeding in nasogastric tube; evisceration of abdominal content through the open wound except in case of protruded omentum without any hypotension and features of peritoneal irritation; air under diaphragm in blunt abdominal injury (not in penetrating injury as external air gets sucked into the peritoneal cavity through the wound).
 
General Clinical Features
  • Features of shock—pallor, tachycardia, hypotension, cold periphery, sweating, oliguria.
  • Abdominal distension.
  • Pain, tenderness, rebound tenderness, guarding and rigidity, dullness in the flank on percussion.
  • Respiratory distress, cyanosis depending on the amount of blood loss.
  • Bruising over the skin of the abdominal wall.
  • Features specific of individual organ injuries.
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Figs 1.255A to C: Stab injury to LIF by an angry husband to his wife causing left common iliac artery transection injury with aortic partial injury. In spite saphenous vein graft reconstruction patient could not survive(Courtesy: Professor Yogishkumar, MS, KMC, Mangaluru).
 
Investigations
  1. Ultrasound abdomen. FAST is Focused Abdominal Sonar Trauma: It is rapid, noninvasive, portable bedside method of investigation focusing on pericardium, splenic, hepatic and pelvic areas. Blood more than 100 ml in cavities can be identified. It is not reliable for bowel or penetrating injuries. It often needs to be repeated.
  2. Diagnostic peritoneal lavage (DPL): It is done in case of blunt injury abdomen. Through a subumbilical lavage catheter one litre of normal s aline/Ringer's lactate is infused into the peritoneal cavity. Patient is changed to different positions and side-to-side. Fluid content is aspirated from the abdomen for assessment.
    It has got 98% accuracy rate.
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    Figs 1.256 and B: Diagnostic peritoneal lavage—incision and technique. 10 French polyvinyl catheter is used. Urinary bladder is emptied by passing a catheter. After injecting xylocaine local anaesthesia into subumbilical region, 2–3 cm vertical subumbilical midline incision is made. Skin, linea alba is incised. Local anaesthesia is infiltrated into the peritoneum again. Peritoneum is held with two haemostats and a purse string suture is placed using polyglactic acid absorbable suture material. Peritoneum is incised for 3 mm length. Catheter (standard peritoneal dialysis catheter) is introduced into the peritoneal cavity. If blood enters the catheter immediately, it means early laparotomy is needed and carried out without continuing the peritoneal lavage. Otherwise, one litre of normal saline is infused into the peritoneal cavity rapidly in few minutes through the catheter using a drip set with elevation of the fluid bottle/bag. Patient is moved well to mix the fluid in all four quadrants. Now bag is lowered below so that fluid from the peritoneal cavity reenters/siphoned into the bag. Collected fluid is analysed for red cells, leukocytes, etc. DPL may not be useful in bowel injury, retroperitoneal injury, diaphragmatic injury, organ haematoma (subcapsular splenic haematoma). If patient is decided for observation catheter can be left in situ for repeat DPL after 6 hours. One has to remember that DPL is not a substitute for clinical assessment and monitoring. In Lazarus-Nelson approach Teflon catheter with a guide wire is used.
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    It is the procedure of choice in physiologically unstable patient with blunt abdominal injury (like with spinal injury, unconscious patient).
  3. CT scan is indicated in assessing retroperitoneum, solid organ injuries. It is noninvasive and highly specific.
  4. Diagnostic laparoscopy (DL) is valuable method in stable abdominal trauma patient.
 
Treatment
Emergency laparotomy.
 
BLUNT TRAUMA OF ABDOMEN
It is common in accidents. It is often missed or lately diagnosed. Ultrasound/CT abdomen or diagnostic peritoneal lavage (DPL) is useful. In many cases on clinical grounds direct exploratory laparotomy is done. Plain X-ray abdomen may show gas under diaphragm.
Difficulty arises in deciding about the need for laparotomy in abdominal trauma in unconscious patients. If severity of external injury is out of proportion to the existing severe shock then exploratory laparotomy is indicated in an unconscious patient. It is also often difficult to diagnose bowel injury in such patients. If it is suspected laparotomy should be undertaken in such patients. Associated spinal injury masks the abdominal findings.
Injuries may be of liver, spleen, GIT, pancreas, mesentery, vascular or diaphragm. Associated chest, pelvis, skeletal and head injuries should be remembered.
 
Features of Blunt Trauma
  • Features of profound shock, progressive distension of abdomen, pain, tenderness, guarding, rigidity, rebound tenderness, dull flank.
  • Features specific of individual organ injury like obliteration liver dullness in bowel injury.
  • Bruising of skin over the abdomen—London's sign.
  • Respiratory distress, cyanosis.
  • Repeated clinical examination is a must in blunt trauma.
 
Evaluation
 
Ultrasound Abdomen
  • It is very useful, simpler, noninvasive method of evaluating the abdomen. Negative ultrasound means no immediate further intervention is needed and also conservative treatment can be undertaken.
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    Fig. 1.257: Blunt injury abdomen. Note the bruising over abdominal skin—London's sign.
  • Advantages of ultrasound: There is no danger of radiation; it can be done bedside; it can be repeated many times; it is cost-effective. Its sensitivity is 90%; specificity is 98%. Focused abdominal sonar (ultrasound) for trauma (FAST) is very useful method.
  • Disadvantages: It is less useful in obesity, with interposition of gas, when fluid is less than 500 ml; retroperitoneal injuries and bowel injuries.
  • Focused abdominal sonar trauma (FAST): It is rapid, noninvasive, portable bedside method of investigation focusing on pericardium, splenic, hepatic and pelvic areas. Blood more than 100 ml in cavities can be identified. It is not reliable for bowel or penetrating injuries. It often needs to be repeated.
 
Diagnostic Peritoneal Lavage (DPL) (by Perry)
It is useful in blunt injury abdomen. It is not very useful in penetrating injury, bowel injury, retroperitoneal and pelvic injuries.
 
CT Scan of Abdomen
It is most commonly used and better investigation for abdominal trauma. It is useful in blunt/penetrating trauma, suspected pancreas, spleen, liver, duodenal, retroperitoneal injuries. Smaller injuries, early haemoperitoneum are better detected. It is noninvasive, highly specific, highly accurate (96%), with low false-positive/low false-negative, noninvasive.
 
Other investigations
  1. Abdominal diagnostic paracentesis (Drapanas and McDonald): Here 18 G short bevel spinal needle is inserted into the peritoneal cavity after injecting local anaesthetic agent into the abdominal wall. With continuous suctioning through syringe, needle is passed at various sites. Positive tap means return of minimum of 0.1 ml of nonclotted blood. False-positive result occasionally can occur due to needle puncture of abdominal wall vessels. Needle should not be inserted close to previous abdominal scar as bowel may be adherent underneath the scar. Change of direction of needle is done by withdrawing the needle tip outer to peritoneum and again 147puncturing the peritoneum. Puncture by 18 G needle of nondistended bowel will seal without any leakage. Peritoneal tap should be avoided if bowel is distended. Bilateral flank tap/four quadrant tap is also done with similar result. Rectus sheath haematoma and false-negative results are the problems.
  2. Diagnostic laparoscopy is very useful. It can be done under local anaesthesia. Haemoperitoneum, solid organ and diaphragmatic injuries are well assessed. But bowel and retroperitoneal injuries are more likely to be missed.
  3. Arteriography through Seldinger technique is useful in suspected cases of renal arterial injury (thrombosis/spasm); intimal tears, traumatic aneurysm and aortic occlusion (after seat belt injury) are well diagnosed with arteriography. Often it can be therapeutic also. Pelvic bleed extending into retroperitoneum is not uncommon which can be assessed by arteriography and also the bleeding vessel can be identified. But venous bleed cannot be assessed by this.
  4. Doppler assessment of major vessels may be beneficial especially for IVC, aorta, iliac vessels, and portal system; but with haemoperitoneum visualisation window may be poor and vessels can be better identified by contrast CT scan.
 
Management Concepts in Abdominal Trauma
  • Evaluation of extent of the injury; number of organs injured and severity of injury; haematocrit assessment (haemoglobin drop up to 6 g% is tolerated well with adequate tissue oxygenation. Rapid drop of haemoglobin needs adequate number of blood to be kept ready for transfusion, like 5/10/bottles or more); central line for volume replacement; urinary catheterisation; administration of systemic antibiotics.
  • Autotransfusion of blood is very useful as a life-saving procedure in such situation. Blood from the cavity is sucked out into a sterile bottle which contains 150 ml of 3.8% sodium citrate dextrose solution. This blood is strained/filtered through gauze and re-transfused. If there is colonic and small bowel injuries auto transfusion is not possible for fear of sepsis due to contamination.
  • Upper midline incision extending down across the left of the umbilicus is the preferred incision. But surgeon should not be hesitant to extend the incision into the thorax or do horizontal T or extend as needed depending on the internal organ injury.
  • First priority after opening the abdomen is immediate control of profuse bleeding using finger compression or mop or pressure. Later once the field is clean; area is assessed for the extent of injury without releasing the compressed finger on the bleeding site. A vascular clamp or bulldog clamp is helpful in such situation. Once it is applied over the site of bleeding, compressing finger can be removed. Vascular suturing using 4 zero or 6 zero polypropylene/resection of the tissue; reconstruction of the area; persistent pressure mop in situ with closure of the abdominal wall with an option of second look surgery in 48 hours are the different options. Individual organs are assessed and graded for injuries and managed accordingly.
  • During laparotomy, entire abdomen should be inspected/palpated carefully for any additional missed injuries. Lesser sac, retroperitoneum, duodenum, pancreas and diaphragm should be checked. Often peritoneum on the margin of the duodenum and right side colon is incised, duodenum and colon is reflected medially to visualise the retroperitoneum. Pelvic structures need special attention. Rectum, urinary bladder injuries are likely to be missed if proper attention is not given. On catheterization, if urine is clear it means urinary system is normal. Portal venous system should be assessed.
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    Figs 1.258A to C: Traumatic blunt injury abdomen causing small bowel injury which is sutured using interrupted horizontal silk sutures.
  • Resection or repair should be decided later once haemostasis is maintained. Whether the injury is to the bowel or organs (liver/spleen/kidney, etc.) resection or repair approach is decided depending on the severity of individual organ injury (based on scale or grade).
  • Mesenteric tear may be the cause for haemoperitoneum. Tear may be perpendicular or parallel to the bowel. If it is perpendicular, haemostasis and approximation of the mesentery is sufficient; if it is parallel tear, then blood supply to corresponding bowel may be compromised and resection of that part of the bowel is indicated. Mesenteric haematoma is left alone if small 148and nonprogressive. Whether there is any colour changes in the adjacent bowel should be observed. If haematoma is large; if it is progressive; if it causes compromised blood supply to the adjacent bowel, then it should be gently evacuated. Mesenteric leaf is opened using curved scissor; clot is evacuated using gentle finger dissection; bleeder is identified and ligated. If there is compromised bowel function, it should be resected. Bleeding from the major vein like superior mesenteric vein is disastrous as tear may not be localised but may be extensive; and even gentle dissection may cause more tear. It is carefully mobilised; vascular clamps are applied and repaired using 5 zero polypropylene sutures.
  • Aortic clamping: Catastrophic bleeding found after opening the abdomen which cannot be controlled and bleeding with profound hypotension are the indications for aortic clamping. Profuse intraperitoneal bleed comes under control temporarily by tamponade effect of tense abdominal wall and it itself temporarily helps the patient. The moment abdomen is opened; tamponade effect is released causing further rapid bleed leading into critical catastrophe. If such event is expected prior to opening the abdomen very quick rapid thoracotomy (prelaparotomy thoracotomy) through left 5th intercostal space is done; left lung is deflated and displaced; pleura over the thoracic aorta is incised; aorta is dissected using finger; vascular clamp or soft intestinal occlusion clamp is applied to occlude the thoracic aorta. Later laparotomy is performed to go ahead with management of the bleeding. If profound bleeding is observed after laparotomy necessitating the aortic clamping, it is done by applying the clamp in infradiaphragmatic part of the aorta. Peritoneum is incised on the right of the abdominal oesophagus in infradiaphragmatic area; aorta is dissected using finger high up close to diaphragm to avoid injury to celiac plexus; clamp is applied across (infradiaphragmatic aortic occlusion).
  • Usually drainage using tube drains on either side of the abdomen is used even though it is controversial. ICT should be placed if thoracotomy is also undertaken.
  • Jejunostomy for enteral nutrition is ideal in all major abdominal injuries. Often gastrostomy is also done along with jejunostomy in case of duodenal and pancreatic injuries.
  • Management of individual organs after grading its severity of the injury—duodenum, pancreas, liver, spleen, bowel, kidney, etc. (Please refer individual chapters for detail—highlights of individual organ injury is given below).
  • Management as critical care (ICU with intensivist); multiple blood transfusions; management of sepsis, maintenance of respiration, management of electrolyte changes, treatment of renal failure, provision of nutrition, prevention of DVT, management of DIC are very essential part of postoperative treatment.
 
DUODENAL INJURY
  • Its severity depends on the type and extent of the injury.
  • It can be haematoma or lacerations.
  • Lacerations can cause duodenal disruption, may be < 50% or >50% or 75% or more.
  • Laceration may extend into the ampulla, distal CBD, pancreas or with duodenal devascularisation.
 
Management
  • CT scan is more relevant investigation.
  • Associated other injuries should be managed accordingly.
  • Haematoma without extension is managed conservatively with nasogastric aspiration, antibiotics and IV fluids.
  • Lacerations are sutured surgically with a stenting or often with bypass like gastrojejunostomy.
  • ERCP stenting or CBD bypass is also often required.
Grading of duodenal injury
Grade I
– Haematoma
Involving single portion of the duodenum.
– Laceration
Partial thickness injury without perforation.
Grade II
– Haematoma
Involving more than one portion.
– Laceration
Disruption less than 50% circumference.
Grade III
– Laceration
Disruption of 50–75% of the circumference of 2nd part of the duodenum; disruption 50–100% of the 1st, 3rd or 4th part of the duodenum.
Grade IV
– Laceration
Disruption more than 75% of 2nd part of the duodenum and involving the ampulla or distal common bile duct.
Grade V
– Laceration
Severe disruption of duodenopancreatic complex.
– Vascular
Duodenal devascularisation.
 
PANCREATIC INJURY
  • It can be in the head or body and tail of the pancreas.
  • It may be associated with injury to duodenum or portal or superior mesenteric veins.
  • It can be contusion or severe lacerations.
 
Management
  • High resolution CT scan is diagnostic.
  • Distal pancreatectomy for injuries distally.
  • Conservative treatment is useful with antibiotics, IV fluids.
  • Whipple's operation or total pancreatectomy is done as a last resort.
  • Drainage of the pancreatic bed is simple and often useful method.
 
Complications
  • Pancreatitis, septicaemia.
  • Pancreatic fistula, pancreatic abscess formation.
    Pancreatic injury has got high mortality (>45%).
 
SMALL BOWEL INJURY
  • It can be blunt injury or stab injury.
  • Blunt injury causes disruption of either duodenojejunal region or at ileocaecal region.
  • Presentation is like haemoperitoneum or features of peritonitis.
  • Monks localising zones in the abdomen signify the location of the small bowel injury.
  • Presence of pattern bruising over the abdominal wall signifies the small bowel injury and its site. It is called as London's sign.
 
Management
  • Plain X-ray abdomen shows gas under abdomen with ground-glass appearance.
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    Figs 1.259A and B: Assault causing stab injury abdomen. On opening the abdomen, multiple perforations were found in the small bowel and was sutured. Patient recovered well.
  • Ultrasound abdomen is useful.
  • Laparotomy and closure of the perforation if it is small.
  • In presence of extensive bowel injury or multiple injuries, resection and anastomosis is done.
  • Any associated injuries should be dealt with accordingly.
 
COLONIC INJURY
  • Left sided injury is treated with proximal colostomy with closure of the wound if it is small, or resection and anastomosis if it is wider area. Closure of colostomy is done at later stages after 3–6 months.
  • Small wound over right-sided colon can be sutured primarily.
  • Ileostomy alone or ileostomy with ileo-transverse anastomosis or right hemicolectomy with ileostomy is indicated in following situations:
    • Extensive peritoneal contamination.
    • Colonic vascular injuries.
    • Haemodynamically unstable patients.
    • Long-term hypotension after trauma.
 
LIVER INJURY
It can be subcapsular haematoma, lacerations, deeper injuries, lacerations with disruption of hepatic lobes or segments or liver injury with vascular injuries like of inferior vena cava or hepatic veins.
Present with features of haemorrhagic shock, distension of the abdomen, tenderness, rebound tenderness, guarding, rigidity.
 
Management
  • Small tear is sutured.
    For larger tears:
    • Deep sutures.
    • Packing.
    • Debridement.
    • Haemocoagulants.
  • Liver resection is not done (not advisable) usually for injuries.
  • Pringle manoeuvre—by compressing the porta near foramen Winslow—to control bleeding (not more than 30 minutes).
  • Blood transfusions.
  • Treatment of associated injuries like of diaphragm, lung, duodenum, colon.
  • Antibiotics.
 
Complications of Liver Injury
  • Haemorrhage, septicaemia, bile leak.
  • Liver failure, haemobilia.
  • Subphrenic abscess, CBD stricture.
 
SPLENIC INJURY
It can be subcapsular haematoma, laceration or hilar injury.
It can be associated with other organ injuries like left kidney, left lobe of the liver, splenic flexure of the colon or pancreas.
It can cause torrential haemorrhage and shock.
It is the most common organ injured in blunt injury abdomen.
 
Management
  • Ultrasound abdomen, diagnostic peritoneal lavage are the investigations.
  • Blood transfusions.
  • Splenorrhaphy is done in selected patients so as to save the spleen.
  • Splenectomy.
  • Management of associated injuries.
 
Complications of Splenectomy
  • Left lung atelactasis.
  • Overwhelming postsplenectomy infection (OPSI).
  • Pancreatitis and pancreatic fistula.
  • Gastric bleeding.
  • Subphrenic abscess.
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RENAL INJURY
  • It is commonly managed conservatively.
  • IVU is the investigation of choice in renal injury.
  • Surgery is indicated when there is hilar injury, progressive bleeding, failure of conservative treatment or perinephric abscess formation.
 
URINARY BLADDER INJURY
Intraperitoneal bladder injury occurs in distended bladder. It is treated always by surgical exploration through transabdominal approach. Bladder tear is sutured with keeping a suprapubic cystostomy using Malecot's catheter.
Extraperitoneal injury can be treated conservatively by placing a Foley's catheter for 2–3 weeks.
 
ABDOMINAL COMPARTMENT SYNDROME
Abdominal compartment syndrome (ACS; Richards and krons, 1984) is organ dysfunction caused by increased intra-abdominal pressure more than 12 mmHg (intra-abdominal hypertension/ IAH); organ dysfunction is usually respiratory, cardiovascular and renal but can be any organ; normal intra-abdominal pressure is being considered as 2–7 mmHg.
Abdominal perfusion pressure (APP) is the pressure which maintains adequate abdominal blood flow. It is measured by subtracting the intra-abdominal pressure (IAP) from mean arterial pressure (MAP). APP in ACS is usually less than 60 mmHg but should be maintained as more than 60 mmHg.
 
Effects
  • Cardiovascular system: It is often sudden, rapidly progressive, decreasing the venous return (due to IVC compression) to heart and increasing peripheral resistance, with decreased right atrial pressure and decreased cardiac output.
  • Respiratory system: Intrapleural pressure is increased proportionately to the abdominal pressure. Upward displacement of the diaphragm, increased peak inspiratory pressure, hypoxia, hypercapnia, acidosis, respiratory failure, ARDS are other problems. It also causes restrictive lung disease.
  • Renal system: Decreased renal blood flow and glomerular filtration causes oliguria, renal failure.
  • Gastrointestinal system: Mesenteric venous hypertension; bowel wall oedema and ischaemia.
  • Central nervous system: Cerebral oedema and hypoxia, unconsciousness.
 
Causes
  • Major abdominal trauma, postoperative haemorrhages, after damage control surgery with abdominal packings, are the common causes; ruptured aortic aneurysm.
  • Closure of the abdomen under tension; forcible reduction of the massive hernia.
  • Bowel wall oedema, mesenteric congestion, acute ascites; profound hypothermia and coagulopathy.
  • Acute gastric dilatation, paralytic ileus, gastroparesis, colonic pseudo-obstruction.
  • Retroperitoneal haemorrhages, pancreatitis.
  • Laparoscopic procedures.
  • Morbid obesity, pregnancy, major burns, continuous ambulatory peritoneal dialysis are precipitating causes.
 
Features and Diagnosis
  • Tensely distended abdomen, progressive oliguria, airway obstruction, occult blood loss.
  • Measurement of urinary bladder pressure: Transducer and manometer methods are available. Bladder acts as a passive reservoir at volume less than 100 ml (now 25 ml saline is used to measure) and it can transmit IAP without imparting any additional pressure from its bladder musculature. Measurement of bladder pressure reflects the IAP pressure. IAP is measured using a urinary catheter in the urinary bladder. Pressure is graded (Burch) as: I—10–15 cm of H2O (will not require decompression); II—16–25 cm of H2O (needs close monitoring); III—26–35 cm H2O (most need decompression); IV—more than 36 cm H2O (all need decompression otherwise will die of cardiac arrest in few hours). Beyond grade III immediate decompression is needed. Initial volume preload is essential otherwise sudden decompression may cause cardiac arrest in asystole due to reduced preload, sudden influx of high potassium, acid and other metabolic by products into the heart. Grade III and IV becomes a surgical emergency.
  • Chest X-ray, ECG monitoring, ICU care, electrolytes, haematocrit and serum creatinine estimation, USG abdomen should be done.
  • Mortality for ACS is 40%.
Intra-abdominal pressure grading
Burch grading in cm of water
World Society of the ACS in mm of Hg (Muckart et al., and Malbrain et al.)
I
10–15 cm of H2O
12–15 mmHg
II
15–25 cm of H2O
16–20
III
25–35 cm of H2O
21–25
IV
>35
≥25
Abdominal compartment syndrome (ACS)
Causes
Multiple trauma and ICU patients—common
Postoperative ileus
Acute abdomen
Acute gastric dilatation
Laparoscopic procedures
Intestinal obstruction
Major burns
Features
Hypoxia, hypercarbia
Decreased urine output – anuric renal failure in severe cases
Tense abdomen—distended
Decreased venous return
Refractory hypoxaemia in severe cases
Bowel ischaemia
Cardiac arrest
Management
Bladder pressure assessment
Ryle's tube aspiration
Hypotension Resuscitation
ICU care
Surgical decompression
151
 
Treatment
  • Abdominal decompression is the only ideal treatment for ACS; technique and timings are decided based on the clinical situation.
  • Temperature and coagulation profile should be made as possible as normal prior to decompression.
  • Silastic sheet created chimneys sutured to fascia around is often used. Pressure free abdominal closure should be the target. Bogota bag, first described by Londoni, chief resident in Bogota, Columbia is cost effective; here irrigation bags are sutured to each other as necessary to get a proper size and is sutured to fascia around using 1 zero nylon suture. Several litres of serosanguineous or ascitic fluid are let out through a plastic stoma bag attached to a closed drainage system. Once patient is haemodynamically stable, definitive closure is performed after 48 hours. Abdominal fascia is closed using nonabsorbable sutures; subcutaneous tissue and skin are closed at a later period. Fluid and electrolyte management, antibiotics, adequate blood or blood product transfusions should be used as needed.
  • Other methods of closure: Towel clips, temporary mesh placement; PTFE mesh repair; vacuum assisted closure are all temporary closure methods. Definitive closure methods – Primary closure of fascia; closure using synthetic mesh if no sepsis in the wound; biological mesh closure; component separation technique; closure using skin graft or flaps.
 
SEAT-BELT INJURIES
  • In an individual with seat-belt, during impact, violent deceleration of human body occurs. Seat-belt impinges heavily on its point of contact with trunk and viscera continue to move forward. It leads into severe contusion of abdominal contents; detachment of bowel from its mesentery due to free forward rapid mobility of the bowel over a relatively fixed mesentery. Solid organ injury occurs only occasionally.
  • Two point anchorages causes' solid organ injuries like of liver/spleen. Lap-belt causes contusion and bowel injury commonly.
  • It is often difficult to identify the injuries due to presence of more obvious other injuries. CT chest and abdomen, diagnostic peritoneal lavage (DPL) are very useful.
  • Petechiae around iliac crest or costal margin are signs wherein one can suspect seat-belt injuries.
  • Distraction fracture of lumbar spine (chance fracture) with hyperaesthesia of T12 and L1 level is often associated. 10% of such fractures are associated with intra-abdominal injuries.
  • Treatment is immediate laparotomy and proceed—bowel suturing/resection/suturing of the organ injuries/splenorrhaphy/splenectomy.
152K. Hand and Foot
CHAPTER OUTLINE
  • ❖ Hand
  • ❖ Hand Infections
  • ❖ Acute Paronychia
  • ❖ Chronic Paronychia
  • ❖ Apical Subungual Infection
  • ❖ Terminal Pulp Space Infection
  • ❖ Infection of Web Spaces
  • ❖ Deep Palmar Space Infection
  • ❖ Space of Parona Infection
  • ❖ Acute Suppurative Tenosynovitis
  • ❖ Compound Palmar Ganglion
  • ❖ Orf
  • ❖ Milker's Nodes/Nodules
  • ❖ Hand Injuries
  • ❖ Dupuytren's Contracture
  • ❖ Volkmann's Ischaemic Contracture
  • ❖ Syndactyly
  • ❖ Mallet Finger
  • ❖ Heberden's Nodes
  • ❖ Spina Ventosa
  • ❖ Foot
  • ❖ Callosity
  • ❖ Corn
  • ❖ Plantar Fasciitis
  • ❖ Ingrowing Toe Nail
  • ❖ Onychographosis
  • ❖ Onychomycosis
  • ❖ Athlete's Foot
  • ❖ Hallux Valgus
 
HAND
 
Surgical Anatomy of the Hand
 
Flexor Retinaculum
  • It extends medially from pisiform and hook of hamate, laterally to scaphoid tubercle and trapezium crest as a strong fibrous band so as to bridge carpus to create a carpal tunnel.
  • Ulnar nerve and vessels, palmar cutaneous branches of median and ulnar nerves, palmaris longus muscle are superficial to the carpal tunnel.
  • Median nerve, tendons of flexor digitorum superficialis, profundus and pollicis longus, radial and ulnar bursa are deep to flexor retinaculum.
 
Palmar Aponeurosis
It is a thickened, modified deep fascia in the palm with its apex pointing proximally (as continuation of palmaris longus) and base distally which in turn gets divided into four parts. They extend over deep transverse ligament into lumbrical tunnel.
 
Blood Supply of the Hand
  • Superficial palmar arch is mainly formed by ulnar artery and completed by superficial palmar branch of radial artery. It gives four digital branches to medial three fingers.
  • Deep palmar arch is formed by radial artery and is completed by deep branch of ulnar artery. It gives three palmar metacarpal arteries which communicate with superficial palmar arch. It also gives communicating, perforating branches to dorsal metacarpal arteries.
 
Muscles of the Hand
  • Thenar muscles: Abductor pollicis brevis, flexor pollicis brevis, opponens pollicis and adductor pollicis.
  • Hypothenar muscles: Palmaris brevis, abductor digiti minimi, flexor digiti minimi and opponens digiti minimi.
  • Lumbricals are four in number—named from lateral to medial.
  • Four palmar interossei.
  • Four dorsal interossei.
 
Nerve Supply
  • Abductor pollicis brevis, flexor pollicis brevis, opponens pollicis and 1st and 2nd lumbricals are supplied by median nerve (5 muscles).
  • Rest of the muscles in hand are supplied by ulnar nerve (15 muscles).
 
Modified Verdan Zone System in the Hand (Tendon Zones)
 
Zone I
From the fingertip up to the attachment of flexor digitorum superficialis (middle of middle phalanx). It contains tendon of flexor digitorum profundus.
 
Zone II
It begins proximal to metacarpophalangeal joint at distal palmar crease and extends up to the attachment of flexor digitorum superficialis at the middle of the middle phalanx. It is called as “No-Man's-Land.” Here flexors are tightly enclosed within a fibro-osseous tunnel. It is the most dangerous zone in hand injuries (critical zone).
 
Zone III
It begins at the distal end of flexor retinaculum (base of the palm) and ends at the transverse crease of the palm. It contains lumbricals attached to flexor digitorum profundus.
 
Zone IV
It begins at the proximal end of the flexor retinaculum and ends at its distal end.
153
 
Zone V
It extends from the proximal end of flexor retinaculum up to distal third of the forearm.
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Fig. 1.260: Anatomy of flexor retinaculum and palmar aponeurosis.
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Fig. 1.261: Modified Verdan zone system in the hand.
 
HAND INFECTIONS
  • Hand is a compact actively functioning unit. It contains neurovascular bundles, muscles, bones and ligaments.
  • Infection may be due to minor injuries or blood borne.
    zoom view
    Fig. 1.262: Infection of finger at middle phalanx level. Note the oedema and position of the finger.
 
General Features of Hand Infection
  • Infection spreads faster in all areas.
  • Causes oedema over the dorsum of hand due to lax skin and more lymphatic network even though infection per se is more over the volar aspect. It looks like frog hand.
  • Restricted movements of fingers and hand. The hand functions like hook, pinch, grip, grasp are lost.
  • Severe pain and tenderness, with fever.
  • Tender palpable axillary lymph nodes are often present.
 
Different Types of Hand Infections
  • Acute paronychia.
  • Chronic paronychia.
  • Terminal pulp space infection (felon).
  • Subungual infection.
  • Web space infection.
  • Mid-palmar space infection.
  • Thenar space infection.
  • Deep palmar abscess.
  • Acute suppurative tenosynovitis.
  • Chronic tenosynovitis of flexor tendon sheath of palm and forearm—compound palmar ganglion.
  • Lymphangitis of the hand.
  • Arthritis of hand joints.
  • Subcuticular abscess
Hand infection can be superficial or deep; it can be localised or spreading.
154
zoom view
Figs 1.263A to F: Different types of hand infections. Note the oedema of hand even on dorsal aspect. Small infective focus can aggravate rapidly and so early proper drainage from deeper plane is important in managing the hand infections. Often it may cause extensive destruction exposing the tendons.
 
Investigations
  • Pus for culture and sensitivity.
  • Blood sugar.
  • Urine sugar and ketone bodies.
  • X-ray of the part.
  • Arterial Doppler of the hand if needed.
 
General Principles of Managing Hand Infections
  • Antibiotic therapy.
  • Position of rest with wrist slightly abducted and extended, thumb and index fingers away (glass-holding position). Position of function is in which thumb and index fingers are pinching firmly with wrist extension.
    155
    zoom view
    Fig. 1.264: Hand positions.
    zoom view
    Figs 1.265A and B: Hand positions in immobilisation and function.
    zoom view
    Fig. 1.266: Hand infection. Infection of ring finger extending into the palm.
  • Elevation of hand reduces the oedema, increases perfusion, promotes healing.
  • Early recognition of localised pus. Once localised, Incision and Drainage is done ideally under general anaesthesia or regional block (not local anaesthesia). Draining incision should not cross the palmar crease. Incision should have adequate length and adequate depth (deep to palmar fascia, otherwise evacuation of pus is inadequate). Care should be taken not to injure neurovascular bundles. Pus should be sent for culture and sensitivity. Slough, if present should be excised thoroughly. Gauze drain is placed. Regular dressings are done with continuation of antibiotics. Communications into other areas of hand should also be drained.
    zoom view
    Fig. 1.267: Infection of little finger with dorsal oedema.
    zoom view
    Fig. 1.268: Hypertrophic scar and keloid in hand and forearm after burn contracture.
  • Bloodless field (using tourniquet) is better to drain pus from hand.
  • Proper measures must be taken after treatment. Initial rest, elevation of hand and later proper physiotherapy and regular exercise of hand and fingers are encouraged to restore normal function.
 
ACUTE PARONYCHIA
  • It is the most common hand infection.
  • It occurs in subcuticular area under the eponychium.
  • Minor injury to finger is the common cause.
  • Suppuration occurs very rapidly.
  • It tracks around the skin margin and spreads under the nail causing hang nail or floating nail.
  • Organisms are Staphylococcus aureus and Streptococcus pyogenes.
  • Quantity of pus is very less around 0.5 ml but it should be drained to relieve sympotoms.
 
Clinical Features
Severe throbbing pain and tenderness (dependent throbbing) with visible pus under the nail root. Nail on touch is very tender (paronychia means “Run around”).
 
Treatment
  • Pus is sent for culture and sensitivity.
  • Antibiotics like cloxacillin, amoxicillin.
    zoom view
    Figs 1.269A and B: Pointing pus in acute paronychia. Quantity of pus is very less usually around 0.5 ml.
    zoom view
    Figs 1.270A and B: Paronychia showing pointing pus in one picture and sloughed area granulating in another picture.
  • Analgesics.
  • The pus is drained by making an incision over the eponychium. Digital block using xylocaine 2% plain (without adrenaline as end artery supply to digits can develop arterospasm) is given as anaesthesia.
  • If there is a floating nail, then the nail is dead and it has to be removed.
  • Recovery is fast.
 
CHRONIC PARONYCHIA
It is commonly due to fungal infection—due to candida infection commonly.
 
Features
  • It is common in females.
  • Nail is diseased with ridges and pigmentation.
  • Itching in the nail bed.
  • Recurrent pain, discharge
  • Secondary bacterial infection may supervene.
  • Investigation: Culture of scrapings for fungus and other causative agents.
  • Treatment
    • Long-term antifungal therapy—local and systemic.
    • Antibiotics for secondary infection.
    • In severe cases removal of nail is required.
 
APICAL SUBUNGUAL INFECTION
  • It is infection of the space between subungual epithelium and the periosteum.
  • 157It occurs after minor trauma or rarely after formation of subungual haematoma.
  • Beneath the free edge of the nail, pus comes to the surface.
  • Excruciating tenderness with small visible pus under the tip (summit) of the nail is the feature.
  • Drainage with ‘V’ incision over the summit is the treatment along with antibiotics.
  • Osteomyelitis is not common.
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Fig. 1.271: Apical subungual infection and pus formation. Note the ‘V’ shaped incision to drain the same.
 
TERMINAL PULP SPACE INFECTION (FELON)
  • It is the second most common hand infection (25%).
  • Index and thumb are commonly affected.
  • Usually by a minor injury like finger prick.
 
Surgical Anatomy
  • Terminal pulp space contains fat and is partitioned by septae which is attached from periosteum of terminal phalanx to skin.
  • Proximally deep fascia is attached to the periosteum distal to the base of terminal phalanx, i.e. distal to the attachment of flexor tendon.
  • So, terminal space is a closed compartment, as the result of which pressure increases when there is infection, compressing terminal artery leading to thrombosis, resulting in osteomyelitis of terminal phalanx.
 
Bacteria
  • Staphylococcus—most common.
  • Streptococcus, Gram-negative organisms.
 
Clinical Features
  • Pain, tenderness, swelling in the terminal phalanx.
  • Fever.
  • Tender axillary lymph nodes.
Often suppuration is severe, forming collar stud abscess which eventually may burst.
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Fig. 1.272: Anatomy of the terminal pulp space.
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Fig. 1.273: Pulp space infection.
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Fig. 1.274: Incision for pulp space drainage.
 
Investigations
  • X-ray of the part is required often to rule out osteomyelitis of terminal phalanx.
  • Pus for culture and sensitivity.
 
Treatment
  • Antibiotics and analgesics.
  • Drainage of terminal pulp space by an oblique deep incision.
  • If there is osteomyelitis of the terminal phalanx, it has to be amputated.
158
 
Complications
  • Osteomyelitis of the terminal phalanx.
  • Pyogenic arthritis of distal interphalangeal joint and tenosynovitis of flexor sheath.
  • Septicaemia—in immunosuppressed individuals.
 
INFECTION OF WEB SPACES
 
Surgical Anatomy
There are three triangular web spaces filled with fat between the dorsal and volar skin. When the space is filled with pus it straddles the deep transverse ligament. Even though pus is volar, it points out dorsally.
Infection of originates from:
  • Abrasion.
  • Infection of proximal volar space of finger.
  • Callosities.
  • Infection of proximal spaces.
  • Trauma.
  • Spread from other palmar spaces and from flexor sheaths through lumbrical canal.
 
Bacteria
  • Staphylococcus.
  • Streptococcus.
  • Gram-negative organisms.
 
Clinical Features
  • Fever.
  • Pain and tenderness.
  • Oedema of dorsum of hand.
  • Maximum tenderness is on the volar aspect.
  • ‘V’ sign—separation of fingers.
  • If untreated, infection may spread into other web spaces and hand spaces.
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Fig. 1.275: Incision for web space drainage.
 
Treatment
  • Elevation of hand.
  • Antibiotics and analgesics.
  • Drainage under regional or general anaesthesia. A horizontal incision is placed on volar skin of the web and deepened to reach the space by dividing fibres of palmar fascia. Pus is drained and sent for culture and sensitivity. If other web spaces are involved they should be drained through a separate incision. Edges of the wound are cut to leave a diamond shaped opening in front. Often counter-incision over dorsal skin of web is needed.
 
DEEP PALMAR SPACE INFECTION
 
Surgical Anatomy
zoom view
Figs 1.276A to C: Anatomy of palmar spaces of the hand and forearm. Midpalmar space is on the medial aspect; thenar space is on the lateral aspect. Space of Parona is on the lower forearm.
159Two deep palmar spaces are present
  • Midpalmar space.
  • Thenar space.
Midpalmar space is bound in front by palmar aponeurosis, behind by medial three metacarpals, laterally by a vertical line from lateral margin of the middle finger. It contains flexor tendons, neurovascular bundles and lumbricals. It is the common site of the infection.
Thenar space is located anterior to lateral two metacarpals. Infection here is usually due to extension from midpalmar space.
 
Midpalmar Space Infection
 
Causes
  • Trauma.
  • Spread from infection of finger spaces and web spaces.
  • Haematogenous spread.
  • Spread from tenosynovitis.
 
Clinical Features
  • Pain and tenderness in the palm.
  • Oedema of dorsum of hand (frog hand).
  • Loss of concavity of palm.
  • Painful movement of metacarpophalangeal joint (but interphalangeal joint movements are normal and painfree).
  • Fever.
  • Palpable tender axillary lymph nodes.
  • Eventually pus may come out of palmar aponeurosis forming collar stud abscess and later sinus formation.
    X-ray of the part is required.
 
Treatment
  • Elevation of the affected limb.
  • Antibiotics and analgesics.
    zoom view
    Fig. 1.277: Incisions to drain midpalmar space infection.
  • Drainage: It is drained under regional/general anaesthesia by placing horizontal/oblique incision parallel to the palmar crease. One should avoid crossing the crease line as much as possible. Palmar aponeurosis is carefully incised vertically to avoid injury of the neurovascular bundles. Alternatively one of the interdigital web spaces is incised horizontally; lumbrical canal (3rd or 4th) is opened to reach the deep palmar space. Pus is drained and sent for culture and sensitivity. Thorough saline irrigation is very essential. Drain is placed through the wound.
 
Thenar Space Infection
  • Thenar space (triangular shape) is located anterior to the lateral two metacarpals and fascia over transverse head of adductor pollicis; behind the short muscles of thumb, flexor tendons of index finger and 1st and 2nd lumbricals. Thenar muscles and flexor pollicis longus are lateral to it; fibrous vertical septum from palmar aponeurosis to 3rd metacarpal bone is medial to it. It is on the outer half of the hollow of the palm. Proximally it extends from flexor retinaculum; distally it extends to transverse palmar crease. It communicates to fascial sheath of 1st lumbrical. It is often associated with midpalmar space infection.
  • It is drained similarly by placing incision on the lateral aspect of the palm or through the first web space incision is done along the first lumbrical canal on the radial side of the index finger. Often incision is made parallel to cleft between index and thumb on the posterior aspect.
  • In some patients, thenar space infection may spread distally to the first web and then dorsally over the first dorsal interosseous muscle, referred to as a pantaloon abscess. In such situation an additional counter incision over the dorsal aspect of the hand is needed while draining.
zoom view
Fig. 1.278: Incision and drainage of thenar space abscess.
160
 
SPACE OF PARONA INFECTION
Forearm space of Parona is a rectangular space situated in the lower part of the forearm above the wrist, in front of pronator quadrates and deep to long flexor tendons. Above it extends up to oblique origin of flexor digitorum superficialis, below up to flexor retinaculum communicating with midpalmar space. Flexor tendon sheath proximally extends into this space. Pus in this space is drained through lateral incisions in the lower part of the forearm.
 
ACUTE SUPPURATIVE TENOSYNOVITIS
It is the bacterial infection of flexor tendon sheaths.
 
Surgical Anatomy
  • Radial bursa is synovial sheath of flexor tendon of thumb which extends to the digit.
  • Ulnar bursa is synovial sheaths of medial four flexor tendons of hand which extends into the digit of the fifth (little) finger.
    zoom view
    Fig. 1.279: Bursae hand.
  • Extensor tendons are devoid of sheaths.
  • Radial and ulnar bursa communicate with each other in 80% of cases.
Common bacteria:
  • Staphylococcus aureus, Streptococcus pyogenes.
 
Clinical Features
  • Symmetrical swelling of entire finger.
  • Flexion of finger—Hook sign.
  • Severe pain on extension.
  • Tenderness over the sheath.
  • Oedema of whole hand, both palm and dorsum (due to lymphatic spread).
  • As ulnar bursa extends into the little finger its infection results in pain and tenderness extending up to little finger but not much to other fingers.
  • In infection of radial bursa thumb is swollen with pain and tenderness over the sheath of the flexor pollicis longus and there is inextensibility of interphalangeal joint.
  • Swelling just above the flexor retinaculum is common.
 
Treatment
zoom view
Figs 1.280A and B: Suppurative tenosynovitis is drained through incision at proximal part and another at digital sheath. Often by placing fine polythene catheter into the sheath, saline wash is given into the area.
  • 161Elevation of the affected limb.
  • Antibiotics and analgesics.
  • Position of rest.
  • Drainage under general anaesthesia. Incisions are placed over the site of maximum tenderness and flexor sheath should be opened up. Many a times multiple incisions are required.
It is drained through two incisions—one over the proximal part of the sheath; other over the distal part of the sheath in the digit—along the crease lines. A fine catheter is passed into the sheath from proximal incision and irrigated with normal saline through this catheter. This catheter is left in situ for further regular irrigations, splinting of hand is necessary with boxing glove dressing.
 
COMPOUND PALMAR GANGLION
  • It is chronic tenosynovitis of flexor tendon sheaths due to tuberculosis (tuberculous tenosynovitis) or rheumatoid arthritis.
  • It can be unilateral or bilateral.
 
Pathology
  • Flexor tendon sheath on either side of the wrist is involved, i.e. both in the volar surface of palm and lower forearm.
  • Swelling contains fluid with typical melon seed bodies.
  • Condition is often bilateral in case of rheumatoid arthritis.
 
Features
  • Swelling in the palm and lower forearm which is smooth, soft, nontender, fluctuant and also cross-fluctuant across flexor retinaculum, nontransilluminating.
  • Wasting of hand and forearm muscles are seen.
  • Matted axillary lymph nodes may be palpable.
  • Primary focus may be present in lungs.
  • Investigations:
    • ESR, chest X-ray.
    • FNAC of axillary lymph node and swelling itself.
 
Treatment
  • Start antituberculous drugs: INH, rifampicin, ethambutol and pyrazinamide for 9 months.
  • Excision of flexor tendon sheath is done along with scraping of caseating material, tubercles, melon seed bodies.
  • Care should be taken not to injure median and ulnar nerves.
 
ORF
  • It is a rare, benign, self-limiting exanthematous disease, also known as contagious pustular dermatitis or infectious labial dermatitis or ecthyma contagiosum or thistle disease or scabby mouth caused by a parapox virus infection. Contracted via direct contact with infected sheep or goats or fomites with orf virus. Human-to-human transmission is not known.
  • It causes a purulent-appearing papule locally and generally without systemic symptoms.
  • Infected locations can include the finger, hand, arm, face and even the penis.
  • It may become progressive and life threatening in immunocompromised host.
  • Treatment—1% cidofovir in progressive disease.
 
MILKER'S NODES/NODULES (Milkmaid Blisters)
  • It is cutaneous condition caused by Paravaccinia virus; transmitted from udders of infected cows.
  • Disease in humans is nearly identical to Orf.
  • Usually has got self-limiting course, running from 14–72 days, with infrequent systemic symptoms and little or no scarring.
 
HAND INJURIES
 
Classification
  • Tidy injuries: They are clean incised wounds and are usually treated by primary suturing but depends on the tissues involved like nerves, tendons and muscles.
  • Untidy injuries: They are lacerated wounds. Treated by debridement and later by delayed primary or secondary suturing.
  • Compartment injuries.
  • Degloving injuries
  • Indetermined injuries which could not be assessed.
 
Assessment of Injury
It should include: Number, extent, depth, deformity and disability, neurovascular injuries, tendon injuries, muscle injuries bone and joint injuries.
zoom view
Figs 1.281A and B: Indeterminate and untidy hand injuries.
162
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Fig. 1.282: Hand injury exposing tendons. Note the marker stitch in the tendon. It needs local transposition flap or groin flap to cover. Skin grafting is not possible over tendons.
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Fig. 1.283: Stuck finger by a ring. It is removed by applying soap, fat, and wax. String method is winding and unwinding a thread under and across the stuck finger. Sawing is done only when every method fails.
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Fig. 1.284: Avulsion injury of finger causing raw area.
 
Principles of Treatment
  • Haemostasis.
  • Use of tourniquet.
  • Wound debridement and cleaning.
    zoom view
    Fig. 1.285: Hand injury which is healing but with severe deformity of fingers.
    zoom view
    Fig. 1.286: Typical deformity of finger which needs correction for proper function.
  • Antibiotics and antitetanus treatment (toxoid and antitetanus globulin).
  • Primary suturing if it is a incised wound or delayed primary suturing if there is odema.
  • Skin grafting or flaps for skin loss.
  • Tendon suturing or tendon graft for tendon injuries.
  • Rest and elevation of the affected parts.
  • Management of fractures by splint, wiring.
  • Nerve repair for nerve injuries.
  • Immobilisation up to 21 days.
  • Later physiotherapy with warm, exercise, was bath active movements.
  • Microsurgical restoration of digits. Reimplantation of the digits.
  • Amputation of digits or metacarpals only when inevitable.
Primary repair of tendons and nerves are of lesser priority in untidy injuries. Priority is wound debridement/wound excision and early skin cover. Cut ends of nerves and tendons are tagged with coloured stitches for future identification purpose.
In hand
Do's
Don'ts
Do examine hand carefully
Do not incise every infected digit
Do think of other diagnosis
Do not make puncture incisions or over pads
Do wait for abscess to localise
Do not injure the digital nerves or vessels
Do place adequate length and depth of incisions
Do not place incisions crossing the crease line
Do immobilise, elevate the hand
Do not close human bites or lacerated wounds
Do give antibiotics and proper dressings
Do not forget to send pus for culture and sensitivity
163
 
DUPUYTREN'S CONTRACTURE
It refers to localised thickening of palmar aponeurosis and later formation of nodules with severe permanent changes in metacarpophalangeal and proximal interphalangeal joints. Terminal interphalangeal joint is not involved as palmar aponeurosis does not extend to terminal phalanx. It is common in males (10:1).
  • It starts in ring and little fingers, with flexion of ring and little fingers. Later involving all fingers.
  • There is thickening and nodule formation in the palm with adherent skin.
  • It is often familial and bilateral 45%.
  • Pads (of fat) develop in knuckles and are called as Garrod's pads (in proximal IP joints).
 
Aetiology
  • Repeated minor trauma, use of vibrating tools.
  • Cirrhosis, alcoholism, smoking,
  • Epileptics on treatment with phenytoin sodium.
  • Diabetics, pulmonary tuberculosis, AIDS.
  • Other metabolic conditions.
  • Familial—autosomal dominant.
zoom view
Figs 1.287A and B: Dupuytren's contracture in the hands. Note the involvement of the ring finger. Note the fibrous band on the other hand as early finding.
 
Complications
  • Restriction of hand function and so disability.
  • Arthritis of MCP and proximal IP joints.
164
 
Treatment
  • Fasciotomy of palmar aponeurosis and later physiotherapy, Z plasty.
  • In severe cases fasciectomy partial or complete.
  • Treatment of the cause.
Recurrence can occur in 5–50% cases.
zoom view
Fig. 1.288: Z plasty done for Dupuytren‘s contracture.
 
VOLKMANN'S ISCHAEMIC CONTRACTURE
It is a vascular injury leading to muscular infarction and subsequent contracture.
 
Causes
  • Supracondylar fracture of the humerus.
  • IV chemotherapy.
  • Burns.
  • Closed forearm crush injuries.
  • Tight plaster after reduction of fracture.
 
Pathogenesis
zoom view
 
Clinical Features
Acute phase:
  • Pain (persistent pain in forearm, hand, fingers—ominous symptom).
  • Pallor.
  • Puffiness (due to oedema).
  • Pulseless (absence of radial pulse; but its presence does not rule out the onset of impending contracture).
  • Paresis.
Late phase: Deformity
Deformity (due to injury to median nerve):
  • Wrist joint extended.
  • Extended metacarpophalangeal joints.
  • Flexed interphalangeal joints.
Volkmann's sign:
In early stage, the fingers can be extended at the interphalangeal joints, only when the wrist is flexed fully. The fingers tend to flex if any attempt to extend the wrist is made.
 
Treatment
In acute phase:
  • Removal of plastic cast applied after fracture reduction.
  • Correction of fracture.
  • Exposure of brachial artery and application of 2.5% papaverine sulphate to relieve the spasm if any.
  • Suture of arterial tear if present, often with placement of arterial graft.
  • Lateral incision over the deep fascia of forearm is placed to decompress the oedema.
In late phase (once deformity occurs):
  • Physiotherapy
  • Dynamic splints.
  • Max-Page operation: Release of flexor muscles (forearm muscles) from their origins from the bone and allowing it slide down until full extension.
  • Excision of fibrous tissue and damaged muscles along with tendon transfer.
  • Arthrodesis.
 
SYNDACTYLY
It is webbing or fusion of fingers.
 
Causes
  • Congenital and hereditary—common.
  • Traumatic like burns.
 
Types
  • Cutaneous—simple.
  • Fibrous.
  • Bony—complex.
  • It can be unilateral or bilateral.
  • Often all four limbs may be involved with webbing of toes.
  • It may be associated with polydactyly or visceral anomalies.
  • If bony type is suspected, X-ray of the part should be taken.
 
Treatment
  • If cutaneous, release of web is done as a staged procedure along with “Z” plasty or skin grafting.
  • If fibrous, release can be done.
  • If bony type, release is difficult because blood supply may be compromised which leads to gangrene of the digit.
165
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Fig. 1.289: Syndactyly.
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Fig. 1.290: Syndactyly and polydactyly of both hands and both feet.
 
MALLET FINGER (Base ball finger)
The terminal phalanx can not be extended because of tear at insertion of extensor tendon or avulsion fracture of the base of the terminal phalanx.
 
HEBERDEN'S NODES
These are seen in osteoarthritis, occurring behind the distal interphalangeal joints of index, middle, little and ring fingers.
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Fig. 1.291: Arthritis of joints of hands.
 
SPINA VENTOSA
Refers to phalangeal tuberculosis (Tuberculous dactylitis). It is called as spina ventosa because of its appearance as “air- filled balloon”.
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Fig. 1.292: Spina ventosa.
 
FOOT
Foot contains 7 tarsal bones, 5 metatarsals, 14 phalanges (total 26 bones). Two sesamoid bones of 1st metatarsal bone are common. There are 4 layers of muscles in foot. Ligaments, muscles, joints, maintain the stability of foot complex. Blood supply is by anterior tibial, posterior tibial and peroneal arteries. Nerve supply is by saphenous, sural, posterior tibial, superficial and deep peroneal nerves.
 
CALLOSITY
  • It is a hard, thickened skin occurs as a protective measure seen in wider area usually over heel and heads of metatarsals.
    zoom view
    Fig. 1.293: Callosity in the foot.
  • A callosity protrudes outwards from the skin.
  • It is greyish-brown, raised, protruded outwards, thickened, hypertrophic skin occurs due to occupation and skeletal structure. It is painless. It is wider lesion. Paring the top layer exposes the shiny translucent dead skin beneath.
  • It is grayish brown hypertrophic raised thick protective phenomenon which occurs commonly in areas of wear and tear like hands and feet. Top roughened layer when peeled off, shiny, translucent, homogenous dead skin can be exposed beneath.
  • It is painless; it can get rubbed easily to create a sore.
  • As it is a protective phenomenon it is best left alone.
166
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Fig. 1.294: Diagram showing differences between corn and callosity.
 
CORN
 
Types
  • Hard corn.
  • Soft corn.
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Fig. 1.295: Corn in the plantar aspect of the foot.
 
Hard Corn
  • It is localised area of thickening over a bony projections like heads of metatarsals.
  • Histologically it differs from callosity by having severe keratoses with a central core of degenerated cells and cholesterol.
  • It presses over the adjacent nerves causing pain. It can get infected causing severe pain and tenderness with inability to walk.
  • It is smaller lesion which is pushed deep into the skin forming a localised palpable painful/tender nodule with a central yellow-white core of dead cornified skin.
  • Corn is common if there is deformity or by wearing tight fitting shoes/foot wears.
  • Corn is narrow, deep and painful/tender.
  • It is common in females.
  • Corn is usually white/gray/yellow coloured, deep seated lesion.
  • Infection, abscess formation and ulceration can occur especially if patient is diabetic.
  • Corn may be associated with bursae causing bursitis.
  • Corn often recurs after excision.
 
Treatment
  • Excision.
  • Local application of salicylic acid preparations or mixture of salicylic acid/lactic acid/collodion may be helpful. Skin softening agents are also tried.
  • Eliminating the pressure is very important to prevent recurrence.
  • Avoid excision of corn unnecessarily in diabetic (especially with neuropathy) and in ischaemic foot.
 
Soft Corn
It usually occurs between 4th and 5th toes due to friction of bases of adjacent proximal phalanges.
 
PLANTAR FASCIITIS (Policeman's Heel)
  • It occurs due to friction or tear of the ossified posterior insertion of the plantar fascia which is common in people who stand or walk for long-time.
  • Treatment: Analgesics, rest, steroid injections to the site.
 
INGROWING TOE NAIL (Onychocryptosis)
  • It is also called as embedded toe nail.
  • It is due to curling of the side of nail inwards, causing it to form a lateral spike resulting in repeated irritation and infection of overhanging tissues in the nail fold.
 
Causes
  • Tight shoes.
  • Improper cutting of nails (very short and convex).
 
Clinical Features
  • It is common in great toe and is often bilateral.
  • Both medial and lateral sides of the toe can be involved.
  • Recurrent attacks of acute and subacute paronychia occurs.
  • Pain, tenderness, swelling of margins of the toe, often along with granulation tissue and foul smelling discharge.
 
Treatment
  • Regular dressing and packing.
  • Antibiotics. Discharge is sent for culture and sensitivity.
  • Nails should be cut concavely or straight without leaving lateral spikes towards soft tissues.
  • Zadik's or Fowler's operation: Skin in lateral margin and root is incised so as to expose the lateral spike and germinal matrix. Infected tissues with pus and germinal matrix of ingrown part of the nail is excised or often entire nail with its root and germinal matrix is excised.
167
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Fig. 1.296: Zadik‘s or Fowler‘s operation.
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Figs 1.297A and B: Ingrowing toe nail. Note the granuloma caused by repeated infection and inflammation.
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Fig. 1.298: Incision for nail excision. Note the germinal matrix. Removal of nail, entire or partial with adjacent germinal matrix is called as radical nail excision.
 
ONYCHOGRYPHOSIS
  • It is curving of nail upwards (Ram's Horn Nail).
  • It occurs due to repeated trauma or fungal infection.
 
ONYCHOMYCOSIS
It is fungal infection of the nail.
 
ATHLETE'S FOOT
  • It is the fungal infection of the skin between the toes— Tinea pedis.
  • Fungi enter through cracks; survive due to moisture in between toes.
  • Skin is swollen, red, with sticky fluid, macerated with blisters.
  • Itching, deep cracks, pain and discharge are common.
 
Treatment
  • Part should be kept dry. Cotton, clean socks should be worn.
  • Oral antifungals, antihistaminics and topical antifungals are used.
  • Condition is contagious.
 
HALLUX VALGUS
  • Here great toe is deviated laterally at first metatarsophalangeal joint. There is outward deviation of great toe with medial deviation of first metatarsal head.
  • It may be due to persistent lateral force or occasionally hereditary.
  • Condition is often bilateral.
  • It is common in females.
  • Thick walled bursa (bunion) over medial aspect of the head of the first metatarsal bone is common.
  • Undue prominence of head of first metatarsal bone is typical often forming an exostosis at this point. Osteoarthritis of 1st metatarsophalangeal joint can occur.
  • Lateral deviation of proximal phalanx over 2nd toe causing crowding of the toes.
  • Initially it is painless; but eventually pain and tenderness develops with infection of bunion and splaying of forefoot.
  • X-ray shows deviation with often osteoarthritis of the metatarsophalangeal joint.
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Fig. 1.299: Hallux valgus deformity.
168
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Fig. 1.300: Hallux varus deformity. It is opposite of hallux valgus deformity.
 
Treatment
Keller's operation: Proximal 1/3rd of the proximal phalanx of great toe and medial part of head of 1st metatarsal bone is excised through medial curved incision. Soft tissue interposition is done.
Mayo's procedure: Medial part of base of the proximal phalanx of great toe and head of 1st metatarsal bone is excised—opposite of Keller's.
Simmond's procedure: Varus osteotomy at the base of 1st metatarsal bone with reinsertion of adductor hallucis tendon is done.
McBride procedure: Transfer of adductor hallucis tendon and lateral head of flexor hallucis brevis from proximal phalanx of great toe to the lateral part of head of 1st metatarsal bone.
Arthrodesis of metatarsophalangeal joint is done to relieve pain.
Excision of bunion, deformity correction, osteotomy, muscle transfers are also done as a combined approach.
169L. Arterial Diseases
CHAPTER OUTLINE
  • ❖ Surgical Anatomy of Thoracic Outlet
  • ❖ Arteries of Upper Limb
  • ❖ Arteries of Lower Limb
  • ❖ Arterial Diseases
  • ❖ Intermittent Claudication
  • ❖ Rest Pain
  • ❖ Limb Ischaemia
  • ❖ Pregangrene
  • ❖ Gangrene
  • ❖ Different Levels of Arterial Obstruction
  • ❖ Other Features of Poor Circulation
  • ❖ Investigations for Arterial Diseases
  • ❖ Diseases of the Arteries
  • ❖ Atherosclerosis
  • ❖ Thromboangiitis Obliterans
  • ❖ Takayasu's Pulseless Arteritis
  • ❖ Raynaud's Phenomenon
  • ❖ Temporal Arteritis
  • ❖ Treatment of Arterial Diseases
  • ❖ Subclavian Steal Syndrome
  • ❖ Acute Arterial Occlusion
  • ❖ Traumatic Acute Arterial Occlusion
  • ❖ Embolism
  • ❖ Reperfusion Injury
  • ❖ Saddle Embolus
  • ❖ Embolectomy
  • ❖ Air/Gas Embolism
  • ❖ Therapeutic Embolisation
  • ❖ Caisson's Disease or Decompression Disease
  • ❖ Aneurysm
  • ❖ Mycotic Aneurysm
  • ❖ Abdominal Aneurysm
  • ❖ Abdominal Aortic Aneurysm
  • ❖ Peripheral Aneurysm
  • ❖ Carotid Artery Aneurysm
  • ❖ Dissecting Aneurysm
  • ❖ Erythromelalgia/Erythralgia
  • ❖ Livedo Reticularis
  • ❖ Polyarteritis Nodosa
  • ❖ Scleroderma/Systemic Sclerosis
  • ❖ Acrocyanosis
  • ❖ Gangrene
  • ❖ Diabetic Foot and Diabetic Gangrene
  • ❖ Trophic Ulcer
  • ❖ Bedsores
  • ❖ Frostbite
  • ❖ Ainhum
  • ❖ Endovascular Surgeries
  • ❖ Upper Limb Ischaemia
  • ❖ Arterial Substitutes
 
SURGICAL ANATOMY OF THORACIC OUTLET
Thoracic outlet is bounded by manubrium sternum in front, spine posteriorly, and the first rib laterally. At the superior aperture of thorax subclavian vessels, brachial plexus traverse the cervicoaxillary canal to reach the upper limb.
Cervicoaxillary canal is divided into proximal Costoclavicular space and distal axilla (divided by first rib).
Costoclavicular space is bounded superiorly by clavicle, inferiorly by first rib, anteromedially by the costoclavicular ligament, and posterolaterally by scalenus medius muscle along with long thoracic nerve.
Scalenus anticus muscle divides the costoclavicular space into two compartments, the anterior one containing subclavian vein and the posterior one containing subclavian artery and brachial plexus.
This posterior compartment is called as Scalene triangle bounded by scalenus anticus anteriorly, scalenus medius posteriorly, and the first rib inferiorly.
Cervical rib narrows this triangle and causes compressive features of the C8, T1 nerve roots and subclavian artery. Anything that narrows costoclavicular space causes Thoracic outlet syndrome.
 
ARTERIES OF UPPER LIMB
Right subclavian artery begins from brachiocephalic trunk (innominate artery) whereas left subclavian artery arises directly from the arch of aorta. From underneath the sternoclavicular joint artery arches over the pleura and apex of lung about 2.5 cm above the clavicle and then reaches the lateral border of first rib to continue as axillary artery.
Subclavian artery is divided into three parts by scalenus anterior muscle.
Axillary artery is divided into three parts by pectoralis minor muscle.
At the lower border of teres major muscle it enters the arm and continues as brachial artery.
About 2.5 cm below the crease of the elbow joint, it bifurcates into radial and ulnar arteries which run in the forearm.
Ulnar artery forms the superficial palmar arch which is completed by superficial palmar branch of radial artery.
Radial artery after passing through the anatomical snuff box enters the dorsum of hand and first intermetacarpal space to form deep palmar arch. It is completed by deep palmar branch of ulnar artery and is 1 cm proximal to superficial palmar arch.
 
ARTERIES OF LOWER LIMB
Abdominal aorta bifurcates at the level of fourth lumbar vertebra (corresponds to the level of the umbilicus in anterior abdominal wall) into two common iliac arteries.
Common iliac artery is about 5 cm in length passes downward and laterally; and at the level of lumbosacral intervertebral disc, anterior to sacroiliac joint, it divides into external and internal iliac arteries. Internal iliac artery supplies pelvic organs.
170External iliac artery continues as common femoral artery at the level of inguinal ligament.
About 5 cm below the inguinal ligament common femoral divides into superficial femoral and deep femoral (Profunda femoris) arteries.
Deep femoral provides collateral circulation around the knee joint and also communicates above with gluteal vessels to maintain collateral circulation around the gluteal region.
Superficial femoral artery at the hiatus in the adductor magnus, continues as popliteal artery up to the inferior angle of the popliteal fossa where it divides into anterior and posterior tibial arteries.
Anterior tibial artery supplies anterior compartment of leg and ankle, continues as dorsalis pedis artery which forms dorsal arterial arch of the foot.
Posterior tibial artery supplies posterior compartment of leg and ends as medial and lateral plantar arteries which forms plantar arterial arch of the foot.
Posterior tibial artery gives peroneal artery which runs close to fibula supplying calf muscles.
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Figs 1.301A and B: CT angiogram of aortoiliac segment showing aortoiliac block due to atherosclerosis. Collaterals are also well-developed.
 
ARTERIAL DISEASES
  • Stenosis due to trauma, atherosclerosis, emboli. It may be:
    • In the brain causing transient ischaemic attacks.
    • In the limbs causing claudication and rest pain.
    • In the abdomen causing pain, bloody stool.
    • In the kidney causing haematuria.
  • Dilatations are aneurysms.
  • Arteritis.
  • Small vessel abnormalities.
 
INTERMITTENT CLAUDICATION
Claudio means “I limp” a Latin word. It is a crampy pain in the muscle seen in the limbs. Due to arterial occlusion, metabolites like lactic acid and substance P accumulate in the muscle and cause pain.
The site of pain depends on site of arterial occlusion.
  • The most common site is calf muscles.
  • Pain in foot is due to block in lower tibial and plantar vessels.
  • Pain in the calf is due to block in femoropopliteal segment.
  • Pain in the thigh is due to block in the superficial femoral artery.
  • Pain in the buttock is due to block in the common iliac or aortoiliac segment, often associated with impotence and is called as Leriche's syndrome.
Pain commonly develops when the muscles are exercising. Cause for pain is accumulation of substance P and metabolites. During exercise increased perfusion and increased opening of collaterals wash the metabolites.
Note:
• Beta blockers may aggravate claudication.
• Claudication is not that common in upper limb but can occur during writing or any upper limb exercise.
 
REST PAIN
  • It is continuous aching in calf or feet and toes or in the region even at rest depending on site of obstruction.
  • It is ‘cry of dying nerves’ due to ischaemia of the somatic nerves. It signifies severe decompensated ischaemia. Pain gets aggravated by elevation and is relieved in dependent position of the limb.
  • Pain is more in the distal part like toes and feet. It gets aggravated with movements and pressure.
  • Hyperaesthesia is common association with rest pain.
  • Rest pain is increased in lying down and elevation of foot; it may be reduced on hanging the foot down.
  • Rest pain is worst at night and so patient is sleepless at night.
  • Rest pain is apparently reduced by holding the foot with hand, probably due to suppression of transmission of pain sensation.
171
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Fig. 1.302: Rest pain in a patient suffering from TAO. Holding the foot reduces the pain slightly.
 
LIMB ISCHAEMIA
 
Causes
  • Atherosclerosis.
  • Embolism (acute).
  • Arteriopathies—Buerger's disease, Raynaud's disease, Takayasu's disease.
  • Diabetes.
  • Scleroderma.
  • Physical agents—trauma, tourniquet, radiation injury.
 
Classification of Limb Ischaemia
Rutherford classification
Grade
Clinical feature
0
Asymptomatic
1
Mild claudication
2
Moderate claudication
3
Severe claudication
4
Ischaemic rest pain
5
Minor tissue loss
6
Major tissue loss
 
Limb ischaemia is also classified as:
  • Functional ischaemia.
  • Critical ischaemia.
 
Functional Limb Ischaemia
Here flow of blood is normal when limbs are at rest; but will not be increased during exercise. It presents as claudication. It is defined as, “Muscle discomfort in the limb reproducibly produced by exercise and relieved by rest within 10 minutes.”
 
Critical Limb Ischaemia
It is persistently recurring ischaemic rest pain for 2 weeks, which requires regular analgesics for > 2 weeks or ulceration or gangrene of the foot or toes with an ankle systolic pressure < 50 mmHg or toe systolic pressure < 30 mmHg. Ankle brachial pressure index (ABPI) will be less than 0.3.
One should check blood pressure in all 4 limbs. ABPI is checked in supine position; systolic blood pressure in upper and lower extremities (two upper and two lower) is checked and higher value of each extremities is taken; ABPI is calculated.
Results—>0.90 is normal; 0.70–0.89 is mild disease; 0.50–0.69 is moderate; <0.50 is severe.
Note:
Calcification can alter the ABPI.
 
PREGANGRENE
It is the changes in tissue which indicates that blood supply is inadequate to keep the tissues alive and presents with rest pain, colour changes, oedema, hyperaesthesia with or without ischaemic ulceration.
 
GANGRENE
It is macroscopic death of tissue in situ with putrefaction.
 
Dry Gangrene
It is dry, desiccated, mummified tissue caused by gradual slowing of bloodstream. There is a line of demarcation and is localised.
 
Wet Gangrene
It is due to both arterial and venous block along with superadded infection and putrefaction. It spreads proximally and there is no line of demarcation. It spreads faster.
172
Organs in which gangrene can develop—appendix, bowel, gallbladder, testis, pancreas.
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Fig. 1.303: Gangrene of great and little toes in a patient with vascular compromise.
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Fig. 1.304: Ischaemic ulcer foot in a diabetic patient.
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Figs 1.305A and B: Gangrene of all toes at their distal phalanges. All ischaemic features are obvious.
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Fig. 1.306: Ischaemic changes in the right leg. Third and fourth toes are gangrenous with line of demarcation. Great and little toes are partly gangrenous. There are ischaemic features in the right foot and leg like hair loss/skin changes/wasting.
 
Line of Demarcation
  • It is a line between viable and dying tissue indicated by a band of hyperaemia. It also indicates that disease is getting localised.
  • Final separation between healthy and gangrenous tissue occurs by development of a layer of granulation tissue in between.
  • It is hyperaesthetic due to exposed nerve endings.
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Fig. 1.307: Clear line of demarcation in gangrenous 4th toe.
 
Types of Separation
  • Separation by aseptic ulceration is seen in dry gangrene.
  • Separation by septic ulceration is seen in infected condition and wet gangrene.
 
DIFFERENT LEVELS OF ARTERIAL OBSTRUCTION
  • Aortoiliac block causes claudication in both buttocks, thighs, and calves; absence of femoral and distal pulses bruit over aortoiliac region. Impotence occurs due to defective perfusion through internal iliac arteries and so into the penis causing erectile dysfunction (Leriche's syndrome).
  • 173Iliac artery obstruction causes claudication in thigh and calf; bruit over iliacs with absence of femoral and distal pulses.
  • Femoropopliteal obstruction causes claudication in calf with absence of distal pulses but with palpable femoral.
  • Distal obstruction shows absence of ankle pulses with palpable femoral and popliteal pulses.
    • Paraesthesia over the skin of the foot is due to shunting of blood from the skin to muscles in deeper plane.
    • Sensation in gangrenous area is absent. But, at the line of demarcation, skin is hyperaesthetic.
 
OTHER FEATURES OF POOR CIRCULATION
  • The affected part is cold with numbness, paraesthesia and colour changes. Observing for colour change is important as, if it is not present one may have to think that numbness could be of neurological origin. On elevation the part blanches, on dependency part becomes purple. Temperature sensation on the ischaemic limb is lost apart from its coldness.
  • Ulceration, gangrene, decreased sensation and movements are the features to be checked.
  • Delayed capillary filling: Blanched nails or pulp of fingers, on pressure, will show delay in refilling (to turn pink) after release of pressure.
  • Delayed venous refilling: Two fingers are placed over the vein. Finger nearest to heart is moved away so as to empty the vein. Distal finger is released to observe the venous refilling. Delay in filling is called Harvey's sign, signifies ischaemia. Venous filling is increased in AV fistulas.
  • Crossed leg test (Fuchsig's test): Patient is asked to sit with the legs crossed one over the other so that the popliteal fossa of one leg will lie against the knee of other leg. Oscillatory movements of foot can be observed synchronous with the popliteal artery pulsation. This movement is absent with blockage of popliteal artery.
  • Disappearing pulse syndrome: Exercise the limb after feeling the pulse. Pulse disappears once patient develops claudication. It is due to vasodilatation and increased vascular space occurring as the result of exercise wherein arterial tension cannot be kept adequately and so pulse will disappear (unmasking the arterial obstruction).
  • Buerger's postural test: Patient lying down on his back is asked to raise the leg above. In normal individuals, limb (plantar aspect of foot) remains pink even after raising above 90°. Ischaemic limb, when elevated shows marked pallor and empty veins. The angle in which pallor develops is called as Buerger's angle of vascular insufficiency. If this angle is < 30°, it indicates severe ischaemia.
  • Systolic bruit may be heard over stenosed artery like subclavian artery, femoral artery, carotid artery, iliacs, renal artery.
  • Adson's test (Scalene manoeuvre): In a patient sitting on a stool, the radial pulse is felt. The patient is then asked to take a deep breath (to allow the rib cage to move upwards so as to narrow the cervicoaxillary channel) and turn the face to same side (to contract scalenus anterior muscle so as to narrow the scalene triangle). If the radial pulse disappears or become feeble it signifies cervical rib or scalenus anticus syndrome.
  • Elevated arm stress test (EAST), or modified Roos test: With both the arms kept in 90° abduction and external rotation position, patient is asked to make a fist and release repeatedly for 5 minutes. In normal side, patient will continue to do the manoeuvre whereas in diseased (Thoracic outlet syndrome) side patient gets pain and paraesthesia with difficulty in continuing the manoeuvre. Patient drops the arm down to relieve the symptoms.
  • Costoclavicular compression manoeuvre (Falconer test): Radial pulse becomes absent when patient draws his shoulders backwards and downwards in excessive military position. This is because at this position, subclavian artery is compressed between first rib and clavicle, leading to feeble or absent radial pulse. Halstead manoeuvre another similar test.
  • Hyperabduction manoeuvre (Wright test): When affected arm is hyperabducted, radial pulse becomes absent or feeble due to compression of artery by pectoralis minor tendon.
  • Allen's test: It is done to find out the patency of radial and ulnar arteries. Both the arteries are compressed near the wrist and allowed to blanch completely in one minute (In the mean time patient closes and opens the fist several times for further venous outflow). Palm appears pale and white. One of the arteries is released and colour of hand is noted. Normally hand will become pink and flushed in no time; whereas in obstruction, the area will still remain pale. Other artery is also released and looked for changes in hand. Often test has to be repeated to get proper information.
  • Abdomen should be examined for the presence of abdominal aortic aneurysms. It presents as pulsatile mass above the umbilicus, vertically placed, smooth, soft, nonmobile, not moving with respiration, resonant on percussion. Expansile pulsation is confirmed by placing the patient in knee-elbow position.
  • Auscultation for arterial bruit over femoral artery, abdominal aorta, subclavian and carotid arteries is done.
 
Palpation of Blood Vessels
  • Dorsalis pedis artery is felt just lateral to the extensor hallucis longus tendon at the proximal end of first web space, felt against the navicular and middle cuneiform bones. It is absent in 10% cases.
  • Posterior tibial artery is felt against the calcaneum just behind the medial malleolus midway between it and tendon Achilles.
  • Anterior tibial artery is felt anteriorly in the midway between the two malleoli against the lower end of tibia just above the ankle joint, lateral to extensor hallucis longus tendon.
  • Popliteal artery is difficult to feel. It is palpated better in prone position with knee flexed about 40–50°, to relax the popliteal fascia. It is felt in the lower part of the fossa over the flat posterior surface of upper end of tibia. In upper end of the fossa, artery is not felt as there is no bony area in intercondylar region.
  • Femoral artery in the groin is felt just below the inguinal ligament midway between anterosuperior iliac spine and pubic symphysis. Often hip has to be flexed for about 10–15° to feel it properly.
  • Radial artery is felt at the wrist on the lateral aspect against lower end of the front of radius.
  • Ulnar artery is felt at the wrist on the medial aspect against lower end of the front of ulna.
  • Brachial artery is felt in front of the elbow just medial to biceps brachii tendon.
  • Axillary artery is felt in apex of the axilla against shaft of the humerus.
  • Subclavian artery is felt against first rib just above the middle of the clavicle.
  • Facial artery is felt against body of mandible at the insertion of masseter.
  • Common carotid artery is felt medial to sternomastoid muscle at the level of thyroid cartilage against carotid tubercle (Chassaignac tubercle) of transverse process of 6th cervical vertebra (in carotid triangle).
  • 174Superficial temporal artery is felt just in front of the tragus of the ear against zygomatic bone.
 
INVESTIGATIONS FOR ARTERIAL DISEASES
  • Segmental pressure measurements: Segmental BP is measured at multiple levels (upper and lower thigh, upper calf and ankle); pressure reductions between levels help to localise the occlusion; normally pressures increase as one moves further down the leg (>20 mmHg gradient abnormal); test is inaccurate in calcified artery walls.
  • Blood tests: Low Hb delays healing due to poor oxygenation; raised WBC count may be due to infection; raised platelet count may precipitate thrombosis (of arteries and veins both); blood sugar and glycosylated haemoglobin (HbA1C) reflects the diabetic problem; lipid profile; peripheral smear; renal function tests (serum creatinine).
  • Doppler to find out the site of block—hand held Doppler can be used (Doppler: Christian Johann Doppler, Austrian physicist).
    • Duplex scan: It is combination of B mode ultrasound and Doppler study. Difference in transmitted beam of the ultrasound and reflected beam is called as Doppler shift which is assessed and converted into audible signals. It is used to study the site, extent, severity of block, and also about collaterals. Audible sound is heard with normal flow, and sound is important. Turbulence is heard when there is stenosed partially blocked artery. Audible sound will be absent if there is complete block. Using Doppler probe blood pressure at various levels can be assessed. Pulse wave tracing along the artery is also important.
      zoom view
      Fig. 1.308: Hand held Doppler is simpler way to identify and assess the artery.
    • Arterial diameter, blood flow rate, velocity of flowing blood, assessment of stenosed segment is properly done using Doppler.
  • Angiography:
    • Angiography is the appropriate investigation for arterial diseases.
    • Retrograde transfemoral Seldinger (Sweden) angiography:
      • It is commonly done angiogram. It is done only when femorals are felt. If femoral pulsation is not felt then angiogram is done either transbrachially (left brachial artery), or transaortic.
        zoom view
        Fig. 1.309: Angiogram showing vessels in both lower limbs; note the significant block on the left side
      • Other angiograms are carotid angiogram, coeliac angiogram, superior mesenteric angiogram, coronary angiogram.
      • Femoral artery is used because it can be easily felt and cannulated to pass an arterial catheter.
      • Water soluble iodine dye (Sodium diatrizoate) is injected. X-rays are taken to see the block, its extent in the affected limb.
      • In TAO cork screw appearance is characteristic. Distal run off through collaterals is also important.
      • If catheter is passed still proximally angiogram of opposite side is possible.
      • Seldinger technique can also be used (to study) to do renal angiogram to detect renal artery stenosis, renal carcinomas, renal anomalies (vascular). But a caution should be remembered that angiogram in limb may precipitate further rapid thrombus formation, worsening ischaemia and precipitating gangrene.
        175
    • Direct aortic angiogram, practiced earlier, is discouraged at present because of the risk of aortic dissection and paraplegia due to blockage/spasm of anterior spinal artery.
    • Digital subtraction angiography (DSA)
      • Here vessel (artery) is delineated in a better way by eliminating other tissues through computer system. AV fistulas, haemangiomas, lesion in circle of Willis, vascular tumours, other vascular anomalies are well made out.
        zoom view
        Fig. 1.310: DSA showing total block of right common iliac artery due to thrombosis.
        zoom view
        Fig. 1.311: CT angiogram showing abdominal aorta, branches and renal vessels.
      • Dye is injected either to an artery or vein. Injecting into a vein is technically easier but larger dose of dye is required. Injecting into an artery is technically difficult but small dose of dye is sufficient.
      • Advantages: Only vascular system is visualised; other systems are eliminated by computer subtraction. Small lesion, its location and details are better observed with greater clarity.
      • Disadvantages: Cost factor and availability.
      • Complications: Anaphylaxis, bleeding, thrombosis.
  • CT angiogram/MR angiogram.
  • Ultrasound abdomen to see aneurysm/aorta and its anatomical changes/other vessels in the abdomen/other organs.
  • Treadmill test/ECG/echocradiography to assess cardiac/coronary status.
  • Plethysmography: It measures the blood flow in limbs. Water-filled volume recorder; air-filled volume recorder; mercury in silastic gauze is used after occluding the venous outflow. It is a noninvasive method. Segmental plethysmography using occlusion cuffs of 65 mmHg pressure is placed at thigh, calf and ankle levels and then quantitative measure of pulsation is done.
  • Ankle-brachial pressure index: Normally it is 1. If it is less than 0.9, it means ischaemia is present. If it reaches 0.3 or below then it signifies severe ischaemia with gangrene.
  • Brown's vasomotor index: Specific nerve of the ischaemic limb is anaesthetised like posterior tibial nerve or ulnar nerve (local anaesthetia or spinal anaesthesia is given to anaesthetise entire limb). If the ischaemic disease is at vasospasm stage (like in TAO), nerve block will relieve the sympathetic vasospasm and skin temperature rises. It is compared to mouth temperature of the patient.
    zoom view
    Figs 1.312A and B: Aortic and aortoiliac CT angiogram.
    It is to assess the degree of vasospasm which is used as a predictor of the efficacy of sympathectomy.
    (Rise in skin temperature minus rise in mouth temperature) divided by rise in mouth temperature is called as Brown's vasomotor index. If it is more than 3.5, it is due to vasospasm, and can be relieved by sympathectomy. If less than 3.5, sympathectomy is not beneficial.
  • Transcutaneous oximetry: By placing polarographic electrodes over the skin over thigh, leg and foot of oxygen tension (tcPO2) can be measured which is reflection of underlying tissue perfusion. Normal tcPO2 in the foot is 50–60 mmHg. Level less than 40 mmHg shows inadequate wound healing. Level below 10 mmHg suggests critical ischaemia with complete failure of wound healing.
  • 176Other tests
    • Xenon 133 isotope method is used to study muscle blood flow. Xenon 133 after mixing with normal saline is injected IM to study its clearance.
    • Two electromagnetic electrodes are placed in contact with arterial wall in opposite directions which pick up moving blood force to feed into electronic amplifier. But it is invasive as artery has to be dissected to place electrodes.
    • Angioscopy to visualize the vessels directly.
 
Treatment Plan for Arterial Diseases
  • Stopping smoking; supervised exercises; regular controlled walk, diet (carbohydrate and lipid free diet); care of limbs.
  • Control of hypertension, diabetes; antilipid drugs like atorvastatin 10 mg or pravastatin 40 mg; low dose aspirin 75 mg; clopidogrel 75 mg; vasodilators; ticlopidine; dipyridamole; cilostazole 100 mg are different drugs used.
  • Percutaneous transluminal balloon angioplasty (PTA) done mainly to iliac arteries, subclavian arteries, renal artery, carotid and occasionally leg arteries and mesenteric or gastrointestinal arteries. PTA with stenting using expandable stents to the arteries is also often done to get a better result.
  • Bypass graft surgeries—aortofemoral; femorofemoral; iliofemoral, etc. Dacron, human umbilical vein (3 mm), saphenous vein; PTFE (Polytetrafluoro ethylene)—are different grafts used.
  • Endarterectomy, atherectomy, thrombectomy, profundaplasty, etc.
 
DISEASES OF THE ARTERIES
  • Atherosclerosis.
  • Thromboangiitis obliterans (TAO) (Buerger's disease).
  • Raynaud's disease.
  • Conditions causing Raynaud's phenomenon: Like scleroderma, rheumatoid arthritis, SLE, granulomatosis, vasculitis of other causes.
  • Embolus.
  • Aneurysms.
  • Other causes: Fibromuscular dysplasia, radiation, Takayasu's arteritis.
 
ATHEROSCLEROSIS
It is a chronic, complex inflammatory condition of elastic and muscular arteries, involving as systemic and segmental. It begins in childhood as fatty streaks.
Risk factors
Definitive
  • Hypercholesterolaemia, and hyperlipidaemia (cholesterol >200 mg%; high LDL (>100 mg%); low HDL (<35 mg%)
  • Cigarette smoking
  • Hypertension
  • Diabetes mellitus
Relative
  • Age—elderly
  • Common in males
  • Hypertriglyceridaemia
  • Sedentary life, obesity
  • Family history
zoom view
Fig. 1.313: Angiogram showing atherosclerosis.
 
Pathogenesis
  • All risk factors cause initial endothelial injury, both mechanical as well as toxic. This reduces significantly normal atheroprotective features of endothelium (barrier function; antiadhesive effect; antiproliferative effect on smooth muscles of arterial wall). Progressive atheromatous plaque formation, thrombosis, migration and proliferation of vascular smooth muscle cell occur. Migrated smooth muscle cells into intima act as neointima and this migration is stimulated by PDGF (platelet derived growth factor released by endothelial smooth muscles, platelets); which (this migrated smooth muscle) newly becomes secretory to produce large quantity of matrix of the plaque. Lipid (LDL) gets oxidised to release factors which promote inflammation and coagulation and factors which prevent production of protective nitric oxide. Macrophages stabilise the plaque.
  • Pathology constitutes of atherosclerotic plaque which contains smooth muscle cells, connective tissue matrix, macrophages and lipid (the feature of atherosclerosis). Ulceration and calcification occurs in these plaques. Ulcerated plaque is highly thrombogenic causing thrombosis and further critical block of the vessel leading to tissue ischaemia and infarction distally.
  • 177Plaques are more at the dividing junctions of the artery where stress and shear force of the blood flow is more. Plaques are dynamic in nature with progression and regression phases.
  • Plaque progression has got a unique ability of adaptation so that as the plaque progresses, lumen caliber is been tried to be preserved until critical stage occurs. Stenosis more than 40% is said to be critical. Beyond this, compensatory mechanism fails causing rapid progression and further stenosis of lumina. Stenosis more than 40% causes atrophy of tunica media making arterial wall mechanically unstable leading into dilatation and aneurysm.
  • Common arteries involved are—infrarenal part of abdominal aorta, coronary arteries, iliofemoral vessels, carotid bifurcation, popliteal arteries. It is less common in upper limb arteries, common carotid, renal and mesenteric arteries.
 
Features and Evaluation
  • It is common after 50 years, but can occur at earlier age group.
  • It occurs in males and females. Family history is common.
  • Smoking, hypertension, diabetes, raised cholesterol are common causes.
  • Veins are not diseased. Arterial wall is thickened on palpation.
  • Thrill and bruit over femoral, renal, carotid arteries may be felt/heard. It suggests localised stenosis with turbulence of blood flow.
  • Features of ischaemia in the affected limb seen. Absence/feeble pulses including main arteries of the limb—femorals. Abdomen should be examined for aortic aneurysm.
  • Transient ischaemic attacks, chest pain, eye problems, mesenteric ischaemia, altered renal function may be associated.
  • Blood sugar, fasting lipid profile, Doppler, angiogram (CT / DSA), US abdomen, ECG, echocardiography are essential investigations. Angiogram shows typical narrowed artery, site, extent, percentage of stenosis, and collaterals.
  • Antiphospholipid antibody (APLA) estimation is done to identify antiphospholipid antibody syndrome (APLS/Hughes' syndrome). It is an autoimmune, hypercoagulable state caused by antiphospholipid antibodies. APLS provokes thrombosis in both arteries and veins as well as causes pregnancy-related complications such as miscarriage, stillbirth, preterm delivery, and severe preeclampsia. It causes lower limb DVT (venous) and arterial thrombosis (causing stroke); it is diagnosed by ELISA test for APLA. It is treated by aspirin and anticoagulant (Warfarin).
 
Management
  • Risk factor modification: Avoid smoking; control of hypertension, diabetes, hypercholesterolaemia; weight reduction by diet, and exercise.
  • Drugs: Antiplatelet agents (aspirin 75 mg, clopidogrel 75 mg); cilostazol 50 mg bd; atorvastatin to reduce cholesterol; pentoxiphylline.
  • Percutaneous transluminal angioplasty (PTA) is very useful for iliac blocks and lower limb blocks.
  • Surgeries:
    • Thrombectomy, endarterectomy, profundaplasty.
    • Reverse/saphenous vein graft.
    • By pass grafts—iliofemoral, aortofemoral, iliopopliteal, femorofemoral grafts.
    • Amputations if limb is gangrenous—toe/below knee, above knee. Forefoot and Syme's amputations are not feasible in vascular conditions.
Note:
Lumbar sympathectomy and omentoplasty are not much useful in atherosclerotic limb. Omental vessels as such are often poorly perfused in atherosclerotic patients due to involvement of coeliac trunk.
 
Aortoiliac Occlusive Disease
Common site of symptomatic atherosclerotic occlusive arterial disease of lower limb is infrarenal abdominal aorta and iliac arteries. Aortic bifurcation is the most common site of occlusion. Often disease may also extend into infrainguinal level.
 
Types of Aortoiliac Occlusive Disease
Type I: Disease localised to distal abdominal aorta and common iliac arteries.
Type II: Wide spread aortic and iliac disease.
Type III: Multiple level diseases along with infrainguinal diseases.
zoom view
Fig. 1.314: Types of aortoiliac occlusive disease.
178
 
Features
  • Common in 5th and 6th decades. Common in males.
  • Claudication in buttock, Leriche syndrome with impotence, distal ischaemia are the features.
  • Femoral artery pulsations below are absent. Systolic bruit over aorta and iliac arteries may be heard suggesting stenosis.
  • Atheromatous plaque may dislodge and may cause embolus causing acute presentation.
  • Aortic angiogram is diagnostic.
 
Management
  • Treatment for diabetes, hyperlipidaemia, etc.
  • Surgical treatment is the mainstay.
    • Direct anatomical reconstruction
      • Aortoiliac endarterectomy is reboring/disobliteration procedure useful for type I disease. Diseased intima, plaque with thrombus is removed by arteriotomy along the entire length which is closed later using 4 zero/5 zero polypropylene continuous sutures (open endarterectomy). In lengthy disease, after making two small arteriotomies at proximal and distal diseased parts, endarterectomy loop is passed to remove the intima with diseased plaque (semi-closed endarterectomy). Advantages: It avoids prosthetic graft and its complications. Problem is—reocclusion and restenosis.
      • Aortofemoral bypass graft is the gold-standard surgical procedure for type I and II disease. Long-term patency rate is 70–80%. Woven Dacron graft is used. Complications are—bleeding, thrombosis, embolisation, graft blockage, graft failure, graft infection, graft leak, aortovenacaval/aortoduodenal fistula, mesenteric ischaemia (colonic), impotence.
    • Indirect extra-anatomical bypass
      It is quicker and technically easier and is suitable to patients who cannot tolerate anatomical bypass. Axillo-bifemoral graft is used, only in such occasional situation.
    • Nonoperative catheter based endovascular procedure
      If stenosis is less than 5 cm percutaneous transluminal angioplasty (PTA) with or without intravascular stents can be done. It is useful for single or multiple short focal stenoses. It is now proved that long-term patency of PTA is equal to surgical intervention.
 
Infrainguinal Arterial Occlusive Disease
It is either part of type III aortoiliac disease (aortoiliac femoral) or femoropopliteal tibial disease. Superficial femoral artery is most commonly involved. Involvement of long segment of the artery is common. Occasionally, a short stenotic segment may be present.
 
Management
  • If the popliteal artery below knee is patent femoropopliteal bypass is the ideal procedure used. Otherwise one of the patent branches is used for bypass. In situ saphenous vein graft is ideal; reverse saphenous vein graft or synthetic femoropopliteal graft can also be used.
  • Profundaplasty may be done to improve the collateral circulation through profunda femoris (deep femoral).
zoom view
Figs 1.315A and B: Aortofemoral bypass graft.
Note:
PTA in infrainguinal blocks is occasionally useful, only when stenosis is short and well-localised; otherwise it is not a good option. Angioplasty with laser drilling is often tried.
 
THROMBOANGIITIS OBLITERANS (TAO) Syn. Buerger's Disease
  • It is a disease very commonly seen in young and middle aged males; seen only in smokers and tobacco users; not usually seen in females due to genetic reasons (but can occur in females very rarely).
  • Almost always starts in lower limb, may start on one side and later on the other side. Upper limb involvement occurs only after lower limb is diseased. Only upper limb involvemnt can occur (not uncommon) but it is rare.
  • It is nonatherosclerotic inflammatory disorder involving medium sized and distal vessels with cell mediated sensitivity to type I and type III collagen.
  • 179It is common in Jewish people; it is rare even in female smokers.
  • Hormonal influence, familial nature, hypersensitivity to cigarette, altered autonomic functions are probable different causes.
  • Lower socioeconomic group, recurrent minor feet injuries, poor hygiene are other factors.
  • It is segmental, progressive, occlusive, inflammatory disease of small and medium sized vessels with superficial thrombophlebitis often may present as Raynaud's phenomenon with microabscesses, along with neutrophil and giant cell infiltration, with skip lesions.
 
Pathogenesis
Smoke contains carbon monoxide and nicotinic acid
↓ ← Carboxyhaemoglobin
Causes initially vasospasm and hyperplasia of intima
Thrombosis and so obliteration of vessels occur, commonly medium sized vessels are involved.
Panarteritis is common
Usually involvement is segmental
Eventually artery, vein and nerve are together involved
Nerve involvement causes rest pain
Patient presents with features of ischaemia in the limb
Once blockage occurs, plenty of collaterals open up depending on the site of blockage either around knee joint or around buttock
Once collaterals open up, through these collaterals, blood supply is maintained to the ischaemic area
It is called as compensatory peripheral vascular disease
If patient continues to smoke, disease progresses into the collaterals, blocking them eventually, leading to severe ischaemia and is called as decompensatory peripheral vascular disease. It is presently called as critical limb ischaemia. It causes rest pain, ulceration, gangrene.
Note:
  • There is vasospasm → intimal hyperplasia → thrombosis → panarteritis → obliteration; tender, cord like veins with superficial migratory thrombophlebitis (30%); with nerve involvement due to vasa nervorum block/spasm. Arterial lumen is blocked but not thickened like atherosclerosis.
  • In 10% disease is bilateral; 10% females may get the disease (but rare); 10% seen in upper limbs.
  • Large arteries are not involved by TAO.
 
Classification of TAO
Type I: Upper limb TAO—rare.
Type II: Involving leg/s and feet—crural/infrapopliteal.
Type III: Femoropopliteal.
Type IV: Aortoiliofemoral.
Type V: Generalised.
 
Clinical Features
  • Common in male smokers between the 20-40 years of age group. It is a smoker's disease.
    zoom view
    Fig. 1.316: Dry gangrene of leg. Patient needed above knee amputation.
  • Intermittent claudication in foot and calf progressing to rest pain, ulceration, gangrene.
  • Recurrent migratory superficial thrombophlebitis.
  • Absence/Feeble pulses distal to proximal; dorsalis pedis, posterior tibial, popliteal, femoral arteries.
  • May present as Raynaud's phenomenon.
 
Investigations
  • Hb%. Blood sugar.
  • Arterial Doppler and Duplex scan (Doppler + B mode U/S).
  • Transfemoral retrograde angiogram through Seldinger technique:
    • 180Shows blockage—sites, extent, and severity.
    • Cork screw appearance of the vessel due to dilatation of vasa vasorum.
    • Inverted tree/spider leg collaterals.
      zoom view
      Figs 1.317A and B: Bilateral lower limb TAO causing gangrene of both feet. Patient needs amputation on both sides.
      zoom view
      Fig. 1.318: Gangrene foot.
    • Severe vasospasm causing corrugated/rippled artery.
    • Distal run off is amount of dye filling in the main vessel distal to the obstruction through collaterals. If distal run off is good then ischaemia is compensated. If distal run off is poor then ischaemia is decompensated.
  • Transbrachial angiogram: If femorals are not felt, then transbrachial angiogram (through left side brachial artery—left subclavian artery—and so to descending aorta) should be done.
  • Ultrasound abdomen to see abdominal aorta for block/aneurysm.
  • Vein, artery, nerve biopsy.
zoom view
Fig. 1.319: Gangrene of all toes in a foot in TAO patient.
zoom view
Fig. 1.320: Ischaemic ulcer foot in a TAO patient.
zoom view
Fig. 1.321: Ischaemic features in upper and lower limbs (four limbs).
 
Treatment
Stop smoking. “Opt for either cigarette or limb, but not both.”
 
Drugs
  • Pentoxiphylline increases the flexibility of RBC's and helps them reach the microcirculation in a better way so as to increase the oxygenation. Its efficacy is more in venous ulcer than arterial diseases (now).
    181
    zoom view
    Fig. 1.322: Skip ischaemic ulcers are common in vascular diseases. It suggests severe ischaemia up to most proximal ulcer level.
    zoom view
    Fig. 1.323: CT angiogram of lower limb (leg area) showing segmental block.
    zoom view
    Fig. 1.324: Angiogram showing block in main vessel with opened up collaterals and adequate distal run off.
    zoom view
    Fig. 1.325: Angiogram showing adequate collaterals.
  • Low dose of aspirin 75 mg once a day—antithrombin activity.
  • Prostacyclins, ticlopidine, praxilene, carnitine.
  • Clopidogrel 75 mg; atorvastatin 10 mg; parvostatin 40 mg; cilostazole 100 mg bid—is a phosphodiesterase inhibitor which improves circulation (ideal drug).
    All drugs act at the collateral level than on the diseased vessel.
  • Analgesics, often sedatives, antilipid drugs like atorvastatin may be needed. Complamina retard (xanthine nicotinate) tablet which was used daily once earlier, is presently not in use. However, graded injection of xanthine nocotinate 3000 mg from day 1 to 9000 mg on day 5 is often practiced to promote ulcer healing, helps to increase claudication distance as a temporary basis. Low molecular dextran may be also used.
  • Naftidofuryl is useful in intermittent claudication; it alters the tissue metabolism.
Note:
Vasodilators and anticoagulants are of no use in TAO.
 
Care of the Limbs
  • Buerger's position and exercise—regular graded exercises up to the point of claudication improves the collateral circulation.
    In Buerger's position, head end of bed is raised; foot end of bed is lowered to improve circulation. In Buerger's exercise leg is elevated and lowered alternatively, each for 2 minutes for several times at time.
  • Care of feet (Chiropady): Exposure of feet to more cold and warm temperature should be avoided; trauma even minor like nail paring or pressure at pressure points in feet should be avoided. Dryness of feet and legs should be avoided by applying oil to the feet and legs. Footwear should be selected carefully. It is better to wear socks with footwear. Heel raise by raising the heels of shoes by 2 cm decreases the calf muscle work to improve claudication.
182
 
Chemical Sympathectomy
  • Sympathetic chain is blocked to achieve vasodilatation by injecting local anaesthetic agent (xylocaine 1%) paravertebrally beside bodies of L 2, 3 and 4 vertebrae in front of lumbar fascia, to achieve temporary benefit. Long time efficacy can be achieved by using 5 ml phenol in water. It is done under C-Arm guidance. Feet will become warm immediately after injection. Problems are—possible risk of injecting phenol into IVC/aorta, spinal cord ischaemia.
 
Surgery
  • Omentoplasty to revascularise the affected limb.
  • Profundaplasty is done for blockage in profunda femoris artery so as to open more collaterals across the knee joint (It often makes better perfusion to the knee joint and flap of below-knee amputation).
  • Lumbar sympathectomy to increase the cutaneous perfusion so as to promote ulcer healing. But it may divert blood from muscles towards skin causing muscle more ischaemic.
    zoom view
    Fig. 1.326: Bilateral TAO. Patient has undergone right-sided above knee amputation and left-sided lumbar sympathectomy. Ischemic ulcer on left-sided foot is seen.
  • Amputations are done at different levels depending on site, severity and extent of vessel occlusion. Usually either below-knee or above-knee amputations are done.
  • Ilzarov method of bone lengthening helps in improving the rest pain and claudication by creating neo-osteogenesis and improving the overall blood supply to the limb.
 
Gene Therapy
  • Intramuscular injection of vascular endothelial growth factor (VEGF) which is an endothelial cell mitogen that promotes angiogenesis.
 
TAKAYASU'S PULSELESS ARTERITIS (Mikito Takayasu, 1938—Ophthalmologist, Japan)
  • It is progressive, initially symptomless panarteritis involving aortic arch and branches of aorta of unknown etiology, probably immunological.
  • It is common in young females (85%); common in Japan; commonly subclavian artery is involved (85%); involves all layers of arteries of upper limb and neck; often bilateral. It remains unnoticed for long time.
 
Features
  • Fever, myalgia, arthralgia, upper limb claudication.
  • Absence pulses in upper limb/limbs, neck; hypertension.
  • Fainting on turning the neck or change in position; atrophy of face.
  • Thrill/bruit along major arteries of upper limb and neck are the features.
  • Optic nerve atrophy without papilloedema.
  • Weakness and paraesthesia of upper limb.
  • Cerebral softening, convulsions, hemiplegia can occur.
  • Occasionally it can be life-threatening. Myocardial infarction; embolism, ischaemia are other complications.
  • DSA; MR angiography and Doppler are the investigations.
 
Treatment
  • To suppress immunity prednisolone 50 mg/day and cyclophosphamide daily is given.
  • Vascular reconstruction.
 
RAYNAUD'S PHENOMENON
It is an episodic vasospasm, i.e. arteriolar spasm. It leads to sequence of clinical features called as Raynaud's syndrome.
183
Coffman criteria for Raynaud's syndrome—“episodic attacks of well-demarcated reversible self-limiting colour changes for 1–20 minutes on exposure to cold/emotional stimuli and is symmetrical/bilateral lasting for 2 years”.
 
Causes for Raynaud's Phenomenon
  • Raynaud's disease:
    • It is seen in females, usually bilateral.
    • It occurs in upper limb with normal peripheral pulses.
    • It is due to upper limb (hand) arteriolar spasm as a result of abnormal sensitivity to cold. Patient develops blanching, cyanosis and later flushing as in Raynaud's syndrome. Occasionally, if spasm persists it results in gangrene.
    • Symptoms can be precipitated and observed by placing hands in cold water.
  • Working with vibrating tools: Like pneumatic road drills, chain saws, wood cutting, fishermen travelling in machine boats—vibration white finger.
    zoom view
    Fig. 1.327: Vasculitis can cause arterial insufficiency.
  • Collagen vascular diseases: Like scleroderma, rheumatoid diseases causing vasculitis (all autoimmune diseases).
  • Other causes: Cervical rib, Buerger's disease, Scalene syndrome.
It is often associated with CREST syndrome (Calcinosis cutis, Raynaud's phenomenon, Esophageal defects, Sclerodactyly, Telangiectasia).
 
Raynaud's phenomenon can be:
  • Primary Raynaud's phenomenon is an idiopathic vasospastic disorder without underlying identifiable causes. Usually there is no significant pain in primary type. Primary is probably due to increased sensitivity of alpha 2 receptors to nonepinephrine; decreased nitric oxide and endothelin 1 in endothelial cells; increased serotonin and thromboxane. It is common in females and younger age group. Usually it is bilateral involving all digits.
  • Secondary Raynaud's phenomenon is vasospasm due to some underlying cause. Significant pain will be present especially during rewarming stage. There are positive autoantibodies; equal in both sexes; occurs at any age group; need not be bilateral.
 
Features (of Raynaud's disease)
  • Commonly bilateral.
  • Common in young females.
  • Raynaud's disease is common in western white women.
  • Usually medial four digits and palm are involved. Thumb is spared.
  • Features of pallor/blanching (syncope), dusky cyanosis (asphyxia), rubor/painful red engorgement (recovery) are the presentation. Occasionally, if vasospasm becomes longer, gangrene or ischaemic ulceration supervenes along the tips of the fingers.
  • Peripheral pulses (radial/ulnar) are normally felt. These pulses will be absent in upper limb TAO.
  • Repeated attacks are common.
 
Investigations
  • Type is identified by angiogram of hand (DSA/MR angiogram), arterial Doppler/Duplex scan.
  • Other investigations required are X-ray of the part, antinuclear antibody (ANA assay) tests specific for different conditions.
  • Assessment of segmental blood pressure gradient from brachial-forearm-wrist-fingers; finger tip thermography; cold recovery time (normal is less than 10 minute, but in Raynaud's it is more, often up to 30 minutes); reactive hyperaemia time (pneumatic cuff is inflated and kept for 5 minutes and released to observe hyperaemia); nail fold capillary microscopy; Laser Doppler flux to assess microvascular perfusion of finger skin—are special methods of evaluations.
  • Other routine investigations for arterial diseases like blood sugar/lipid profile/hypercoagulability status.
 
Treatment
  • Treat the cause.
  • Avoid precipitating factors—protect from cold/proper dress/hand warmer electrical or chemical/hand gloves. Avoid smoking even though it is not direct etiological cause (other than upper limb TAO), but it may possibly aggravate the disease. Avoid vibrating tools.
  • Vasodilators/pentoxiphylline/low dose aspirin (75–100 mg per/day). Calcium antagonist (nifedipine 20 mg) is useful. Steroids may be useful in case of secondary Raynaud's.
  • ACE inhibitors, nitrates, endothelin inhibitors (bosentan), epoprostenol—prostaglandin a potent vasodilator and antiplatelet drug (continuous intravenous infusion can be given), iloprost—prostacycline analogue, PG E1, misoprostol (oral PG E 1)—are all tried at different stages of the disease.
  • Cervical sympathectomy—is used for nonhealing digital ulceration. Not very beneficial to Raynaud's syndrome.
Note:
Avoid oral contraceptives, beta blockers and ergot preparations in Raynaud's disease.
184
 
TEMPORAL ARTERITIS
  • There is localised inflammatory giant cell infiltration of arterial wall (giant cell arteritis) involving superficial temporal, facial, retinal, upper limb, coronary and vertebral arteries.
  • It is common after 50 years. Common in females (2:1).
  • Claudication of facial muscles, ischaemic severe headache, tender, thrombosed superficial temporal artery and its branches are the features.
  • Retinal ischaemia leading into irreversible blindness is dangerous feature. Involvement of coronary artery may cause myocardial infarction.
  • Temporal artery biopsy is diagnostic—shows giant cell granuloma with CD4+ T lymphocytes.
  • High dose long-term prednisolone 80 mg/day is needed. In involvement of retinal artery IV hydrocortisone/methylprednisolone may be needed initially.
 
TREATMENT OF ARTERIAL DISEASES
 
a. Medical
 
General Measures
  • Stop smoking, reduction of weight, exercise.
  • Change in lifestyle, care of feet.
  • Control of diabetes and hypertension.
  • Buerger's position and exercise.
 
Drugs
  • Nifedipine, praxilene, pentoxiphylline, low dose aspirin, prostacycline, dipyridamole, ticlopidine.
  • Clopidogrel (75 mg).
  • Cilostazol (type III phosphodiesterase inhibitor) 100 mg BD—inhibits platelet aggregation.
  • Oral anticoagulants are used only if there is history of embolism or atrial fibrillation.
  • Prostaglandins, growth factors, vascular endothelial growth factor (VEGF), E2Fdecoy (blocks intimal and smooth muscle cell proliferation), mesoglycan (breaks blood clot), testosterone, herbals like garlic (reduces viscosity of blood) are other newer drugs under use and trial.
  • B vitamins and folic acid reduces homocysteine level (which is a risk factor).
  • Inositol, L-carnitine (1500 mg), magnesium 500 mg (not in renal failure or with diarrhea), vitamin E and C are other agents often used to improve walking distance.
  • Heparin is used only in acute phase or embolism.
 
b. Surgery
  • Percutaneous transluminal balloon angioplasty (PTA): Through transfemoral Seldinger approach, initially angiogram is done. Then under guidance (fluoroscopic) stenosed area is approached. First guidewire is introduced through which balloon catheter is passed. Balloon of the angioplasty catheter is inflated at stenosed area for one minute and repeated if required. Plaques should rupture. Catheter is withdrawn. It is useful in cases of localised stenosed areas.
Note:
  • Often nonexpandable or self-expandable stents are used if stenosed segment is not dilated adequately through balloon—PTA with stenting.
  • PTA for carotid artery stenosis is risky and not ideal as there will be possible release of microemboli during dilatation procedure which can precipitate stroke. Specialised balloon catheters with umbrella tip which can trap the microemboli may be used in these places.
 
Types
  • Conventional: Here balloon is inflated along the lumen to break the plaque circumferentially.
  • Subintimal: Here balloon is inflated after passing subintimal plane to break the plaque.
    zoom view
    Fig. 1.328: Conventional and subintimal types of PTA.
 
Complications
  • Thrombosis, bleeding, sepsis.
  • Embolism, dissection, retroperitoneal haematoma.
  • Pseuodoaneurysm formation.
 
Advantages
  • It is done under local anaesthesia.
  • Procedure can be repeated if needed.
  • Stent can be placed at a later stage if needed.
  • It is done when stenosis is less than 5 cm. In ideal indications its efficacy is equal to surgery.
 
Disadvantages
  • It is less useful for lengthy blocks or stenosis more than 5 cm.
    zoom view
    Fig. 1.329: Percutaneous transluminal balloon angioplasty (PTA). Note the inflated balloons on both side iliac arteries.
    185
    zoom view
    Figs 1.330A and B: DSA showing left-sided aortoiliac block and correction after doing PTA.
  • It is dangerous to do in stenosis of carotid artery where endarterectomy is ideal.
  • Atherectomy:
    It is removal of atheroma either through open surgery or by percutaneous route from the wall of the vessels.
  • Thrombectomy:
    It is removal of thrombus through an arteriotomy of larger vessels. Done in aortoiliac, femoropopliteal region.
  • Endarterectomy:
    • It is removal of thrombus along with diseased intima through an arteriotomy. Endothelium of the vessel is removed, hence the name.
      zoom view
      Figs 1.331A and B: DSA showing superior mesenteric artery stenosis. It is corrected by PTA.
      zoom view
      Fig. 1.332: Thrombectomy.
      zoom view
      Fig. 1.333: Endarterectomy technique. Both thrombus and diseased intima are removed through an arteriotomy. Often ring stripper is used to remove the atheromatous plaque.
    • It is done in carotid, aortoiliac and occasionally aortofemoral blocks. It is also called as disobliteration/reboring. There are three methods—(1) Open method—Arteriotomy is done along the entire diseased segment; endarterectomy is done by removing thrombus, diseased intima with plaque along the plane of media. Arteriotomy is closed using 5 zero polypropylene suture and patient is heparinised. (2) Semiclosed method—Here two arteriotomies are done on either ends of the level of obstruction; loop endarterectomy stripper is passed from one end to complete the endarterectomy; two arteriotomies are closed. (3) Wiley's eversion endarterectomy—Here artery is cut transversely at the junction of diseased and normal nondiseased segment; diseased intima with plaque is circumferentially dissected; artery is everted out to extract the diseased intima like a tube; everted artery is reduced and sutured to normal end of the artery. Advantages are—it avoids prosthetic graft and its complications. Problem is—reocclusion and restenosis.
  • Placement of intraluminal stent for localised stenosis.
  • Profundaplasty:
    • It is done when there is localised block in opening of profunda femoris (deep femoral). Profunda femoris is opened, thrombus if present, is removed. Opening is widened using either venous or synthetic (Dacron or PTFE) grafts. This procedure allows collaterals across the knee joint to open through profunda femoris and so gives good blood supply below-knee level and may prevent patient going in for above-knee amputation.
      186
      zoom view
      Fig. 1.334: Profundaplasty for deep femoral block.
      (May be able to save knee joint with below-knee amputation with better prosthesis.)
    • Lateral angiogram view is needed to identify the orifice of profunda femoris. Disease involves invariably only at the orifice without extending distally towards 1st perforator branch. Endarterectomy at the junction and closure with a venous patch widens the opening adequately.
  • Reverse saphenous vein graft:
    In case of femoropopliteal block, saphenous vein is dissected out, reversed and sutured above to the femoral artery and below to popliteal segment so as to bypass the blood through reverse saphenous vein graft. Saphenous vein is reversed to nullify the action of valves so as to allow easy flow of blood.
  • In situ saphenous vein graft:
    It is arterialisation of saphenous vein. Saphenous vein intact in same position is sutured above and below the blocked femoropopliteal region to bypass the blood across. Venous valves are removed through valvulotomy instrument so as to allow the blood to pass. Here nutrient supply of vein is left intact with proximal part of the vein sutured to wider part of the femoral artery, narrow distal part is sutured to narrow part of the artery.
  • Arterial/venous grafts:
  • Different procedures
    • Aortofemoral bypass graft (end to side)—5% mortality.
    • Ileofemoral bypass graft.
    • Femorofemoral bypass graft
    • Femoropopliteal graft.
    • Femorodistal graft.
    • Axillofemoral graft.
    Problems with grafts: Leak, infection, thrombosis, cost factor, availability, reblock.
Note:
Angioscope is used to visualise the valves in saphenous vein or to visualise the completion of the by pass grafts like femorodistal graft.
zoom view
Fig. 1.335: Bypass graft (Aortoiliac).
zoom view
Fig. 1.336: Femoropopliteal bypass graft.
  • Cervicothoracic preganglionic sympathectomy:
    It is removal of 2nd and 3rd thoracic ganglia which contains cells of postganglionic fibres supplying the upper limb. Preganglionic white rami communicantes fibres from 2nd and 3rd sympathetic nerves enter thoracic T1 ganglion and supplies head and neck region through upper part of the stellate ganglion. Preganglionic sympathetic nerve entering the 2nd and 3rd ganglia from below, supplies sympathetic fibres for upper limb through the lower part of the stellate ganglion. In cervical sympathectomy for upper limb ischaemia, lower part of stellate ganglion with Kuntz nerve is divided. For head and neck hyperhidrosis entire stellate ganglion should be removed which leads to development of Horner's syndrome. For hyperhidrosis of axillary area, along with stellate ganglion upper four thoracic ganglia has to be removed.
187
zoom view
Fig. 1.337: Aortofemoral bypass graft (End to side).
zoom view
Fig. 1.338: On table picture of aortofemoral arterial graft.
 
Approaches
  • Supraclavicular approach:
    Through a supraclavicular incision sternomastoid, (omohyoid is retracted or divided) scalenus anterior muscles, are divided. Phrenic nerve is displaced medially; subclavian artery is pushed downwards; thyrocervical trunk is identified and ligated securely, suprapleural membrane is depressed, stellate ganglion is identified in the neck of the first rib. All rami communicantes from second and third ganglia are divided. Grey ramus from second ganglion to first thoracic nerve called as Kuntz nerve, is also divided.
  • Transthoracic/Axillary approach (Hedley Atkins):
    This gives better visibility and easier removal of rami, lower down compared to supraclavicular approach. Patient is placed in lateral position; transverse incision is made just below the hair bearing line; intercostobrachial nerve is preserved. Thorax is opened at 2nd space. Sympathetic chain is identified at the neck of 1st rib.
  • Thoracoscopic sympathectomy is the choice, and popular approach at present.
    Advantages are better visibility with magnification, less trauma of access (wound), faster recovery, and precise.
    zoom view
    Fig. 1.339: Cervical sympathectomy scar in the neck and patient has developed Horner's syndrome. Healed ulcer over tip of index finger on left side is seen. Patient is asymptomatic after sympathectomy.
  • Lumbar sympathectomy:
    Indications
    • Peripheral vascular disease like TAO.
    • To promote healing of cutaneous ulcers.
    • To change level of amputation and to make flaps to heal better after amputation.
    • Causalgia of lower limb (it is common in upper limb).
    • Hyperhidrosis of lower limb is rare.
    Principle
    • It increases the cutaneous blood supply thereby promoting healing of ulcer and skin flaps in amputation. It is a preganglionic sympathectomy. Ganglion L2 and L3 supplies legs below knee level. L1 supplies upper part of thigh and buttock region. 188L1 lies under the crus of diaphragm. L4 lies under the common iliac vessels below.
    • It increases the blood flow for 2–4 weeks by abolishing constriction of arterioles and precapillary sphincters (basal and reflux). It produces transient small increase in distal perfusion; increases the nutritive perfusion to promote ulcer healing; alters the pain perception and pain impulse transmission temporarily.
 
Procedure
Under general or spinal anaesthesia, ganglia are approached through a transverse incision in the loin at the level of umbilicus, through extraperitoneal approach, by dividing external oblique, and internal oblique, and splitting transverse abdominis muscles. Inferior vena cava on right side, aorta on left side are identified. Sympathetic chain is identified by its rami, over transverse processes of lumbar spines. L2, L3, L4, L5 ganglia are removed. L2 is identified by its size (Larger) and more number of rami. L1 is retained on one side in bilateral cases. If both are removed it will lead to failure of ejaculation and so sterility (Dry ejaculation).
  • Its effects are only temporary (3–4 weeks). Long-term results are doubtful. It can be combined with omentoplasty.
  • It can also be done along with below-knee amputation to increase the blood supply of skin flap so as to have better healing.
  • Limb will become warmer immediately after sympathectomy.
zoom view
Fig. 1.340: Lumbar sympathectomy scar with ischaemic ulcer foot showing healing sign.
Note:
Lumbar sympathetic chain may be mistaken for lymph nodes, fat, tendon of psoas muscle, genitofemoral nerve.
  • Chemical sympathectomy:
    • It is done in lateral position using a long spinal needle under local anaesthesia. Position is confirmed by injecting dye under fluoroscopy. Later 5 ml of phenol in water or absolute alcohol is injected lateral to the vertebral bodies of fourth and second lumbar vertebrae. Care should be taken to see that the needle does not enter IVC or aorta.
    • Procedure is contraindicated in patients with bleeding disorders and in patients who are on anticoagulants.
  • Omentoplasty:
zoom view
Figs 1.341A to C: Omentoplasty procedure for revascularisation of the ischaemic limb.
Omentum is supplied by omental vessels
zoom view
Four layers of omentum has got omental arcades of vessels (Arc of Burkow). Omentum is also rich in lymphatics. It has got adhesive property. By retaining one of the pedicles, omentum can be mobilised 189so as to reach the limb to maintain the circulation. It can also be mobilised up to the ankle. It promotes ulcer healing, reduces the pain and controls the features of ischaemia. It can also be used in upper limb ischaemia. But, if patient continues to smoke, disease spreads to these omental vessels also. Often it can be mobilised to both lower limbs in bilateral diseases.
zoom view
Fig. 1.342: Incisions for omentoplasty in the abdomen (upper midline) and in lower limb.
Complications of omentoplasty:
  • Abdominal sepsis.
  • Incisional hernia, where omental pedicle is tunneled into the limb from the abdomen.
  • Adhesions and intestinal obstruction.
Procedure: Under general anaesthesia, abdomen is opened with upper midline incision. Omental vessels are identified. Omentum with its blood supply is carefully mobilised to get an adequate length. Lengthened, mobilised omentum is brought into the subcutaneous plane through abdominal wall, lateral to the lower part of rectus muscle. Later this pedicle is mobilised in the subcutaneous tunnel across the leg, burried in the deep fascia.
  • Other treatment methods:
    • Amputations are done at different levels depending on extent of gangrene, site of block, amount of collaterals.
    zoom view
    Fig. 1.343: Below knee amputation stump which is also ischaemic. Patient underwent below knee amputation for gangrene foot. But patient might need above knee amputation.
 
SUBCLAVIAN STEAL SYNDROME
Following obstruction of the first part of subclavian artery, vertebral artery provides collateral circulation to the arm by reversing its blood flow. This causes cerebral ischaemia with syncopal attacks, visual disturbances, diminished blood pressure in the affected limb.
zoom view
Fig. 1.344: Subclavian steal syndrome.
  • It is more common on left side.
  • Vertebrobasilar symptoms like dizziness, syncope, visual disturbances, vertigo can occur.
  • Pain, heaviness, paraesthesia and fatigue in the arm which is aggravated by exercise.
  • Radial pulses on both sides are asymmetrical.
  • Blood pressure on the diseased side will be 20 mmHg less compared to normal side.
  • Javid test: Here compression of carotid artery makes ipsilateral radial pulse feeble.
 
Investigations
Duplex scan and angiogram. DSA is useful.
 
Treatment
  • Transluminal balloon angioplasty.
  • Endarterectomy or bypass graft.
    (Common carotid—subclavian graft).
 
ACUTE ARTERIAL OCCLUSION
It is a condition of acute lack of tissue perfusion due to sudden cessation of circulation. Main axial artery of the limb is blocked presenting within minutes to hour after occlusion.
It is common in lower limb, upper limb; but can occur in mesenteric, cerebral, coronary arteries.
 
Causes
  • Embolism is the most common cause in developing country.
  • Trauma.
  • Thrombosis of an artery: Normal artery can develop sudden 190acute thrombosis in certain special situations with hypercoagulable status like malignancy, leucaemia, antiphosholipid antibody syndrome, protein C/protein S/antithrombin deficiency; polycythaemia rubra vera, thrombocytosis. It is commonly observed in external iliac artery, profunda femoris artery and popliteal artery.
  • Thrombosis of a bypass graft is common cause in western countries which occurs at the site of anastomosis.
 
Pathophysiology
Distal ischaemia begins immediately after acute obstruction. Most sensitive peripheral nerves are first involved, and then muscles, subcutaneous tissue and skin are affected in order. Irreversible ischaemia occurs in 6 hours. Golden period is 1–6 hours. Ischaemia may get aggravated by—propagation of thrombus below and above the block occluding the orifices of collaterals, fragmentation of embolus, associated thrombosis, acute compartment syndrome.
Acute ischaemia causes endothelial injury of capillaries, arterioles and venules with luminal obliteration. Raised capillary permeability causes fluid leakage into extravascular space forming massive tissue oedema deep to deep fascia which by raising the intracompartmental pressure further reduces the perfusion leading into acute compartment syndrome.
 
Features
  • Pain which is continuous, severe, steady, bursting.
  • Pallor of the distal part with extreme cold limb.
  • Pulselessness—sudden loss of earlier palpable pulse.
  • Paraesthesia—sensory disturbances like tingling, numbness or complete loss of sensation.
  • Paresis—damage to motor nerve and muscle leading into paralysis as a late grave feature.
  • Poikilothermia—change in the temperature (cold).
    Pain, paraesthesia, paresis are due to ischaemia of peripheral nerves which are sensitive to hypoxia.
 
TRAUMATIC ACUTE ARTERIAL OCCLUSION
 
Causes
  • Thrombus due to trauma.
  • Subintimal haematoma.
  • Acute compartment syndrome.
  • During femoral or brachial arterial catheterisation for either diagnostic or therapeutic procedures.
 
Clinical Features
History of trauma, pain, swelling at the site, pallor, pulselessness, cold limb.
 
Investigation
Duplex scan, angiogram.
 
Treatment
  • Wound is explored and tear in the artery is identified. It is sutured using nonabsorbable monofilament material, polypropylene 6-0. Often venous or dacron graft is required for interposition.
  • Proper antibiotics and heparin are required to prevent thrombosis of the vessel. Later patient is advised to take oral warfarin for maintenance.
  • Compartment syndrome is common in anterior compartment of leg and in front of forearm. Here because of the closed compartment, pressure increases following fracture, haematoma which compresses over the vessel. It leads to blockade of vessel causing acute ischaemia of the limb presenting with severe pain, pallor, pulselessness.
    • Treatment: Immediate decompression by longitudinal fasciotomy, is the treatment of choice, wherein deep fascia is cut adequately to relieve the compression. Otherwise limb may go for severe ischaemia, gangrene and may land in amputation.
  • Associated fractures, haematoma, vessel tear has to be managed accordingly.
 
EMBOLISM
(‘Embolus’ means in Greek—peg; first this term was used by Virchow in 1854)
It is due to a solid, liquid or gaseous, material which is floating and travelling in the bloodstream, eventually blocking the vessel on its pathway.
  • Arterial emboli:
  • Venous emboli are due to DVT causing pulmonary embolism.
  • Venous-arterial paradoxical emboli: Seen in intra-cardiac shunt (ASD) or intrapulmonary shunts (AV malformations) (Osler-Weber-Rendau syndrome).
  • Fat embolism.
  • Air embolism.
 
Effects of Arterial Embolism
191
 
Sites of Lodging of Emboli
The most common site is lower limbs (75%). 10% brain; 10% upper limb; 5% superior mesenteric and renal arteries.
In the lower limb the most common site is at the bifurcation of common femoral artery (40%); popliteal artery (15%); common iliac artery (12%); aortic bifurcation (10%).
 
Features of Embolism
  • Earlier history of claudication is absent but history suggestive of disease for source of emboli will be present.
  • Sudden, dramatic, rapid development of pain with numbness.
  • Limb becomes rapidly cold and mottled with blebs.
  • Loss of sensation and movements.
  • Absence of distal pulses but forcible, expansile, prominent proximal pulse. For example—prominent femoral artery pulsation with embolic bock at popliteal level.
  • Toxic features.
  • Collapsed veins, cold limb distal to the level of block, oedema and presence of blebs distally.
  • Muscle which is soft normally while palpating will feel doughy initially but later becomes stiff. Once stiffness of muscle is found embolectomy benefit is bleak.
Differences between embolism and thrombosis
Features
Embolism
Thrombosis
Source
Present
Not present
Pulse
Proximal and contralateral pulses normal
Same and opposite side pulses may be absent
Temperature
Severely cold
Cold or normal
Angiography
Sharp cut off sign
Diffuse tapered disease
Collaterals
Very few—not well-developed
Well-developed
 
Investigations for Arterial Embolism
  • Emergency Doppler angiogram, ECG and echocardiography. Angiogram is gold standard in all acute limb ischaemia. It differentiates between embolism and thrombosis; status of vessel proximally and distally. Angiography should ideally be done from contralateral limb or through left brachial.
    zoom view
    Fig. 1.345: Right leg showing features of acute embolism.
  • Relevant tests for origin of emboli. Prothrombin time, APTT, BT, CT, platelet count should be done.
Note:
Once embolism occurs irreversible changes occur distally in 6 hours, so ideal period for intervention is within 6 hours.
 
Classification of Severity of Acute Limb Ischaemia
Class I: Viable—no pain; no neurological deficit; Doppler shows audible signal. Venous flow present.
Class IIa: Marginally threatened—no pain; numbness/paraesthesia; no audible Doppler signal. Venous flow present.
Class IIb: Immediately threatened—persistent pain; sensory and motor loss; no Doppler signal. Venous flow present.
Class III: Irreversible—paralysis and anaesthesia. No venous flow.
Ischaemia up to class IIb with normal venous flow is called as Early; ischaemia which is class III, with muscle rigor, marbled skin and without any venous flow is Late. This late ischaemia is more likely to land with amputations even though revascularisation can be tried.
 
Treatment
 
Treatment of Embolism and Thrombosis of Acute Limb Ischaemia
Immediate infusion of 5000–10,000 units of IV heparin and relief of pain are needed first.
 
Surgical
  • Embolectomy (surgical exploration and removal of clot) is the choice for embolus. It is done either by interventional balloon 5 French (Fogarty, 1963) embolectomy or open method. It is the standard treatment for arterial embolism. It can be repeated several times until adequate bleeding occurs.
  • For acute thrombosis causing acute limb ischaemia, open thrombectomy with or without bypass may be the surgical treatment; but it is not the standard treatment for acute thrombosis (Standard is thrombolysis, Dotter and co, 1974).
 
Endovascular therapy
  • Intrarterial thrombolysis using urokinase.
  • Percutaneous mechanical thrombectomy—it is done either by suctioning clot via catheter or dissolution of thrombus by pulverisation and aspiration by high speed motors or fluid jets.
  • Ultrasound accelerated thrombolysis using catheter based or transdermal using acoustic cavitation to ablate thrombus.
Embolectomy
  • It is done as early as possible as an emergency operation.
  • Under fluoroscopic guidance, Fogarty catheter (interventional radiology) is passed beyond the embolus and balloon is inflated. Catheter is withdrawn out gently with embolus. Procedure has to be repeated until embolectomy is completed and good back bleeding occurs. Angiogram is repeated to confirm the free flow.
  • Postoperatively initially heparin and later oral anticoagulants are used. Procedure is done under general anaesthesia or local anaesthesia.
  • 192Open arteriotomy and embolectomy can be done by direct approach and later the arteriotomy has to be sutured. Postoperatively anticoagulants and antibiotics are given.
Intra-arterial thrombolysis using fibrinolysins
After passing arterial catheter, angiogram is done and agents are injected intra-arterially through the arterial catheter.
 
Drugs used are:
  • Streptokinase (Here lysis occurs in 48 hours). Dose is 2.5 lac IV over 30 minutes; or intra-arterialy 20,000 units/hour followed by one lac unit in 24 hours.
  • Urokinase. It is commonly used for thrombolysis. It converts plasminogen to plasmin which breaks fibrin clots. Initial bolus of 2,50,000 IU is given followed by an infusion of 4,000 IU/min for 4 hours, later continuous infusion of 2,000 IU/min to complete the lysis. Even though controversial, it is of usual practice to infuse 1000 IU/hour of heparin to prevent new thrombus formation. Check angiography should be done during therapy. Multiholed catheter (5 French) is used for infusion.
  • Tissue plasminogen activator (TPA)—Alteplase, Reteplase—here lysis occurs in 24 hours. TPA is better and ideal; but it is costly. It has very less side effects. TPA dose is 50 mg over 2 hours IV.
  • TPA pulse-spray method—here lysis occurs in 6 hours.
Advantages of thrombolysis
Disadvantages of thrombolysis
  • Gentle angiographic clot removal
  • Useful only for class I and IIa acute ischaemia
  • Survival and limb salvage is equal
  • Bleeding at the site and elsewhere is possible
  • It is mainly useful for acute thrombus
  • 25% rate of failure
  • For embolus it is used often as an adjunct along with embolectomy
  • It avoids surgery
 
Anticoagulant Therapy
  • It is to prevent recurrent emboli formation. Immediate infusion of heparin 5,000 units intravenously is helpful to prevent further extension of thrombus. Later oral anticoagulants may be added.
 
Complications of Revascularisation in Acutely Ischaemic Limb
  • Reperfusion injury
  • No reflow’ phenomenon: It is due to severe capillary oedema causing poor peripheral tissue hypoperfusion in spite of major vessel revascularisation.
  • Acute compartment syndrome can occur due to massive ischaemic oedema especially of skeletal muscles deep to deep fascia which compress on venules exceeding tissue interstitial pressure causing further compromise in tissue perfusion. Compartment pressure when measured using transducer needles will be more than 40 mmHg or > 30 mmHg for 3 hours or above the mean arterial pressure. Presents with muscle weakness, sensory changes, leg pain which is aggravated by dorsiflexion of toes.
  • Other complications are—sepsis, reblock, bleeding and catheter-related complications.
 
REPERFUSION INJURY
  • It occurs after reestablishment of arterial flow to an ischemic tissue bed which further leads to tissue death causing specifically peripheral muscle infarction. It is due to sudden release of oxygen free radicals which blocks the microcirculation, with release of high levels of potassium (hyperkalaemia) and myoglobin (myoglobinaemia and myoglobinuria). Haemodynamically patient becomes unstable with lactic acidosis, intracellular changes, interstitial oedema and cardiac dysfunction. It is often life-threatening.
  • Haimovici triad of revascularisation injury (1960)—(1) Muscle infarction; (2) Myoglobinuria; (3) Acute renal failure.
  • Severe ischaemia causes oedema in the muscular compartment with raise in compartment pressure more than the essential capillary perfusion pressure causing acute compartment syndrome. It is common in the anterior compartment of the leg. It is basically in the skeletal muscles deep to deep fascia. Compartment pressure when measured using transducer needles will be more than 40 mmHg or > 30 mmHg for 3 hours or above the mean arterial pressure. Muscle weakness, sensory changes, leg pain which is aggravated by dorsiflexion of toes.
  • ‘No re-flow’ phenomenon due to tissue oedema causes capillary perfusion block. Even though compartment syndrome and ‘no reflow’ phenomemenon are separate entities they are always seen together along with reperfusion injury.
  • Metabolic acidosis, acute tubular necrosis causing acute renal failure and cardiac arrhythmias may set in and become life-threatening.
  • Features are—toxaemia; oliguria; persistent pain and oedema in the leg with muscular tenderness; raised blood urea and serum creatinine with features of acute ischaemia in the limb. Raised creatinine level (renal failure), creatine kinase (muscle lysis) are typical.
  • Treatment:
    • Mannitol to prevent renal failure; fluid therapy.
    • Fasciotomy to reduce raised compartment pressure. All four compartments of lower limb should be decompressed surgically. Long vertical lateral deep fasciotomy incision in the calf behind the fibula along the deep fascia and its fibular attachments is a must. Bleeding is common after fasciotomy as patient is heparinised. Infection of the wound can occur. Later, once the patient is stabilised and oedema subsides with healthy wound, secondary suturing or skin grafting is done. If after fasciotomy, patient survives then it is with eventual development of Volkmann's ischaemic contracture.
    • Antibiotics and supportive therapy.
193
 
SADDLE EMBOLUS
It is an embolus blocking at bifurcation of aorta.
 
Causes
  • Mural thrombus after myocardial infarction.
  • Mitral stenosis with atrial fibrillation.
  • Aortic aneurysm.
    zoom view
    Fig. 1.346: Saddle embolus blocking the bifurcation of abdominal aorta. It causes severe, rapid, dramatic symptoms.
The embolus which blocks at aortic bifurcation is usually large.
 
Clinical Features
  • Features of sudden, rapidly progressive ischaemia in both lower limbs.
Note:
In aortic bifurcation thrombus, there is earlier history of claudication in the buttock often with Leriche's syndrome. Symptoms are slow and gradual but not dramatic. Collaterals between aorta and iliac arteries have well-formed and so sudden, rapid development of gangrene will not occur.
  • Gangrene of both lower limbs.
  • Features of associated infection.
 
Investigations
  • Arterial Doppler, aortic angiogram.
  • Ultrasound abdomen.
 
Treatment
  • Initially, heparin is injected intravenously—10,000 units and later 5,000 units subcutaneously 8th hourly.
  • Embolectomy can be done using Fogarty's catheter.
  • Open arteriotomy and embolectomy can also be tried.
  • Antibiotic prophylaxis is given to prevent infection.
 
EMBOLECTOMY
 
Indications
  • Acute embolic blockade of artery commonly seen in common femoral, cranial vessels, mesenteric vessels.
  • It should be done within 6 hours as after 6 hours irreversible changes occur—Golden hour.
  • It is usually done under local anaesthesia under C arm guidance with anaesthetist monitoring the patient. It can be done under spinal or general anaesthesia.
    zoom view
    Fig. 1.347: Embolectomy technique.
 
Methods
  • Interventional method is usually employed using Fogarty's catheter. Good back bleed signifies completeness of embolectomy.
  • Open arteriotomy method is done directly over the artery followed by suturing the artery.
Note:
  • Intraoperative arteriogram is a must to confirm the adequacy of blood flow and completion.
  • Intraoperative thrombolysis as an adjunct to save the limb using urokinase 2,50,000 IU for minutes into distal artery may be beneficial.
  • Prophylactic fasciotomy is needed in delayed cases to prevent reperfusion injury.
  • Postoperative systemic heparin and later oral anticoagulant is given.
  • Treatment for atrial fibrillation, atherosclerotic stenosis and other causes is needed.
194
zoom view
Figs 1.348A and B: Fogarty's catheter. It is 80 cm in length with 4 to 7 French size. It is used for embolectomy. Note the inflated balloon at the tip.
 
After Embolectomy
Patient is placed in ICU care.
Monitoring with—PTT, thromboplastin time.
 
FAT EMBOLISM (Ernst Von Bergmann, in 1873)
  • 90% of major trauma especially with fractures develop fat embolism from aggregation of fat globules and chylomicrons derived from bone marrow. Fat globules release fatty acids which act as toxins.
  • It is common in fracture long bones, and multiple fractures. It is observed after intramedullary nailing, liposuction, joint reconstruction, parenteral lipid infusion, cardiopulmonary bypass, and pathological fractures.
  • Only 5–10% will develop fat embolism syndrome (FES). FES shows respiratory distress (ARDS), and skin manifestations. Approximately 20–30% of the population have a patent foramen ovale; fat emboli pass through the pulmonary circulation causing the systemic manifestations of FES, particularly involving the brain and kidneys. As a result of the occluded cerebral vasculature, patients exhibit encephalopathy, localised cerebral edema. FES has got 20% mortality.
 
Features
  • Pulmonary: Cyanosis, tachypnoea, right heart failure, froth in mouth and nostrils, fat droplets in sputum, eventually respiratory failure.
  • Cutaneous: Petechial haemorrhages in the skin.
  • Cerebral: Drowsy, restlessness, disoriented, constricted pupils, pyrexia and coma.
  • Retinal artery emboli is the earliest sign to appear, causing striae haemorrhages, fluffy exudates confirmed on fundoscopic examination.
  • Kidney: Blockage in renal arterioles results in fat droplets in urine.
Gurd and Wilson criteria for FES
Major criteria
Minor criteria
  • Symptoms and radiologic evidence of respiratory insufficiency
  • Cerebral sequelae unrelated to head injury or other conditions
  • Petechial rash—over upper body, axillae
  • Tachycardia (heart rate >110/min)
  • Pyrexia (>38.5°C)
  • Retinal changes or petechiae
  • Renal dysfunction
  • Jaundice
  • Acute drop in hemoglobin level
  • Sudden thrombocytopaenia
  • Elevated erythrocyte sedimentation rate
  • Fat microglobulinaemia
 
Differential Diagnosis
  • Pulmonary embolism.
  • Thrombotic thrombocytopenic purpura.
 
Investigations
  • Presence of fat lobules in the blood obtained by pulmonary capillary wedging is diagnostic.
  • Haemoglobin estimation, platelet count and total WBC count.
  • Chest X-ray shows snow storm appearance.
  • CT chest is useful; CT head is done to rule out causes of intracranial injuries.
  • Transesophageal echocardiography (TEE) may be of use in evaluating the intraoperative release of marrow contents into the bloodstream during intramedullary reaming and nailing.
  • Bronchoalveolar lavage with staining for fat will show lipid inclusions.
 
Treatment
  • Adequate oxygenation with ventilator support (ICU care).
  • Hydration, nutrition, achieving haemodynamic stability, prevention of DVT, avoiding volume overload with proper fluid therapy.
  • Methylprednisolone may be useful; but use of heparin, low molecular dextran and other steroids are controversial even though commonly used.
  • Albumin transfusion may be helpful as it binds with fatty acids to reduce the lung injury.
  • Early fixation of the fractures; placement of IVC filters will prevent the chances of fat embolism or emboli reaching into the lungs.
195
 
AIR/GAS EMBOLISM
 
Causes
  • Through venous access like IV cannula, most common cause.
  • During artificial pneumothorax.
  • During surgeries of neck and axilla.
  • Traumatic opening of major veins sucking air inside, causing embolism.
  • During fallopian tube insufflation; laparoscopic surgeries.
  • During illegal abortion.
 
Features
It causes respiratory distress, haemoptysis, convulsions, unconsciousness, visual and hearing disturbances, fatigue and numbness, paralysis, haemodynamic instability and coma.
 
Treatment
  • Patient is placed in Trendelenburg left lateral decubitus position. The Trendelenburg position keeps left ventricular air bubble away from the coronary artery ostia (which are near the aortic valve) so that air bubbles do not enter and occlude the coronary arteries. Left lateral decubitus positioning helps to trap air in the non-dependent segment of the right ventricle (where it is more likely to remain instead of progressing into the pulmonary artery and occluding it). The left lateral decubitus position also prevents the air from passing through a potentially patent foramen ovale (present in as many as 30% of adults) and entering the left ventricle, from which it could then embolise to distal arteries.
  • Hyperbaric oxygen is useful in both venous and arterial gas/air embolism as it reduces the ischaemia, reduces the bubble size; in arterial gas embolism it removes the nitrogen from the bubble so that to improve perfusion and oxygenation.
  • By passing a needle, the air has to be aspirated from the right ventricle. Often requires life-saving open thoracotomy to aspirate the excess air causing the block.
 
THERAPEUTIC EMBOLISATION
 
Indications
  • Haemangiomas.
  • AV fistulas.
  • Malignancies like renal cell carcinoma, hepatoma.
  • Cerebrovascular problems.
  • To arrest haemorrhage from GIT, urinary and respiratory tract.
    • In bleeding duodenal ulcer or gastric ulcer, embolisation is done to occlude gastroduodenal artery or left gastric artery respectively.
    • It is also useful in bleeding oesophageal varices, secondaries in liver (mainly due to carcinoids), hepatoma.
 
CAISSON'S DISEASE OR DECOMPRESSION DISEASE
It occurs due to rapid decompression from high altitude, aircraft, compressed air chambers, deep sea divers causing bubbling of nitrogen which blocks the small vessels.
  • In joints and muscles it causes excruciating pain (bends).
  • Spinal cord ischaemia causing neurological deficits.
  • Lungs may be affected causing choking with chest pain, tightness and dry cough.
  • Treatment
    • Oxygen therapy.
    • Recompression and gradual decompression in special chamber.
 
ANEURYSM
It is an abnormal permanent dilatation of localised segment of arterial system. Diameter will be 50% more than expected normal diameter of that artery in aneurysm. Atherosclerosis which is the most common (90%) facilitating cause of aneurysm is due to destruction and loss of stability of tunica media.
True aneurysm contains all three layers of artery.
False aneurysm contains single layer of fibrous tissue as wall of the sac and it usually occurs after trauma.
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Fig. 1.349: True and false aneurysms. In true type, all layers are intact. In false type all layers breached with haematoma having a false capsule.
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Fig. 1.350: Fusiform and saccular types of aneurysms.
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Fig. 1.351: Thoracic aortic aneurysm.
 
Causes
  • Acquired:
    • Degenerative: Atherosclerosis (most common cause— 90%); mucoid degeneration of intima and media (in South African young Negroes).
    • Traumatic: Direct; indirect like in post-stenotic dilatation by cervical rib; traumatic AV aneurysmal sac; aneurysm due to irradiation (due to dryness and destruction of vasa vasorum causing weakening).
    • Infective: Syphilis; mycotic; tuberculosis (in lung); arteritis; acute sepsis.
    • Collagen diseases like Marfan‘s syndrome, polyarteritis nodosa, Ehler-Danos syndrome.
  • Congenital:
    • Berry aneurysm; cirsoid aneurysm; congenital AV fistula.
 
Sites
  • Aorta.
  • Femoral.
  • Popliteal.
  • Subclavian.
  • Cerebral, mesenteric, renal, splenic arteries.
Berry aneurysms are multiple aneurysms occurring in circle of Willis.
 
Clinical Features of Aneurysms
  • Swelling at the site which is pulsatile (expansile), smooth, soft, warm, compressible, with thrill on palpation and bruit on auscultation. Swelling reduces in size when pressed proximally.
  • Distal oedema due to venous compression.
  • Altered sensation due to compression of nerves.
  • Erosion into bones, joints, trachea or oesophagus.
  • Aneurysm with thrombosis can throw an embolus causing gangrene of toes, digits, extending often proximally also.
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Fig. 1.352: Chest X-ray showing aortic aneurysm.
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Figs 1.353A to D: Different methods of aneurysm repair. (A) Matas aneurysmorrhaphy for saccular aneurysm; (B) Excision and Dacron grafting; (C) Ligation and exclusion of the aneurysm using autologous vein graft; (D) Excision of aneurysm and bypass using autologous vein graft.
 
Differential Diagnosis
  • Pyogenic abscess: Abscess has to be always confirmed by aspiration; especially in axilla, popliteal region, groin.
  • Vascular tumours.
  • Pulsating tumours: Sarcomas, pulsating secondaries.
  • Pseudocyst of pancreas mimics aortic aneurysm.
  • AV fistula.
 
Investigations
  • Doppler study, duplex scan, angiogram, DSA.
  • Tests relevant for the cause, like blood sugar, lipid profile, echocardiography.
 
Treatment
  • Reconstruction of artery using arterial grafts.
  • Arterial endoaneurysmorrhaphy—MATAS. It is done usually for peripheral saccular aneurysm. Matas aneurysmorrhaphy may be restorative or endo-obliterative or reconstructive.
  • Therapeutic embolisation.
  • Clipping the vessel under guidance (e.g. cranial aneurysms).
  • Older methods which are now not used but popular earlier were—wiring of the aneurysmal sac/wrapping of the aneurysmal sac/ligatures at different levels (ligation just proximal to aneurysmal sac—Anel's; ligation proximally proximal to an arterial branch—Hunter's; ligation just distal to aneurysmal sac—Brasdor's; ligation distally distal to an arterial branch—Wardrop's; ligature one proximal and another distal to aneurysmal sac—Antylus').
 
MYCOTIC ANEURYSM
  • It is a misnomer.
  • It is not due to fungus but due to bacterial infection.
  • Common bacteria are gram-positive organisms like Staphylococcus aureus (most common) and Streptococcus.
  • Common aetiology is bacterial endocarditis but could be any infective site.
  • Common vessels involved are aorta, visceral, head and neck and intracranial.
  • Commonly it is saccular, multilobed, with a narrow neck.
  • Patient presents with fever, toxaemia and tender pulsatile mass if it is in the periphery.
  • Investigations: Leucocytosis. Positive blood culture, MR or CT angiogram are relevant.
 
Treatment
  • Broad-spectrum antibiotics
  • Resection of aneurysm; debridement and drainage of the infected aneurysm with adequate blood transfusions.
  • Extra-anatomic bypass through uninfected tissue planes to avoid contamination of the graft.
  • Long-term antibiotic therapy is necessary.
  • It has got 25% mortality.
Note:
Microbial arteritis with aneurysm is a different entity is due to bacteraemia occurring in an atherosclerotic vessel due to Salmonella infection).
 
ABDOMINAL ANEURYSM
  • Abdominal aortic aneurysm is the most common aortic aneurysm.
  • Splenic artery aneurysm is the 2nd most common type.
  • Incidence is 2%. It is more common in males.
  • Transverse diameter of aorta in an aneurysm should be 3 cm or more.
  • Common in elderly; common in males (4:1); chance of getting aneurysm in genetically related first degree relatives is 10 times more.
  • 198Common in smokers (8:1with nonsmokers); in 55% of patients Chlamydia pneumoniae is identified.
Note:
Smoking is an important factor.
 
ABDOMINAL AORTIC ANEURYSM (AAA)
 
Causes
  • Atherosclerosis (as degenerative process) is the most common facilitating cause (95%)—aortic wall contains smooth muscle cell matrix, elastin, collagen; elastin (in tunica media) is the main load bearing part with collagen (in adventitia) as safe net in the wall to provide tensile strength preventing aneurysm formation. Elastin in medial layer of aorta is degraded and reduced significantly in infrarenal aorta in relation to collagen, absence or less vasa vasorum in infrarenal aorta and atherosclerotic unstability of the medial wall of aorta cause infrarenal aorta more prone to develop aneurysm. Increased proteolytic activity of aortic medial wall due to increased matrix metalloproteinases (MMP) (derived from aortic smooth muscle cells and macrophages) cause elastin and collagen degradation and increase in diameter of aneurysm. Collagen degradation in adventitia causes rupture.
  • Familial aortic aneurysm (associated with 25% of AAA) is more prevalent in females to reduce male-to-female ratio to 2:1. It is related to decrease in type III collagen, α1 antitrypsin and lysyl oxidase. Marfan's, Ehler Danlos syndromes are related genetically.
  • Others: Syphilis, dissection, trauma, collagen diseases, infection, arteritis, cystic medial necrosis, association with Chlamydia pneumoniae (55%).
 
Asymptomatic Type
  • It is found incidentally either on clinical examination or on angiography or on ultrasound.
  • Repair is required if diameter is over 5.5 cm on ultrasound.
  • It is identified during routine abdominal palpation or while assessing or operating for some other abdominal conditions.
 
Symptomatic without Rupture (Clinical features/presentations)
  • It presents as back pain, abdominal pain, mass abdomen which is smooth, soft, nonmobile, not moving with respiration, vertically placed above the umbilical level, pulsatile both in supine as well as knee-elbow position with same intensity, resonant on percussion.
  • Common in males (4:1); common in smokers.
  • GIT, urinary, venous symptoms can also occur.
  • Hypertension, diabetes, cardiac problems should be looked for and dealt with.
  • In infrarenal type upper border is clearly felt.
  • Lower limb ischaemia and embolic episodes can occur.
  • Being a retroperitoneal mass back pain is common—may be due to retroperitoneal stretching, nerve irritation or vertebral erosion.
  • 5% present as inflammatory aneurysm adherent to ureters, left renal vein, inferior vena cava and duodenum. Expanding aneurysm blocks lymphatics causing inflammation and fibrosis; or it may be due to infection and fibrosis of earlier localised ruptured abdominal aortic aneurysm. Such chronically inflamed aneurysm will not rupture further; but it is always symptomatic with fever and severe pain in abdomen and back. It needs surgical repair through retroperitoneal approach.
  • Aortocaval fistula, presents as high output cardiac failure with continuous bruit in abdomen and severe lower limb ischaemia (steal phenomenon).
  • Aortoenteric fistula is due to erosion of aneurysm into 4th part of duodenum presenting as GI bleed, malaena, shock. It is treated by duodenal closure, aortic ligation, aneurysmal exclusion with extra-anatomic bypass graft with gastrojejunostomy. Contamination is the major threat here.
  • Aneurysm in a patient with horseshoe kidney which is anterior to aorta is difficult to manage. Left retroperitoneal approach is needed. EVAR is not possible.
 
Investigations
  • Blood urea, serum creatinine.
  • US (most widely used noninvasive test; but neck of the aneurysm, dimensions and relation to renal arteries are difficult to assess), aortogram, DSA, CT scan (most precise). US is an effective screening tool. Screening is done in cardiovascular patients in men (60–85 years), in women (60–85 years); men and women above 50 years with family history; annually in asymptomatic AAA with 4.0–4.5 cm size, with size >4.5 cm once in every 6 months.
  • CT angiogram, MR angiogram.
  • Blood sugar, lipid profile, other relevant investigations like ECG, echocardiography, cardiac and pulmonary assessment.
Note:
X-ray will show eggshell calcification. CT scan is more reliable and precise investigation of choice—gives better information regarding extent on sides/neck, size, dimensions, size and site of the thrombus, calcification, relation of renal arteries, inflammation and fibrosis and adjacent tissues. MRI may be better only in renal failure patients.
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Figs 1.354A and B: USG abdomen showing abdominal aortic aneurysm.
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Fig. 1.355: Abdominal aortic aneurysm showing widened aortic wall with thrombosis in the periphery in CT angiogram.
 
Differential Diagnosis
  • Retroperitoneal mass, pseudocyst of pancreas, retroperitoneal cyst mimic abdominal aortic aneurysm especially when it is thrombosed.
  • Mesenteric ischaemia, acute pancreatitis, perforated duodenal ulcer may mimic ruptured aneurysm.
  • Other conditions causing back pain like disc prolapse, sciatica.
 
Treatment
 
Conservative/Medical Treatment
  • It is done in low-risk abdominal aortic aneurysm (age below 70 years; active physically without cardiac, respiratory, renal impairment and noninflammatory aneurysm); if aneurysm size is < 5 cm; if growth rate is < 0.5 cm/year.
  • It includes risk factor modifications; stopping smoking; control of blood pressure (propranolol), cholesterol; usage of drugs—alpha blockers, elastase inhibitors (NSAID—indomethacin), matrix metalloproteinases (MMP) inhibitor (doxycycline).
  • Periodic size measurement of an aneurysm using ultrasound once in 6 months to find out growth rate is essential during conservative treatment.
 
Surgical Treatment
  • Indications for surgery
    • Asymptomatic aneurysm more than 5.5 cm.
    • Growth rate more than 0.5 cm/year.
    • Painful, tender aneurysm.
    • Thrombosed aneurysm, aneurysm with distal emboli.
  • Open surgical repair
    • It is called as endo-aneurysmorrhaphy with intraluminal graft placement (Crawford, 1960). It is done under GA with epidural support. Major challenges during anaesthesia are—blood loss, haemodynamic control, problems during clamping and declamping of aorta, temperature control, renal hypoperfusion, left ventricular strain.
    • Incision is commonly lengthy midline transperitoneal or supraumbilical transverse. Retroperitoneal approach is used in horseshoe kidney, abdominal wall stoma, inflammatory aneurysm, suprarenal extension, peritoneal dialysis, hostile abdomen. Retroperitoneal approach favors rapid control of proximal aorta but prevents visualisation of abdomen.
    • After laparotomy, duodenum and small bowel are retracted laterally and above; left renal vein which is in front of aorta is dissected and retracted; occasionally it may require to be ligated and it is safer provided left gonadal and left suprarenal veins are intact. Distal arterial clamps are applied first along common or external and internal iliac arteries on both sides. Proximal aortic clamp is applied at infrarenal level. Aorta is opened longitudinally midline towards right to avoid injury to orifice of inferior mesenteric artery. Atheroma, thrombus is removed until adequate back-bleeding occurs. Lumbar vessels are ligated from the luminal side. Knitted Dacron graft after preclotting or woven Dacron graft or ePTFE tube graft is used. Graft is anastomosed above and below using 200polypropylene sutures (4 zero). Inferior mesenteric artery can be reimplanted. Clamps are released first below. Colonic and limb perfusion is checked for adequacy. Graft is covered with aneurysmal sac.
    • Minimal incision aortic surgery (MIAS) is done in thin individual with midline abdominal incision 12 cm in length with its 9 cm part above the umbilicus. Specialised retractors and vascular clamps are used for this. Advantages are less postoperative pain, ileus and incisional hernia.
  • Endovascular aneurysm repair (EVAR)
    • In 1991 Juan Parodi and Julio Palmaz first did EVAR. It is less invasive, less morbid with less mortality rate and shorter hospital stay. It is basically aneurysm exclusion method. It is useful in old age and patients who are not fit for surgery. EVAR is basically a prophylactic procedure. EVAR is indicated if aneurysm is less than 5.5 cm in men and less than 5.0 cm in women. It is usually done in patients after 65 years.
    • It is endoluminal stent graft placement into the aneurysmal segment of aorta using interventional radiology with Seldinger's technique approach through femoral artery.
    • Dacron or ePTFE with integral metallic stent for support and firm attachment is used as stent/endovascular prosthesis.
    • One aortic and iliac (of one/same side) stent is commonly used together which is passed through same side common femoral. Other iliac is maintained with a separate stent approached through opposite common femoral.
    • Procedure can cause endoleak, thrombosis, embolism, malposition/displacement of stent, sigmoid ischaemia, renal failure, failure of stent function causing recurrence and infection.
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Figs 1.356A and B: Aorto bifemoral dacron graft (Woven) with right femoral exposed
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Figs 1.356A to C: Abdominal aortic aneurysm with aortofemoral graft placement(Courtesy: Dr Ashok Shetty, mch, Cardiothoracic Surgeon, Mangaluru).
 
Symptomatic Ruptured Aortic Aneurysm
  • Risk of rupture is 1%, if diameter is within 5.5 cm in size. Risk increases to 20% once the diameter = 7 cm.
It may be anterior rupture (20%) into the free peritoneal cavity causing severe shock and death very early; or posterior rupture (80%) with formation of retroperitoneal haematoma of large size causing severe back pain, hypotension, shock, absence of femoral pulses and with a palpable mass in the abdomen.
  • Management of Ruptured Aortic Aneurysm
    • Immediate diagnosis by ultrasound.
    • Resuscitation.
    • Massive blood transfusions (10–15 bottles).
    • Emergency surgery is the only life-saving procedure in these cases.
Patient has to be shifted to the operation theatre. Abdomen is opened. Vascular clamps or bull dog clamps are applied to the aorta above and below the aneurysm. Adventitia is opened and the clot is removed. Aneurysm is excised and the arterial graft either PTFE (Polytetrafluoroethylene), knitted dacron graft, or woven dacron graft is placed. The graft is sutured to the vessel above and below using monofilament, nonabsorbable suture material, polypropylene 5-zero.
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Fig. 1.357: Infrarenal aortic aneurysm repair. It is the most common site of aortic aneurysm. Adventitia of aorta is opened; aneurysm is excised; graft is sutured above and below; adventitia is wrapped around.
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Figs 1.358A and B: Endovascular aneurysm repair (EVAR). Aortic and one side iliac stent is used as one unit modulus which is passed through same side common femoral artery; opposite side iliac part is inserted as separate modulus through opposite CFA.
 
PERIPHERAL ANEURYSM
  • Peripheral aneurysms are less common compared to aneurysms in the cavity. Such surface aneurysms are easily visible and better amenable for clinical examination. But same time it may be mistaken for abscess and inadvertent wrong attempt of incision and drainage can occur leading to disastrous consequences.
  • Popliteal type is the most common one. Peripheral aneurysms occur in descending order of frequency in popliteal, femoral, subclavian, axillary and carotid arteries.
  • Expansile pulsation which is confirmed using two finger placement with thrill and bruit is typical. Infection, thrombosis make it less pulsatile mimicking an abscess.
  • Erosion into adjacent bone and skin, rupture are known to occur. Distal emboli may lead into digital gangrene.
  • Pressure on the affected artery proximally reduces the size, and eliminates the thrill/bruit; pressure distal to aneurysm increases the prominence of the aneurysm swelling with bounding pulsation.
  • 202X-ray, arterial Doppler, angiogram, echocardiogram are needed.
  • Treatment is open repair using arterial graft or endovascular stenting.
 
Popliteal Aneurysm
  • Is most common (70%).
  • 65% are bilateral.
  • 25% cases are associated with abdominal aortic aneurysm.
  • 75% cause complications in 5 years.
 
Presentations
  • Swelling in popliteal region which is smooth, soft, pulsatile, well-localised, warm, compressible, often with thrill and bruit. It may mimic a pyogenic abscess.
  • Thrombosis and emboli from popliteal aneurysm can cause distal gangrene which may spread proximally and may lead to amputation.
  • Rupture may cause torrential haemorrhage.
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    Fig. 1.359: Femoral artery aneurysm with impending rupture—needs emergency surgical intervention. It is rare type.
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    Fig. 1.360: Popliteal aneurysm about to rupture. It is the most common peripheral aneurysm.
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    Fig. 1.361: Radial artery aneurysm.
  • Investigations
    • Duplex scan, angiogram.
    • CT scan, MRI.
  • Treatment
    • Aneurysmorrhaphy.
    • Repair with arterial graft using PTFE, Dacron.
    • Endoluminal stenting.
 
CAROTID ARTERY ANEURYSM (EXTRACRANIAL)
Incidence is less than 4% of peripheral aneurysms.
Most common site: Common carotid artery bulb, often extends into the internal carotid artery.
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Fig. 1.362: Carotid aneurysm.
 
Causes
  • Atherosclerosis, trauma.
  • Syphilis, Marfan's syndrome.
  • Ehler-Danlos syndrome.
  • Congenital.
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Differential Diagnosis
  • Carotid body tumour.
  • Neurofibroma arising from the vagus.
  • Abscess in neck.
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    Figs 1.363A and B: Basilar artery aneurysm—angiogram (Courtesty: Dr Muralidhar Pai, MCh, Mangaluru ).
 
Complications
  • Rupture.
  • Thrombosis.
  • Hemiplegia.
 
Investigations
  • Doppler of neck, carotid angiogram.
  • DSA, CT angiogram.
 
Treatment
  • Reconstruction of the artery using vascular graft.
  • Ligation of the bulb as a life-saving procedure, but results in hemiplegia.
  • Intravascular stents.
 
DISSECTING ANEURYSM
It is a misnomer. It is not an aneurysm, only an aortic dissection.
It is the dissection of media of the aorta after splitting through intima creating a channel in the media of the vessel wall.
 
Causes
  • Hypertension (It is associated in 80% of dissecting aneurysms).
  • Cystic medial necrosis.
  • Marfan's syndrome and collagen diseases.
  • Trauma.
  • Weakening of the elastic layers of the media due to shear forces.
 
Features
  • It is always seen in thoracic aorta, common in ascending aorta (70%).
  • It is uncommon in other parts of aorta or other vessels.
  • It can occur in aortic arch or thoracic descending aorta.
  • This dissected aortic channel gets lined by endothelium, often reopens distally into the aorta causing double-barrelled aorta which, in fact, prevents complications.
  • It is commonly associated with aortic insufficiency.
Atherosclerosis is not a usual cause for dissecting aneurysm.
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Fig. 1.364: Dissecting aneurysm.
 
Clinical Features
  • Pain in the chest, back which is excruciating.
  • Features of ischaemia due to blockage of different vessels.
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Treatment
Antihypertensives.
Surgery: Using Dacron graft reconstruction of aorta has to be done with cardiopulmonary bypass.
 
ERYTHROMELALGIA (ERYTHRALGIA)
  • It is also called as Mitchell's disease; an episodic attack precipitated by heat, exertion and stress; common in lower limbs. Primary type is familial and autosomal dominant. Secondary type is seen in gout, erythrocyanosis frigida, polycythaemia, viral infection, mushroom poisoning, drug induced (verapamil, ergots, fluoroquinolines). There is microvascular and neuropathic changes.
  • There is severe burning pain in the limbs with redness and sensation of heat. Warmness in the skin; often excoriation or ulceration, flushing, prominent veins, severe hyperesthesia are the usual features.
  • Treatment: Mechanical cooling by elevating the limb (Note: Should not place the affected limb in cold water which may flare up the problems); aspirin; pregabalin, gabapentin, IV lignocaine are different drugs used in this condition.
 
LIVEDO RETICULARIS
It is a condition with arteriolar spasm along with obstruction of capillaries by tiny blood clots with dilatation of venules, causing lace like purplish discoloration. Persistent, mottled, reddish-blue dermal streaks that do not blanche is typical. It may be idiopathic or related to vasculitis due to autoimmune conditions along with SLE or drug induced. Condition worsens by cold. Treating the cause; PUVA bath; warming the limb; exercise are different therapies.
 
POLYARTERITIS NODOSA
  • It is a necrotising inflammatory reaction with commonly microscopic polyarteritis and nodule formation, often of small and medium-sized arteries (not capillaries), causing ischaemia of lower and upper limb.
  • Visceral arterial (mesenteric) involvement (70%) can cause abdominal pain, GI bleed; mucosal ulceration and perforation of small bowel. Massive hepatic infarction, cholecystitis can develop.
  • Renal artery can cause loin pain, haematuria, and renal hypertension.
  • Coronary artery also can get involved causing myocardial infarction.
  • Disease is common at bifurcation of medium/small sized arteries leading to localised aneurysms.
  • It is common in males (3:1); fever, weakness, myalgia, arthralgia are early features.
  • Presents with localised small aneurysms, like multiple 5–10 mm nodules, palpable along the course of the artery.
  • In late stage presents with myocardial infarction, renal failure, sepsis, GI bled.
  • HBsAg is positive in 40% patients of polyarteritis nodosa.
  • Angiogram of renal, mesenteric, peripheral arteries will show aneurysms at branching points.
  • Biopsy of tender nodule, tender muscle is useful for diagnosis.
  • Treatment is prednisolone 60 mg daily with cytotoxic drugs.
  • Prognosis is poor with rapid death in early years.
 
SCLERODERMA/SYSTEMIC SCLEROSIS
  • It is a progressive disease causing fibrosis of skin, GI tract, lungs, heart and kidney.
  • It is common in females (4:1) at 4th/5th decade.
  • It is considered as vasculitis even though earlier considered as collagen disease.
  • Pathology consists of cytotoxic endothelial injury causing interstitial oedema, severe fibroblast proliferation causing fibrosis of affected vessels, and dilatation and proliferation of remaining capillaries as telangiectasis.
  • Thin epidermis, thick dermis with more collagen with absence of appendages and rete pegs are typical.
  • Lower 2/3rd oesophagus is sclerosed (50%) with increased collagen in submucosa with atrophied mucosa and muscularis. Dysphagia is common.
  • Diffuse interstitial fibrosis, thickening of alveolar membrane and pulmonary hypertension occurs.
  • Synovial thickening causes arthritis; fibrosis of skeletal muscles; interstitial myocardial fibrosis causes bundle branch block, pericardial effusion.
  • Glomerulosclerosis in kidney is common (50%). Renal failure is common.
  • Fibrosis of thyroid, periodontal membrane can occur. Malabsorption syndrome is common due to small bowel involvement.
  • Involvement of digital arteries present as Raynaud's phenomenon.
  • Calcinosis, Raynaud's, oesophageal hypomotility, sclerodactyly, and telangiectasia are the presentation of CREST syndrome.
  • Investigations—anaemia, raised ESR, elevated IgG, presence of antinuclear antibodies and anticentromere antibodies (in CREST)—are different laboratory findings. Skin and peripheral arterial biopsy is confirmative.
  • Treatment—is difficult. Drugs like D pencillamine, colchicines, p amino benzoic acid, vitamin E, dimethyl sulfoxide, ranitidine are tried at various levels. Vasodilators, warming and massaging skin, avoiding detergent soaps, oil and hydrophilic ointment application are used.
    Steroids, oxygen therapy for irreversible pulmonary fibrosis; haemodialysis for renal failure; digitalis and other drugs for cardiac failure are needed later.
  • Death is due to cardiac/pulmonary/renal failure.
 
ACROCYANOSIS (CRURUM PUELLARUM FRIGIDUM)
  • It is persistent, painless cyanosis seen in fingers and often in legs with paraesthesia and chilblains affecting young females.
  • It is chronic persistent arteriolar constriction with slow rate of blood flow.
  • Trophic changes and ulcerations are not seen.
  • Cyanosis which is persisting may aggravate on exposure to cold.
  • It may be associated with endocrine dysfunction.
 
Treatment
  • Vasodilators.
  • Cervical sympathectomy (effective).
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Raynaud's phenomenon
Acrocyanosis
  • Episodic
  • Persistent
  • Painful
  • Painless
  • Acute arteriolar spasm
  • Chronic constriction
  • Ischaemic changes are common
  • Ischaemic changes are not seen
 
GANGRENE
It is macroscopic death of tissue in situ (in continuity with adjacent viable tissue) with putrefaction (there will be loss of function also).
 
Causes
  • Secondary to arterial occlusion like atherosclerosis, emboli, diabetes, TAO, Raynaud's disease, ergots.
  • Infective: Boil, carbuncle, gas gangrene, Fournier's gangrene, cancrum oris.
  • Traumatic: Direct, indirect.
  • Physical: Burns, scalds, frostbite, chemicals, irradiation, electrical.
  • Venous gangrene.
 
Clinical Features
  • Colour changes: Pallor, greyish, purple, brownish black due to disintegration of haemoglobin to sulphide.
  • Absence of pulse, loss of sensation, loss of function.
  • Line of demarcation between viable and dead tissue by a band of hyperaemia and hyperaesthesia along with development of a layer of granulation tissue.
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Fig. 1.365: Gangrene foot with ischaemic ulcer.
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Fig. 1.366: Dry gangrene—great toe.
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Figs 1.367A and B: Gangrene of foot and leg. Note the line of demarcation. But skip lesion proximally shown signifies more proximal spread of gangrene which may need above knee amputation.
In dry gangrene the separation occurs by aseptic ulceration with minimum infection and the gangrene is dry and mummified.
In wet gangrene, separation takes place by septic ulceration. Often demarcation is vague with skip lesions more proximally and so landing with higher level of amputations. Even after amputation skin flap may show die back process, leading to failure of taking up of flap of amputation and so requiring still higher level of amputation.
  • Proximal ischaemic features may be present with rest pain, colour changes, hyperaesthesia—pregangrene.
 
Investigations
  • Hb%, blood sugar.
  • Arterial Doppler, angiogram (Seldinger technique).
  • US abdomen to find out the status of aorta.
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Differences between dry gangrene and wet gangrene
Dry gangrene
Wet gangrene (Moist)
Clear line of demarcation is seen
Line of demarcation is vague
Dry, shriveled, mummified
Oedmatous, putrified, discoloured (H2S)
Slow, gradual loss of blood supply
Sudden loss of blood supply
Separation is by aseptic ulceration
Septic ulceration causes separation
Limits to the demarcation
Can extend proximally rapidly
Causes are atherosclerosis, TAO
Emboli, trauma are the causes
Limited amputation is sufficient
Major higher amputation is often needed
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Fig. 1.368: Ischaemic features of right hand; compare to left side which is normal.
 
Treatment
Limb saving methods:
  • Drugs: Antibiotics, vasodilators, pentoxiphylline, praxilene, dipyridamole, small dose of aspirin, ticlopidine.
  • Care of feet and toes:
    • The part has to be kept dry.
    • Any injury has to be avoided.
    • Proper footwear is advised (Microcellular rubber footwear, MCR).
    • Measures for pain relief is taken.
    • Nutrition supplementation is done.
    • The limb should not be warmed.
    • Pressure areas has to be protected.
    • Localised pus has to be drained.
  • Cause is treated.
  • Diabetes is controlled.
  • Surgeries to improve the limb perfusion: Lumbar sympathectomy, omentoplasty.
Profundaplasty, femoropopliteal thrombectomy or endarterectomy, arterial graft bypass are done according to the need.
Life-saving procedures:
Amputations may have to be done ofen.
Level of amputation is decided on skin changes, temperature, line of demarcation, Doppler study.
  • Below-knee amputation is a better option as BK prosthesis can be fitted better and also the movements of knee joint are retained. There is no need of external support and limp is absent.
  • In above-knee amputation range of movements are less, limp is present, and often requires third (stick) support to walk.
Different amputations done are Ray amputation, below-knee amputation (Buerger's amputation), Gritti-Stokes transgenial amputation, above-knee amputation.
Lisfranc's, Chopart's, Symes', Modified Symes' amputations are not commonly used in ischaemic limb as flaps will not survive.
 
DIABETIC FOOT AND DIABETIC GANGRENE
Foot is a complex structure with many layers of muscles, ligaments, joints, arches, fat, thick plantar fascia, vascular arches, neurological system which maintains weight-bearing, gravity, normal walk, stability and gait (swing and stance phases).
 
Pathogenesis of Diabetic Foot/Gangrene
  • High glucose level in tissues is a good culture media for bacteria. So infection is common.
  • Diabetic microangiopathy causes blockade of microcirculation leading to hypoxia.
  • Diabetic neuropathy: Due to sensory neuropathy, minor injuries are not noticed and so infection occurs. Due to motor 207neuropathy, dysfunction of muscles, arches of foot and joints occurs. And loss of reflexes of foot occurs causing more prone for trauma and abscess. Due to autonomic neuropathy, skin will be dry, causing defective skin barrier and so more prone for infection.
  • Diabetic atherosclerosis itself reduces the blood supply and causes gangrene. Thrombosis can be precipitated by infection causing infective gangrene. Blockage occurs at plantar, tibial, and dorsalis pedis vessels.
  • Increased glycosylated haemoglobin in blood causes defective oxygen dissociation leading to more hypoxia. At tissue level there will be increased glycosylated tissue proteins, which prevents proper oxygen utilisation and so aggravates hypoxia.
 
Clinical Features
  • Pain in the foot.
  • Ulceration.
  • Absence of sensation.
  • Absence of pulsations in the foot (Posterior tibial and dorsalis pedis arteries).
  • Loss of joint movements.
  • Abscess formation.
  • Change in temperature and colour when gangrene sets in.
  • Patient may succumb to ketoacidosis, septicaemia or myocardial infarction.
 
Investigations
  • Blood sugar, urine ketone bodies.
  • Blood urea and serum creatinine.
  • X-ray of part to look for osteomyelitis.
  • Pus for culture and sensitivity.
  • Doppler study of lower limb to assess arterial patency.
  • Angiogram to look for proximal blockage.
  • Ultrasound of abdomen to see the status of abdominal aorta.
  • Glycosylated haemoglobin estimation.
 
Treatment
  • Foot can be saved only if there is good blood supply.
    • Antibiotics—decided by pus C/S.
    • Regular dressing.
    • Drugs: Vasodilators, pentoxiphylline, dipyridamole, low dose aspirin.
    • Diabetes is controlled by insulin only.
    • Diet control, control of obesity.
    • Surgical debridement of wound.
    • Amputations of the gangrenous area. Level of amputation has to be decided by skin changes and temperature changes or Doppler study.
    • Care of feet in diabetic:
      • Any injury has to be avoided.
      • MCR footwears must be used (Microcellular rubber).
      • Feet has to be kept clean and dry, especially the toes and clefts.
      • Hyperkeratosis has to be avoided.
zoom view
Fig. 1.369: Diabetic foot with ischaemic ulceration and gangrene.
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Fig. 1.370: Gangrene of 3rd and 5th toes in a diabetic. Patient already underwent amputation of 4 the toe earlier for gangrene.
 
TROPHIC ULCER
  • Aetiology: Diabetic neuropathy, spinal injury and diseases, other neuropathies.
  • Common Sites: Heel, heads of metatarsals, sacrum, ischium, occipital region. Bedsore is a trophic ulcer.
  • Clinical Features: They are deep, punched out, nonmobile ulcers, with bone as its base.
  • Investigations: X-ray spine, nerve conduction studies, blood sugar, Hb%.
  • Treatment
    • 208Nutrition is improved.
    • Anaemia is treated.
    • Diabetes is controlled.
    • Regular dressing is done.
    • Pressure and injuries has to be avoided.
 
BEDSORES (Decubitus Ulcer) (Pressure Sores)
Bedsore is a trophic ulcer with bone as the base.
It is nonmobile, deep, punched out ulcer.
It is common in
Old age Bedridden
Tetanus
Patients with orthopaedic and head injuries
Diabetic Paraplegic
Comatose
Sites of bedsore are occiput, heel, sacrum, ischium, scapula.
Factors: Malnutrition, pressure, anaemia, sensory loss, moisture.
zoom view
Fig. 1.371: Large bedsore over the sacrum in a abedridden patient. Note the size and slough on the surface.
 
Treatment
  • Change of positions is always encouraged.
  • Use of water bed, ripple bed is advised.
  • Moisture has to be avoided.
  • Soaking by urine, sweat, pus, and faeces has to be taken care off.
  • Good nursing, regular dressing, good nutrition are necessary.
  • Antibiotics, blood transfusions are very essential.
  • Excision of dead tissue followed by skin grafting or local rotation flaps may have to be done.
  • Rehabilitation.
 
FROSTBITE
  • It is due to exposure to cold wind or high altitude.
  • It is common in old age during cold spells.
  • Damage to vessel wall occurs causing oedema, blistering, gangrene formation.
  • Part is painless and waxy.
  • Cells get frozen at – 5°C. Initially redness and oedema (1st degree); blister formation (2nd degree); skin necrosis (3rd degree); gangrene (4th degree) develops gradually.
 
Treatment
  • Gradual warming is done. Part should be wrapped with cottonwool and rested. Warming is gradually done with 44°C in 30 minutes with warm water. Limb elevation is done to reduce oedema. Intra-arterial vasodilators may help.
  • Warm drinks, analgesics, paravertebral injections to sympathetic chain, hyperbaric oxygen are effective.
  • If gangrene develops, amputation is needed.
 
AINHUM
Ainhum also known as ‘dactylolysis spontanea’ is a painful constriction of the base of the fifth toe frequently (occasionally other toes also) followed by bilateral spontaneous auto-amputation a few years later. Grooving → pain → constriction deepens → tendon, nerve and vessel involvement → bone gets cut spontaneously without any bleeding (auto-amputation) in many (2–5) years.
  • Commonly affects males (can also occur in females).
  • Common in blacks, in Negroes.
  • History of running barefoot in childhood is common.
  • Fifth toe is commonly affected.
  • A fissure develops at the interphalangeal joint which becomes a fibrous band, that encircles the digit causing necrosis (Gangrene of little toe).
  • Often it can be bilateral.
zoom view
Fig. 1.372: Bilateral Ainhum involving 4th and 5th toes of both feet. Note the constriction ring in the toes.
Treatment: It is early “Z” plasty. Amputation is often required later. Most often autoamputation occurs.
Note:
Yoruba people of Nigeria named ainhum.
 
ENDOVASCULAR SURGERIES
It is mainly used in peripheral vessels like femoropopliteal, renal, coronary, cerebral vessels.
 
Types
  • Balloon angioplasty: It is useful in short segment stenosis in large vessles like renal vessels, iliofemoral, coronary vessels. It is less effective compared to open surgery.
  • Intravascular stenting: Balloon expandable and self-expanding stents are used at stenosed area.
  • Endovascular grafts (PTFE, DACRON).
  • 209Endovascular atherectomy.
  • Angioscopy: Flexible, small, fibreoptic scopes to visualise vessel wall with sufficient irrigation to avoid opacification by blood.
  • Intravascular ultrasound: To evaluate the vessel wall morphology.
 
Complications
  • Thrombosis.
  • Rupture.
  • Sepsis.
  • Fluid overload.
  • Air embolism.
 
UPPER LIMB ISCHAEMIA
It is a rare uncommon entity compared to lower limb ischaemia but important because of its difficulty in managing. Higher-level amputations are rare in upper limb ischaemia.
Its incidence is rare (5%) due to abundant collateral supply, infrequency of atherosclerosis, decreased metabolic demand and smaller muscle mass.
It mostly affects distal small arteries (90%).
Symptoms are usually delayed.
 
Types of Upper Limb Ischaemia
  • Acute.
  • Chronic.
 
Acute type
Causes:
  • Embolism—common: 30% of the peripheral emboli lodge in upper extremity. The most common site is at the bifurcation of brachial artery (40%); next common is at axillary artery (12%). Embolism is due to:
    • Cardiac origin (70%)—valvular lesions (atrial fibrillation, endocarditis), IHD, paradoxical.
    • Others—aneurysms, thoracic outlet syndrome, plaque.
  • Trauma—most common: Brachial artery injury is seen in 30% of civilian trauma with arterial injuries, blunt injuries, fractures and dislocations, penetrating injuries.
  • Iatrogenic.
  • Post AV fistula ‘Steal syndrome’.
  • Aortic dissection.
zoom view
Fig. 1.373: Upper limb ischaemia with gangrene extending proximally towards elbow joint.
 
Chronic Type
Causes:
  • Arteritis—aortoarteritis, Takayasu arteritis, giant cell arteritis, connective tissue disease/vasculitis—scleroderma, SLE, RA, PAN, etc.
  • Atherosclerosis—most common cause in USA.
  • TAO of upper limb.
  • Others—fibromuscular dysplasia; postirradiation—lung, breast; occupational injuries; vibration injury, hypothenar hammer syndrome; hypercoagulable states; APLA, polycythemia, cold agglutinins.
 
Raynaud's Phenomenon
  • It is episodic vasospasm. It is common in upper limb.
  • Raynaud's disease: It is primary Raynaud's phenomenon—no cause could be demonstrated (Idiopathic).
  • Raynaud's syndrome: It is secondary Raynaud's phenomenon—secondary to a demonstrable lesion like SLE, scleroderma, TAO or atherosclerosis.
  • Symptoms: Pain, discolouration, sensation of cold and numbness, pronounced on exposure to cold, and under stress.
  • Signs: Cyclical colour changes—Pallor, Cyanosis and Rubor with swelling; seen in fingers, toes, nose, ear lobes and lips.
  • Pathology of Raynaud's phenomenon: Exaggerated vasomotor response to stress; more common in females; no structural changes in the vessels, except in late stages; recurrent attacks can lead to atrophy of skin, subcutaneous tissue and muscles, ischaemic ulcers and gangrene.
210
zoom view
Fig. 1.374: Left upper limb ischaemia with gangrene of three fingers and ischaemic changes in hand, forearm and arm.
zoom view
Fig. 1.375: Gangrene of left index finger. Patient has undergone cervical sympathectomy.
 
Investigations in Upper Limb Ischaemia
  • Lab tests for vasculitis, hypercoagulable states, and atherosclerotic risk factors.
  • X-rays—for cervical rib; clavicular and first rib fractures; fractures and dislocations in extremity; pulmonary lesions of connective tissue disorders.
  • Arterial Doppler study.
  • Angiogram (Subclavian angiogram)—CT/MR; conventional.
  • CT scan neck and thorax.
  • Blood sugar, lipid profile, cardiac evaluation.
zoom view
Fig. 1.376: Upper limb angiogram showing blocks in subclavian artery.
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Figs 1.377A and B: (A) Carotid subclavian bypass; (B) Subclavian carotid transposition.
 
Management of Upper Limb Ischaemia
  • Treatment of the cause.
 
Treatment of Embolus
  • Time since the first symptom is very important.
  • Clinical assessment of extent of ischaemia, immediate anticoagulation with heparin, Doppler study and angiogram of the arterial system, evaluation for the source of embolus—are the protocols.
  • Embolectomy
    • 211Brachial embolectomy: Local/regional/general anaesthesia is used. Longitudinal incision in the arm is used for proximal embolus; Lazy S-shaped incision across the elbow is done for embolus extending into the bifurcation and to expose the branches.
 
Treatment in Trauma
  • General evaluation and resuscitation.
  • Control of bleeding in open wound: Pressure bandage/manual compression (DO NOT USE TOURNIQUET).
  • Time since the event and clinical assessment of limb perfusion.
  • Stabilisation of fractures and dislocations
  • Doppler study of arterial system, angiogram if required.
  • Arterial repair; bypass graft either venous or synthetic.
 
Treatment of chronic Ischaemia
  • Medical management
    • Risk modification—diabetes, hypertension, dyslipidemia, smoking, homocystinaemia, exercise training.
    • Antiplatelets—aspirin/ticlopidine/clopidogrel.
    • Anticoagulants—heparin/warfarin.
    • Xanthines/pentoxiphylline/cilostazol.
    Cilostazol—suppresses cAMP phosphodiesterase III rise in cAMP levels with antiplatelet, antithrombotic effects; induces vasodilatation; increases plasma HDL cholesterol; decreases plasma triglycerides.
  • Catheter based interventions
    • Atherectomy.
    • Angioplasty ± stenting by conventional or subintimal approach.
    • Stent grafts.
    • Cryoplasty.
  • Surgery
    • Endarterectomy.
    • Bypass surgery.
    • Sympathectomy, extraperiosteal resection of the cervical rib.
 
Bypass Surgeries in Upper Limb Ischaemia
  • Conventional bypass
    • Aorto-subclavian/axillary bypass.
    • Subclavian: Axillary/brachial bypass.
    • Brachiodistal bypass.
  • Extra-anatomical bypass
    • Carotid: Subclavian/Axillary bypass.
    • Subclavian: Subclavian bypass.
    • Axillary: axillary bypass.
  • Subclavian: Carotid transposition.
 
Treatment of Raynaud's Phenomenon
  • Avoiding triggering agents
  • Drugs (vasodilators)—calcium channel blockers, angiotensin II receptor blockers, alpha-1 adrenergic blockers, Sildenafil, prostaglandin E1.
  • Surgery—sympathectomy.
Note:
Individual topics about causes of upper limb ischaemia are discussed in different places.
 
ARTERIAL SUBSTITUTES
Ideal arterial substitute is not yet developed. Ideal arterial substitute should be strong, durable for patient's life, bio-compatible, nonthrombogenic, should be resistant for infection, easily available, should have a long-term patency rate, and should have elastic property of normal artery.
Features of ideal graft
Strong
Should be leak proof on restoration of blood flow
Durable for patient's life
Should not chemically or physically degenerate
Non-thrombogenic
Should not cause any abnormal reaction to surrounding tissues
Biocompatible
Should not occlude when flexed
Resistant to infection
Should not damage blood contents
Flexible
Should maintain long-term patency
Should have elastic property of normal artery
Carrel and Guthrie first did venous autograft into arteries of dogs. They did extensive histological study of viable and nonviable grafts. Lexer in 1907 used saphenous vein for axillary artery repair. Murray started to use intraoperative heparin. Enaz Moniz and dos Santos originated technique of arteriography. Gross and his colleagues in 1948 started to use viable arterial allografts. Later it was found that, as of graft is considered tissue viability is not essential for success of graft uptake.
 
Classification of Arterial Substitutes
  • Arterial allograft—not used.
  • Arterial autograft—internal mammary artery (common), internal iliac artery.
  • Arterial xenograft—bovine carotid artery graft—not used.
  • Venous autograft—long saphenous vein (common), small saphenous vein, basilic vein, cephalic vein.
  • Venous allograft—umbilical vein graft.
  • Prosthetic grafts
    • 212Textile grafts
      • Dacron graft—knitted or woven or crimping or velour types. Dacron is polyethylene terephthalate.
      • Teflon graft—knitted or woven crimping or velour types.
    • Non-textile semi-inert polymer graft:
      • ePTFE graft—expanded polytetrafluoroethylene graft.
Preclotting the noncoated knitted or woven Dacron graft is done to seal the graft and to prevent leak, and to create a smooth lining at graft—blood interface. This step is not necessary for PTFE or newer grafts.
 
Complications of Graft
  • Neointimal fibrous hyperplasia at suture lines of the graft is due to surgical trauma, PDFG, arterial smooth muscle proliferation.
  • Graft infection—incidence is 2%. It is more in lower limb graft than abdominal graft. Peroperative cephalosporin administration reduces the rate of graft infection. If infection occurs graft should be removed and revascularisation is achieved using a saphenous vein graft.
  • Graft failure is rare but can occur. It is due to fiber degeneration, manufacturing defect, diffuse dilatation of graft (is due to expansion of the knit in knitted Dacron).
  • Anastomotic false aneurysm (3%) occurs just adjacent to suture line towards host artery. It is tearing of the artery adjacent to suture line due to mismatched graft artery compliance, improper suture placement, and arterial degeneration. There will be partial or total separation of the graft from the host with blood collection in a covering of fibrous capsule. Eventually it will rupture/may cause thrombosis and embolism. Treatment is graft—artery reanastomosis with insertion of additional piece of graft.
213M. Vascular Lesions and Hamartoma
CHAPTER OUTLINE
  • ❖ Vascular Anomalies
  • ❖ Haemangioma
  • ❖ Vascular Malformations
  • ❖ Cirsoid Aneurysm
  • ❖ Arteriovenous Fistula
  • ❖ Campbell De Morgan Spots
  • ❖ Parry-Romberg Disease
  • ❖ Hamartomata
 
VASCULAR ANOMALIES
  • It is a collective term used for haemangioma and vascular malformations.
  • Haemangioma is a benign tumour containing hyperplastic endothelium with cellular proliferation with increased mast cells. Growth in tissue culture is observed. It is absent at birth, seen by 1 month in 30%. It usually shows biphasic growth phase with slow involution. 95% of cases achieve spontaneous involution. Fast growing type can cause platelet trapping and thrombocytopenia. Associated skeletal changes are not common but can occur. But bone erosion by the lesion can occur. It is common in girls (3:1).
  • Vascular malformations are single layer endothelium lined spaces derived from arterial, capillary, venous or lymphatic system. There is no growth in tissue culture. Raise in mast cells is not seen. 90% cases are seen at birth; only few at later period. It is equal in both sexes (1:1). Quiescent endothelium with vessels showing progressive ectasia is the feature. Intravascular coagulation and mild thrombocytopenia can develop. Skeletal changes and overgrowth are common. Spontaneous involution is not common.
  • Disfigurement, tissue destruction, deformity, dysfunction, telangiectasia, skin scarring are common.
  • Szilagyi classification—(1) Cavernous haemangioma; (2) Microfistulous AV communications; (3) Macrofistulous communications; (4) Anomalous mature vascular channels.
  • Humburg classification—(1) Predominantly arterial/venous/lymphatic defects with aplasia or obstructive dilatation which is limited or infiltrative; (2) Predominantly AV shunting defects with deep/superficial limited or infiltrating lesions; (3) combined vascular defects—arterial, venous and haemolymphatic which may be limited or infiltrating.
  • Diagnosis is made clinically and by radiological imaging—coloured Doppler, DSA, MRI. MRI is better than CT to identify the flow (MR angiogram is ideal). Haemangiomas show intense parenchymal staining; vascular malformations show ecstatic vessels without much parenchyma; AVM shows rapid venous shunting.
 
HAEMANGIOMA
  • It is the most common tumour in children (in 10% of term deliveries).
  • It shows cellular endothelial hyperplasia with increased mast cells.
  • Onset is few weeks after birth with biphasic growth showing initial rapid growth with gradual involution over 5–7 years.
  • It is benign vascular endothelial tumour, common in girls (3 : 1).
  • It is commonly seen in skin and subcutaneous tissue but can occur anywhere in the body like in liver, brain, lungs or other organs.
  • It grows rapidly in first year and 70% involutes in 7 years.
  • Early proliferative lesion is bright red, irregular; deep lesion is bluish coloured. Involution causes colour fading, softness, shrinkage leaving crepe paper like area.
  • Commonly it is central; common in head and neck region (60%).
  • Often large haemangiomas may be associated with visceral anomalies. Head and neck haemangioma is associated with ocular and intracranial anomalies; sacral with spinal dysraphism. Multiple cutaneous haemangiomas may be associated with haemangioma of liver causing hepatomegaly, cardiac failure (CCF), anaemia.
  • Ulceration, bleeding, airway block and visual disturbances are common complications.
  • A definitive even though rare, but important life-threatening complication is platelet trapping and severe thrombocytopenia presenting as ecchymosis, petechiae, intracranial haemorrhage massive GI bleed.
  • Raised angiogenic (fibroblastic) growth factor which is secreted in patient's urine is useful lab investigation to differentiate it from vascular malformations.
zoom view
 
Capillary Vascular Malformations
  • Salmon patch (stork bite):
    • It is actually capillary vascular malformation also called as naevus simplex; it is very commonly seen in 40% of newborns.
    • It presents at birth. It commonly occurs in nape of the neck (50%), face, scalp and limbs. It usually involves wide area of skin. It is caused by an area of persistent fetal dermal circulation. With age, it goes for spontaneous regression and disappears completely (usually in one year). Hence masterly inactivity is the treatment.
  • Port-wine stain (Naevus flammeus):
    • It presents at birth and persists throughout life without any change. Spontaneous regression will not occur. It presents as smooth, flat, reddish blue/intensely purple area; common in head, neck and face; often with maxillary and mandibular dermatomes of 5th cranial nerve. Eventually surface becomes nodular and keratotic.
    • It persists throughout life. It is less common; seen in 0.3% of all newborns. It is also a capillary vascular malformation.
    • It is actually a capillary malformation even though considered under haemangioma. It results from defect in maturation of sympathetic innervation of skin causing localised vasodilatation of intradermal capillaries.
    • It is often associated with Sturge-Weber syndrome, Klippel-Trenaunay-Weber syndrome and Proteus syndrome.
    • It needs treatment—laser (pulsed dye/diode); excision and grafting; cosmetic coverage. Expected result by treatment is not possible many times.
Note:
Presently word ‘capillary haemangioma’ is restricted to strawberry type only; salmon patch and port-wine stain are actually classified under vascular malformations.
zoom view
Fig. 1.378: Salmon patch.
zoom view
Fig. 1.379: Port-wine stain (Naevus flammeus).
 
Capillary Haemangioma
  • Strawberry haemangioma:
    • It may start at birth or child is normal at birth; between one to three weeks it appears as red mark which rapidly increases in size in 3 months to form strawberry/raspberry haemangioma. It contains immature vasoformative tissues. There will be eventually intravascular thrombosis, fibrosis and mast cell infiltration.
    • It is a true capillary haemangioma.
    • It is 20 times more common than port wine stain.
    • It is common in white girls. Male to female ratio is 1 : 3.
    • It is common in head and neck region.
    • It is clinically compressible, warm with bluish surface.
    • Bleeding can occur after minor trauma and also ulceration.
    • It involves skin, subcutaneous tissues and often muscles also.
    • After one year of age, it slowly begins to disappear, and completely in 7–8 years (70% in 7 years).
    • It is the most common haemangioma.
zoom view
Fig. 1.380: Strawberry haemangioma.
215
 
Treatment
  • They are treated by wait and watch policy commonly—allowed for spontaneous regression.
  • Pulsed dye laser (diode laser), surgical excision and reconstruction. Feeding vessels may need to be ligated after wide exposure before achieving complete extirpation. Sclerotherapy/cryotherapy/CO2 snow therapy cause unpleasant scarring.
  • Preoperative embolisation facilitates surgical excision and reduces the operative blood loss. When once embolisation done, surgery should be done as early as possible otherwise recurrence occurs and much more worried formation of enlarged collaterals can occur.
  • Materials used are—foam, plastic spheres, stainless/platinum steel coils, ethanol, polyvinyl alcohol foam of 1000 µ meters size, and rapidly polymerizing acrylic. Problems are tissue necrosis, reaction, normal tissue embolisation. Procedure is done with interventional radiology under image intensifier guidance.
  • Rapidly growing haemangioma may need systemic/oral and intralesional steroid therapy.
  • Antiangiogenic interferon 2a may be useful.
  • Life-threatening platelet trapping may be controlled by cyclophosphamide chemotherapy.
  • Haemangioma with drug resistant CCF can be treated with radiotherapy.
 
Cavernous Haemangioma
  • It is present at birth and consists of a multiple venous channels.
  • Its size increases gradually and may cause problems.
  • It often contains feeding vessels which is of surgical importance.
  • Sites: Head, neck, face, limbs, tongue, liver and other internal organs.
  • Large or multiple cavernous haemangiomas can cause congestive heart failure (hyperdynamic) due to shunting of large quantity of blood.
  • Cavernous haemangioma with dyschondroplasia is called as Maffucci syndrome.
  • Cavernous haemangioma is often mixed with lymphatic component also (mixed vascular and lymphatic).
zoom view
Figs 1.381A and B: Cavernous haemangioma in (A) tongue and (B) knee.
 
Clinical Features
  • It is smooth, soft, well-localised, warm, fluctuant, compressible, nonpulsatile swelling with bluish surface occurring in skin and subcutaneous tissue (often in mucosa like oral cavity) without any transillumination.
  • Compressibility and bluish surface is diagnostic. When swelling is pressed it reduces partially/often completely but when pressure is released it slowly attains its original size and shape. Vascular and lymphatic malformations are compressible.
  • It is usually nontender unless it gets infected or undergoes thrombosis or causes haemorrhage.
 
Differential Diagnosis
  • Lymphangioma: It is brilliantly transilluminant unless it is infected or fibrosed.
  • Lipoma, cold abscess, lymph cyst—clinically it is easier to differentiate.
 
Complications
  • Haemorrhage.
  • DIC.
  • Thrombosis.
  • Infection, ulceration and septicaemia.
  • Erosion into the adjacent bone.
  • High output cardiac failure.
 
Investigations
  • Ultrasound, Doppler.
  • Angiogram to find out feeding vessel.
  • Platelet count.
  • MRI/MR angiogram to see feeding vessels and deeper extension.
zoom view
Figs 1.382A and B: Cavernous haemangioma in the cheek near angle of the mouth and in the tip of the tongue. Haemangioma tongue is one of the causes of macroglossia.
zoom view
Figs 1.383: Laparoscopic view of cavernous haemangioma of liver. It is the most common benign tumour of the liver.
 
Treatment
  • Sclerosant therapy: It is the initial first line of therapy. It causes aseptic thrombosis and fibrosis of the cavernous haemangioma with less vascularity and smaller size. It is directly injected into the lesion. Sodium tetradecyl sulphate/hypertonic saline are used. Often multiple injections are needed to achieve complete required effect. Later excision of the lesion is done.
  • Ligation of feeding artery and often at later stage excision is done once haemangioma shrinks.
  • Therapeutic embolisation.
  • If small and located in accessible area, excision is the initial therapy.
  • Laser ablation—diode pulsed laser is becoming popular because of good control of bleeding. CO2/Nd:YAG laser is also equally effective.
 
VASCULAR MALFORMATIONS
  • Secondary to defect in development of vascular components, in 8th week of intrauterine period.
  • Single layer endothelium lined spaces derived from arterial, capillary, venous or lymphatic system showing ectasia.
  • There is no growth in tissue culture. Raise in mast cells is not seen.
  • Associated with many syndromes.
  • Can be located in skin or in deeper planes.
  • Present at birth and grows in proportion to child's growth. Pale skin which later darkens over the age or faint blue mass is the presentation.
  • Spontaneous involution is not common.
  • Capillary malformation (CM) type is due to lack of sympathetic control.
  • Venous malformation (VM) type is most common vascular malformation which shows hypoplasia, hyperplasia or aplasia of superficial or deeper system. It is seen in subcutaneous plane as faint blue compressible mass with morning pain and stiffness of the area.
  • Lymphatic malformation (LM) type can be microcystic (lymphangioma) or macrocystic (cystic hygroma). It can cause lymphoedema,217 soft tissue and bony hypertrophy, asymmetry (face), macrochelia, macroglossia, macrotia, cellulitis.
  • Low/slow flow malformations can cause skeletal hypoplasia; high/fast flow malformations can cause hypertrophy. AVM is high flow type.
  • Consumption coagulopathy (DIC) can occur.
  • It is equal in both sexes (1:1).
  • Doppler is commonly used investigation; but MRI (MR angiogram is ideal) with contrast is ideal to identify and to differentiate low and high flow types.
  • Treatment—conservative with compression garments and sclerotherapy. Laser photocoagulation is the choice for superficial malformations; multiple sittings may be needed; complete clearance may not be achieved. Surgical excision can be done. Preoperative embolisation may be needed.
Vin rose patch:
It is a congenital intradermal pale pink vascular malformation with dilatation of vessels in subpapillary dermal plexus. It may be associated with haemangiomas; AV malformations in limbs; congenital lymphoedema.
 
CIRSOID ANEURYSM
  • It is actually a rare arteriovenous fistula / malformation of the scalp usually of congenital origin but occasionally can be traumatic. 90% occur in relation to superficial temporal artery but few occur additionally also in relation to occipital arteries. It should be differentiated from the true aneurysm of the superficial temporal artery. Cirsoid means varix.
  • It is a rare variant of capillary haemangioma occurring in skin, beneath which abnormal artery communicates with the distended veins.
  • Commonly seen in superficial temporal artery and its branches.
  • Often the underlying bone gets thinned out due to pressure.
  • Occasionally extends into the cranial cavity.
  • Ulceration is the eventual problem which will lead to uncontrollable haemorrhage.
 
Clinical Features
Pulsatile swelling in relation to superficial temporal artery, which is warm, compressible, with arterialisation of adjacent veins and with bone thinning (due to erosion). It feels like a ‘pulsating bag of worms’.
 
Investigations
  • Doppler study, CT scan.
  • Angiogram, X-ray of the part.
 
Treatment
  • Ligation of feeding artery and excision of lesion, often requires preliminary ligation of external carotid artery.
  • Intracranial extension requires formal neurosurgical approach.
  • Endovascular therapy is also useful.
 
ARTERIOVENOUS FISTULA (AVF)
It is an abnormal communication between an artery and vein.
 
Types
  • Congenital—is arteriovenous malformation.
  • Acquired (Trauma is common cause).
 
Congenital Arteriovenous Malformation (Fistula)—AVM (AVF)
During developmental period AV communications occur.
It is high flow type of vascular malformation. It is 30% of all vascular malformation. 90% of AVM contains both arterial and venous components. Shuting of blood with thrill and bruit with hyperdynamic circulation is common.
 
Sites
  • Limbs, either part or whole of the limb is involved. It may be localised to toes or fingers.
  • Lungs.
  • Brain—in circle of Willis.
  • Other organs like bowel, liver.
 
Clinical Features
Structural changes in the limb:
  • Limb is lengthened due to increase in blood flow since developmental period.
  • Limb girth is also increased.
  • Limb is warm.
  • Continuous thrill and continuous machinery murmur all over the lesion.
  • Dilated arterialised varicose veins are seen due to increased blood flow and also due to valvular incompetence.
  • Often there is bone erosion or extension of AVF into the bone as such.
Physiological changes
Because of the hyperdynamic circulation, there is increased cardiac output and so often congestive cardiac failure.
 
Investigations
  • Angiogram—MR angiogram is ideal.
  • Doppler study.
  • X-ray of the part.
  • ECG, echocardiography.
 
Treatment
  • Conservative—sclerotherapy, compression, avoiding injury.
  • Indications for intervention
    • Absolute: Haemorrhage, ischaemia, CCF.
    • Relative: Pain, functional disability, cosmesis, limb asymmetry.
    • Emergency: Torrential bleeding usually after trauma (example—road traffic accidents).
Interventions
  • Surgical ligation of feeding vessels and complete excision of the lesion. Often if lesion is extending into deeper planes it is technically difficult; but with usage of tourniquet, careful meticulous dissection and ligation of all vessels will lead into successful excision of entire lesion.
  • Therapeutic embolisation/preoperative embolisation hasten the proper surgical excision.
  • In emergency bleeding, adequate transfusion of blood, tourniquet usage, intraoperative embolisation and then excision of entire lesion is done. Occasionally when extensive AVM is present often involving the entire limb, amputation is the final option left as a life-saving procedure.
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Fig. 1.384: MR angiogram of AV malformation in cranial cavity.
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Fig. 1.385: MRI picture of AV malformation.
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Figs 1.386A and B: Hypertrophic changes due to AV malformation.
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Figs 1.387A to E: Congenital arteriovenous malformation involving right upper limb, axillary region and part of right half of neck and face. Note the limb lengthening and widened girth. Limb is warmer. Limb should be measured at each level. Auscultation reveals continuous bruit over the limb. Note the dilated tortuous veins due to hyperdynamic circulation.
219
 
Acquired Arteriovenous Fistula (AVF)
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Fig. 1.388: AV fistula.
 
Causes
  • Trauma in (most common cause):
    • Femoral region.
    • Popliteal region.
    • Brachial region.
    • Wrist.
    • Aorta—vena caval.
    • Abdomen.
It may be following road traffic accidents, penetrating wounds, cock-fight injury (common in South India).
  • After surgical intervention of major vessels.
  • Therapeutic: For renal dialysis, AVF is created (Cimino fistula) to achieve arterialisation of veins and also to have hyperdynamic circulation. It is done to have easy and adequate venous access for long time haemodialysis. Common sites are wrist, brachial, and femoral region.
 
Pathophysiology
  • Physiological changes: Cardiac failure due to hyper-dynamic circulation.
  • Structural changes:
 
Changes at the Level of Fistula
Blood flows from high pressure artery to low pressure vein causing diversion of most of the blood. Between the artery and vein, at the site of fistula, dilatation develops with formation of fibrous sac called as aneurysmal sac. This presents as warm, pulsatile, smooth, soft, compressible swelling at the site with continuous thrill and continuous machinery murmur.
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Figs 1.389A and B: Acquired arteriovenous fistula in the wrist over radial vessels. It should be palpated for compressibility and thrill. It should be auscultated for bruit.
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Fig. 1.390: AV fistula created for treating chronic renal failure has formed an aneurysm. It may rupture to cause severe haemorrhage. Thrombosis or sepsis also can occur in this.
 
Changes Below the Level of the Fistula
Because of diversion of arterial blood distal part becomes ischaemic. Because of high pressure arterialisation of veins and valvular incompetence occurs causing varicose veins.
 
Changes Proximal to the Fistula
  • Hyperdynamic circulation causes cardiac failure. Cardiac failure may be very severe in traumatic AVF (often resistant to drug therapy).
  • If pressure is applied to the artery proximal to the fistula, swelling will reduce in size, thrill and bruit will disappear, pulse rate and pulse pressure becomes normal. This is called as Nicoladoni's sign or Branham's sign.
 
Investigations
  • Doppler, angiogram.
  • ECG, echocardiography.
 
Treatment
  • Excision of fistula and reconstruction of artery and vein with graft.
    Done in early stages—larger vessels. Venous or Dacron graft is used.
  • In emergency situation, quadruple ligation, i.e. both artery and vein above and below are ligated without touching the fistula and sac. Patient recovers well from cardiac failure.
  • Therapeutic embolisation may be tried.
Hunter's ligation should be avoided. It is used as life-saving measure because it invariably causes limb ischaemia and gangrene even though patient recovers from cardiac failure. It is ligation of artery proximally so as to make cardiac function normal. But it invariably steals the blood from the limb leading to gangrene.
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Fig. 1.391: Reconstruction of AV fistula using graft.
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Figs 1.392A and B: (A) Quadruple ligation of AV fistula. (B) Hunter's ligation is ligation of artery proximal to AV fistula. It should not be done as it causes diversion of all blood from periphery leading to gangrene of distal part.
 
CAMPBELL DE MORGAN SPOTS
  • It is usually smaller (0.2 to 6 mm) in size, circular, elevated and bright red swelling.
  • It is common in trunk. Common in elderly.
  • Also called as cherry angiomas.
  • Usually it does not require treatment.
  • When needed, excision or electrodesiccation or laser removal is done.
 
PARRY-ROMBERG DISEASE
  • It is hemifacial atrophy of skin, soft tissue and bone.
  • Common in females.
  • It usually begins at twenties.
  • Atrophy of skin, fat, muscle, cartilage and bone causing coupe de sabre deformity.
  • It is a self-limiting disease.
  • Aesthetic reconstruction is offered when severe deformity develops.
 
HAMARTOMATA
Hamartano means ‘I miss’ (Greek). Or ‘fault’ or ‘misfire’ or ‘error’—(missing the mark in spear throwing).
Note:
Presently this terminology is not very much in use.
  • It is a benign lesion with aberrant differentiation producing a mass of disorganised but mature specialised cells or tissue indigenous to the particular site.
  • It is tumour like overgrowth of tissue or tissues proper to that part.
  • It may be single lesion or multiple lesions.
  • Haemangiomas, lymphangiomas, AV malformations, neural malformations are the examples.
 
Treatment
  • Depends on site, type, extent.
  • Cryotherapy, ligation of feeding vessels, sclerotherapy, excision or laser therapy.221
N. Venous Diseases
CHAPTER OUTLINE
  • ❖ Anatomy of Veins of Lower Limb
  • ❖ Physiology of Venous Blood Flow in Lower Limb
  • ❖ Deep Vein Thrombosis
  • ❖ Varicose Veins
  • ❖ Venous Ulcer
  • ❖ Compression Therapy for Varicose Veins
  • ❖ Thrombophlebitis
  • ❖ Klippel-Trenaunay Syndrome
  • ❖ Anticoagulants
  • ❖ Heparin
  • ❖ Oral Anticoagulants
  • ❖ Direct Thrombin Inhibitors
  • ❖ Antiplatelet Drugs
  • ❖ Pulmonary Embolism
 
ANATOMY OF VEINS OF LOWER LIMB
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Fig. 1.393: Anatomy of lower limb veins.
 
Deep Veins
  • Tibial, popliteal, femoral veins are called as “veins of conduits” which drain blood into iliac veins and then to IVC.
  • Pumping veins: They are venous sinuses existing in the calf muscles which pump blood towards major veins. They are better termed as musculovenous pumps. They are also called as the peripheral heart.
 
Superficial Veins
  • Long (Great) saphenous vein (LSV / GSV): It begins from the medial part of the dorsal venous arch of the foot runs in front of the medial malleolus ascends up to the posteromedial aspect of the knee joint, and then ascends upwards in the thigh towards the saphenous opening. Saphenous opening lies 3.75 cm below and lateral to the pubic tubercle. It pierces the cribriform fascia to enter the femoral vein. LSV contains 12–20 valves. It is the longest vein in the body. In the lower part of the leg LSV is closely associated with saphenous nerve which can get damaged during surgeries to LSV varicosity. Tributaries of GSV are—posterior arch vein, anterior vein of the leg, anterolateral vein, posteromedial vein and sometimes accessory saphenous vein.
  • Short (Small) saphenous vein (SSV): Lateral marginal vein of the foot behind the lateral malleolus continues as SSV ascending upwards along the lateral margin of the tendoachilles. It runs along 222the middle of the back of the leg between two heads of the gastrocnemius into the lower part of the popliteal fossa and ends into the popliteal vein. It has got 6–12 valves. Sural nerve runs closely along the SSV which may get injured during surgery. Saphenopopliteal junction is variable, but usually located at popliteal fossa; it can be above or below the actual site.
  • Posterior arch vein of Leonardo from medial ankle to the LSV below.
  • Anterior arch veins to popliteal veins.
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Fig. 1.394: Bilateral varicosity of great saphenous veins.
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Fig. 1.395: Long saphenous vein, anatomy and its tributaries.
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Figs 1.396A and B: Short saphenous vein varicosity.
Note:
Superficial veins have got multiple valves; blood always drains from superficial veins towards deep veins. Inferior vena cava (IVC) and iliac veins do not have valves. Superficial veins of lower limb drains skin and subcutaneous tissues (10% of blood). Veins can accommodate large quantity of blood hence called as capacitance vessels.
 
Perforator Veins
They are the veins which connect superficial to deep veins at various levels. They travel from superficial fascia through an opening in the deep fascia before entering the deep veins. The direction of blood flow here is from superficial to deep veins. These perforators are also guarded by valves so that the blood flow is unidirectional, i.e. towards deep veins. Reversal of flow occurs due to incompetence of perforators which will lead to varicose veins.
 
PHYSIOLOGY OF VENOUS BLOOD FLOW IN LOWER LIMB
  • Veins are thin-walled vessels with collapsible walls, that assume an elliptical configuration in collapsed state and circular configuration in the filled state.
    zoom view
    Fig. 1.397: Long saphenous vein with perforator incompetence with venous ulcer.
  • Venous valves are abundant in the distal lower extremity and the number of valves decreases proximally, with no valves in superior and inferior vena cava.
 
Venous Return
  • Arterial pressure across the capillary increases the pumping action of vein.
  • Calf musculovenous pump: During contraction phase of walking, pressure in the calf muscles increases to 200–300 mmHg. This pumps the blood towards the heart. During relaxation phase of walking, pressure in the calf falls and so it allows blood to flow from superficial to deep veins through perforators. Normally while walking, pressure in the superficial system at the level of ankle is 20 mmHg.
  • During walking, foot pump mechanism propels blood from plantar veins into the leg.
  • Gravity.
Note:
Pressure in arteriolar end of the capillary is 32 mmHg; venular end of capillary is 12 mmHg.
 
DEEP VEIN THROMBOSIS
Deep vein thrombosis (DVT) is called as phlebothrombosis. It is semisolid clot in the vein which has got high tendency to develop pulmonary embolism and sudden death. Common site of beginning of thrombus is soleal veins which later propagate proximally, often getting detached to cause acute massive pulmonary embolism or moderate sized emboli can cause pyramidal/wedge shaped pulmonary infarcts.223
 
Aetiology: Factors
 
Causes
  • Following childbirth.
  • Trauma—to leg, ankle, thigh, pelvis.
  • Muscular violence.
  • Immobility: Bed ridden patients, individuals on long duration air or bus travel (Traveller's thrombosis).
  • Debilitating illness, obesity, immobility, bed rest, pregnancy, puerperium, oral contraceptives, estrogens.
  • Postoperative thrombosis (Most common cause): Common after the age of 40 years. Incidence following surgeries is 30%. In 30% of cases both legs are affected. Usually seen after prostate surgery, hip surgery, major abdominal surgeries, gynaecological surgeries, cancer surgeries. Bedridden for more than 3 days in the postoperative period increases the risk of DVT.
  • Spontaneous thrombosis is common in visceral neoplasm like carcinoma pancreas or carcinoma stomach. It is often migrating type.
  • Thrombus may start in a venous tributary which eventually may extend into the main vein causing DVT.
  • Axillary vein thrombosis
    • It can occur spontaneously, following compression by cervical rib, by various causes of thoracic inlet syndrome, or arm being in the hyperabduction state for prolonged period (e.g. painting the ceiling), after axillary lymph node block dissection, after radiotherapy to axilla, occasionally as a complication of venous cannulation.
    • Upper limb DVT is rare compared to lower limb DVT (5% of all DVT). It may be axillary or subclavian vein or both.
    • But 30% of upper limb DVT can cause pulmonary embolism.
    • Primary upper limb DVT is Paget-Schroetter syndrome, is due to subclavian vein compression that occurs in thoracic outlet syndrome. It may be precipitated by exertion of arms, swimming, exercise, etc.
    • Idiopathic upper limb DVT is rare. Occult underlying malignancy should be thought of.
    • Secondary upper limb DVT is due to CVP line, pacemaker thrombocytosis, malignancy, surgeries, radiotherapy, etc.
    • Unilateral arm, forearm swelling with bluish discolouration, pain, pitting oedema, often with skin blebs are the features.
    • Investigations are—Duplex scan, MR venography (as clavicle obscures proper duplex evaluation), BT, CT, PT, APTT, platelet count estimation.
    • Treatment is similar, with heparin/LMWH/warfarin, thrombolysis using tissue plasminogen activator, elevation of the arm, using compression stockings.
  • Polycythaemia vera, thrombocytosis.
  • Deficiencies of antithrombin III, protein C, protein S, factor V of Leiden, thrombophilia.
  • Recent myocardial infarction, heart failure, nephrotic syndrome.
  • Thrombosis can occur in individuals who sit with computers for long time—‘ethrombosis’.
 
Phlegmasia alba dolens
It is DVT of femoral vein (deep femoral vein commonly) causing painful congestion and oedema of leg, with lymphangitis, which further increases the oedema and worsens the situation (white leg).
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Fig. 1.398: Deep vein thrombosis (DVT) in both legs. 30% cases of DVT are bilateral.
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Fig. 1.399: Right leg venous gangrene. Note the discolouration, blebs and oedema.
 
Phlegmasia caerulea dolens
It is extensive DVT of iliac and pelvic veins causing blue leg with either venous gangrene or areas of infarction.
 
Clinical Features
  • Fever—earliest symptom.
  • Pain and swelling in the calf and thigh (often). Pain is often so severe that the patient finds it difficult to flex (or move) the leg.
  • Leg is tense, tender, warm, pale or bluish with stretched and shiny skin.
  • Positive Homan's sign: Passive forceful dorsiflexion of the foot with extended knee will cause tenderness in the calf.
  • Mose's sign: Gentle squeezing of lower part of the calf from side-to-side is painful. Gentleness is very important otherwise it may dislodge a thrombus to form an embolus.
  • Neuhof's sign: Thickening and deep tenderness elicited while palpating deep in calf muscles.
  • Most often, DVT is asymptomatic and presents suddenly with features of pulmonary embolism like chest pain, breathlessness and haemoptysis.
  • After applying tourniquet at saphenofemoral junction, patient is made to walk and without removing the tourniquet, limb is elevated—persisting prominent superficial veins will be observed in DVT—Linton's test.
 
Investigations
  • Venous Doppler.
  • Duplex scanning
    It shows noncompressible vein which is wider than normal. On compression over calf muscles, it does not show any augmentation of flow. Normal venous sound at the area of femoral vein which disappears during inspiration is conspicuously absent in DVT.
  • Venogram
    • Contrast material is injected into venous system to get detailed idea of the veins after applying tourniquet into superficial system. Occlusive and nonocclusive thrombus can be differentiated by this. But as it is invasive one, it is not commonly done at present. MR venogram is under trial at present. Impedance plethysmography is used to measure the rate of venous emptying. Vein occlusion is done using cuff around upper thigh which is confirmed by flat electrical wave pattern. When cuff is released rapid flow of wave is observed in normal; sluggish flow of wave is seen in DVT.
      zoom view
      Fig. 1.400: US showing IVC thrombosis.
  • Radioactive I125 fibrinogen study
    • Sodium iodide 100 mg orally is given to the patient 24 hours before the test to block the thyroid activity. I125 labelled fibrinogen 100 μ curies is injected intravenously. First radioactivity of heart is measured by placing the scintillation counter over precordium. Reading obtained by this is adjusted as 100%. After that legs are elevated using adjustable stands and to prevent venous pooling, scintillation counter is placed over the calf. Counting in the leg is done from below upwards at 5 cm intervals. Procedure is done in preoperative period; on 1st, 3rd and 6th postoperative days. A 20% or more raise in percentage value suggests deep vein thrombosis in leg. I125 labelled fibrinogen is used (earlier I131 labelled fibrinogen was used) because it has got shorter radioaction; its detectability is done with much lighter and mobile apparatus.
  • Haemogram with platelet count; D-dimer test/analysis of fibrin degradation products (FDP) are relevant tests used. D-dimer test is measurement of cross-linked degradation products which interprets the plasmin activity on fibrin. Negative D-dimer test is of more value.
  • Ventilation—perfusion scanning with mismatched defects; pulmonary artery CT scan with filling defect; pulmonary angiography are the investigations to confirm the pulmonary embolism.
 
Treatment
  • Rest, elevation of limb, bandaging the entire limb with crepe bandage.
  • Anticoagulants: Heparin/low molecular weight heparin, warfarin, phenindione.
  • For fixed thrombus:
    • Initially high dose of heparin of 25,000 units/day for 7 days is given. Then later patient is advised to continue warfarin for 3–6 months. Dose is controlled by assessing Activated Partial Thromboplastin Time (APTT). Duration of heparin treatment is usually for 7–10 days. Dose of heparin is often calculated as— 80 units/kg bolus of heparin followed by 15 units/kg of infusion.
    • Low molecular weight heparin is preferred to heparin.
    • Warfarin should be started as early as possible (same day of 225heparin therapy). Day one and day two—10 mg each day; day three—5 mg. On day three prothrombin time should be done. Warfarin is given for 3–6 months with regular monitoring, depending on the cause, risk group, and severity of DVT. INR should be maintained between 2.0 to 3.0.
    • Oral anticoagulants being teratogenic cannot be used during pregnancy. LMWH is the drug of choice used during pregnancy and postpartum period.
  • For free thrombus:
    • Fibrinolysins: Streptokinase, 6 lakhs to start with and later one lakh hourly. It is commonly infused directly into the affected vein through a venous catheter. Urokinase or tissue plasminogen activator may also be used to dissolve thrombus (it should not be given when patient is on heparin).
    • Venous thrombectomy is done using Fogarty venous balloon catheter.
    • Thrombotic emboli is prevented from reaching the heart by filtering it at IVC level using intracaval filters—Kim ray Greenfield filter, suture sieve plication, stapler plication, vena caval ligation, Mobin Uddin umbrella filter.
    • Special thrombectomy device of 7–9 French sheath is passed through the thrombosed segment to have partial mechanical thrombectomy and through that thrombolytics (tissue plasminogen activator) are infused. Thrombus can be removed nowadays through balloon angioplasty tube. Open venotomy and thrombectomy also can be done.
Modified Well's criteria for predicting pulmonary embolism (PE)
Points
Clinical symptoms and signs of DVT
3
Alternative diagnosis less likely PE
3
Heart rate >100
1.5
Immobilization more than 3 days or surgery within last 4 weeks
1.5
Previous DVT or PE
1.5
Haemoptysis
1.0
Malignancy in last 6 months
1.0
Score <4 = PE unlikely; score >4 = suggestive of PE.
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Fig. 1.401: Palma operation for iliofemoral block. Using opposite saphenous vein femoral vein is connected to other femoral vein.
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Fig. 1.402: Crepe bandages applied to both legs in bilateral varicose veins and DVT.
  • Palma operation: In iliofemoral thrombosis, common femoral vein below the block is communicated to opposite femoral vein through opposite long saphenous vein.
  • May-Husni operation: When blockage is in popliteal vein, popliteal vein below the block is anastomosed to long saphenous vein (end-to-end) so as to bypass the blood across the popliteal block.
 
Prevention of DVT
  • Care has to be taken to see for proper positioning of legs with no pressure on the calf muscles.
  • Pressure bandage to the legs has to be applied during major surgeries, laparoscopic surgeries. During postoperative period, 226elevation, massaging, pressure bandage, early ambulation, maintaining hydration are essential measures.
  • Low dose heparin is given in suspected cases, in major surgeries and continued during postoperative period till the patient is ambulated. 5,000 units is given subcutaneously 2 hours before surgery. Low molecular weight heparin is preferred drug than heparin as it can be used once a day; it does not require monitoring; it does not cause thrombo-cytopenia (like heparin); and there is lesser risk of bleeding.
  • Various measures like graduated static compression, elastic stockings, electrical stimulation of calf muscles, pneumatic compression are used to prevent sluggish flow of blood.
  • Dextran 70, intravenously 500 ml during surgery and another 500 ml postoperatively in 24 hours can also be used to prevent DVT.
  • Smoking increases the viscosity of blood and so should be stopped.
  • Patients on oral contraceptives or oestrogens should stop the drug 6-8 weeks prior to any elective surgery.
 
VARICOSE VEINS
They are dilated, tortuous, elongated veins in the leg. There is reversal of blood flow through its faulty valves.
  • It is permanently elongated, dilated vein/veins with tortuous path causing pathological circulation.
  • Risk factors being heredity; female sex; occupation that demands prolonged standing; immobility; raised intra-abdominal pressure like in sports, tight clothing, pregnancy, raised progesterone level and altered estrogen-progesterone ratio, chronic constipation, high heels.
  • Prevalence of varicose veins is 35%; severe varicose veins is 10%; chronic venous insufficiency (CVI) is 8%; ulcer is 2%.
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Figs 1.403A to C: Typical varicose vein and with skin changes and venous ulceration.
 
Classification I
  • Long/great saphenous vein varicosity.
  • Short/small saphenous vein varicosity.
  • Varicose veins due to perforator incompetence.
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Figs 1.404A to C: (A) Great saphenous vein varicosity. (B) Small saphenous vein varicosity. (C) Perforator incompetence (blow outs).
 
Classification II
  • Thread veins (or dermal flares/telangiectasis/spider veins/Hypen veins are 0.5–1 mm in size): Are small varices in the skin usually around ankle which look like dilated, red or purple network of veins (Venulectasia). Spider naevi/venous flares are common in females.
  • Reticular varices (1–3 mm in size): Are slightly larger varices than thread veins located in subcutaneous/subdermal region.
  • Varicose veins: They are dilated, tortuous, elongated superficial veins located in the subcutaneous tissue (saphenous compartment) equal or more than 3 mm in diameter measured in standing position.
  • Combination of any of the above.
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Fig. 1.405: Thread veins are up to 1 mm diameter; reticular veins are 1-3 mm in diameter.
Note:
  • Atrophic blanche is localized white atrophic skin surrounded by hyper pigmentation and dilated capillaries.
  • Saphena varix is a large groin varicosity at SFJ which disappears on lying down and imparts an impulse and thrill on coughing.
    227
    zoom view
    Fig. 1.406: Atrophic blanche.
  • Small varicose vein is <4 mm in diameter. Large varicose vein is >4 mm in diameter.
  • Corona phlebectatica are blue telangiectasias on the medial aspect of the foot below the malleolus around ankle level. More than 5 such lesions are the best independent predictor of the skin changes.
 
Classification III
 
Ceap Classification of Lower Limb Varicose Veins (2004)
 
Pathogenesis
Incompetence of venous valves
Stasis of blood
Chronic ambulatory venous hypertension
Defective microcirculation
RBC diffuses into tissue planes
Lysis of RBC's
Release of haemosiderin
Pigmentation
Dermatitis
Capillary endothelial damage
Prevention of diffusion and exchange of nutrients
Severe anoxia
Chronic venous ulceration (Fibrin cuff theory).
  • Inappropriate activation of trapped leucocytes release proteolytic enzymes which cause cell destruction and ulceration—White cell trapping theory. Fibrin deposition, tissue death, scarring occurs together, called as lipodermatosclerosis.
  • Secondary valvular failure → venous reflux → venous wall dilatation → effects. Weakening of the venous endothelial wall and valves occur due to raised venous wall tension by—(1) Shearing stress pressures of blood flow, (2) increased matrix metalloproteinases (MMPs) activity on endothelium and smooth muscle cells reducing structural integrity of venous wall with decreased elastin content in the media of the vein, (3) Changes in normal venous constriction and relaxation properties, (4) Recurrent inflammation.
  • Venous system in the lower limb is maintained by—(1) Valvular competence, (2) Venous patency, (3) Calf muscle pump which is venous channel/plexus within the soleus muscle. Any change in any of these systems can cause venous insufficiency.
  • Chronic venous insufficiency (CVI) is a syndrome resulting from continuous chronic venous hypertension/ambulatory venous hypertension [AVP] (>80 mmHg venous pressure at ankle) in the erect posture either on standing or exercise (in normal people venous pressure in superficial system falls during calf contraction). CVI consists of postural discomfort, varicose veins, oedema, pigmentation, induration, dermatitis, lipodermatosclerosis and ulceration. CVI patients may be having superficial vein incompetence (30%) with or without perforator incompetence or deep vein incompetence (30%) or having previous DVT with complete obliteration or partial recanalisation with incompetence called as post-thrombotic syndrome (30%).
  • Varicose vein is a condition of progressive deterioration even often with interventions.
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Figs 1.407A and B: Lipodermatosclerosis is pigmentation, thickening, and induration of the skin due to venous diseases.
Predisposing factors for varicose veins are—age, sex, race, obesity, height, left > right, occupation, family history, erect posture.
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Fig. 1.408: Typical site of venous ulcer. Note the pigmentation and chronicity.
 
Aetiology of Varicose Veins
Varicosities are more common in lower limb because of erect posture and long column of blood has to be supported which can lead to weakness and incompetency of valves. Incidence is 5% of adult population.
  • Primary varicosities due to:
    • Congenital incompetence or absence of valves.
    • Weakness or wasting of muscles—defective connective tissue and smooth muscle in the venous wall.
    • Stretching of deep fascia.
    • Inheritance (family history) with FOXC2 gene.
    • Klippel-Trenaunay syndrome, avalvulia, Parkes-weber syndrome. Here varices are of atypical distribution.
  • Secondary varicosities:
    • Recurrent thrombophlebitis.
    • Occupational—standing for long hours (traffic police, guards, sportsman).
    • Obstruction to venous return like abdominal tumour, retroperitoneal fibrosis, lymphadenopathy, ascites.
    • Pregnancy (due to progesterone hormone), obesity, chronic constipation.
    • AV malformations—congenital or acquired.
    • Iliac vein thrombosis.
    • Tricuspid valve incompetence.
 
Clinical Features
It is more common in females (10 : 1). Often it is familial. Familial varicose veins begin in younger age group, seen bilaterally, involves all veins including deep veins.
229
 
Signs
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Figs 1.409A and B: Thread (<1 mm) and reticular veins (1–3 mm).
  • Visible dilated veins in the leg with pain, distress, nocturnal cramps, feeling of heaviness, pruritus.
  • Pedal oedema, pigmentation, dermatitis, ulceration, tenderness, restricted ankle joint movement.
  • Bleeding, thickening of tibia occurs due to periostitis.
  • Positive cough impulse at the saphenofemoral junction.
  • Saphena varix—a large varicosity in the groin, which becomes visible and prominent on coughing.
  • Brodie-Trendelenburg test: Vein is emptied by elevating the limb and a tourniquet is tied just below the sapheno-femoral junction (or using thumb, saphenofemoral junction is occluded). Patient is asked to stand quickly. When tourniquet or thumb is released, rapid filling from above signifies saphenoemoral incompetence. This is Trendelenburg test I.
    In Trendelenburg test II, after standing tourniquet is not released. Filling of blood from below upwards rapidly can be observed within 30–60 seconds. It signifies perforator incompetence.
  • Perthe's test: The affected lower limb is wrapped with elastic bandage and the patient is asked to walk around and exercise. Development of severe cramp like pain in the calf signifies DVT.
  • Modified Perthe's test: Tourniquet is tied just below the saphenofemoral junction without emptying the vein. Patient is allowed to have a brisk walk which precipitates bursting pain in the calf and also makes superficial veins more prominent. It signifies DVT.
    zoom view
    Fig. 1.410: Site of saphena varix-in the lower part of groin just below the inguinal ligament.
    zoom view
    Fig. 1.411: Brodie-Trendelenburg test. Note the reversal of blood flow while releasing the tourniquet.
    DVT is contraindicated for any surgical intervention of superficial varicose veins. It is also contraindicated for sclerosant therapy.
  • Three tourniquet test: To find out the site of incompetent perforator, three tourniquets are tied after emptying the vein.
    • At saphenofemoral junction.
    • Above knee level.
    • Another below knee level.
    Patient is asked to stand and looked for filling of veins and site of filling. Then tourniquets are released from below upwards, again to see for incompetent perforators.
  • Schwartz test: In standing position, when lower part of the long saphenous vein in leg is tapped, impulse is felt at the saphenous junction or at the upper end of the visible part 230of the vein. It signifies continuous column of blood due to valvular incompetence.
  • Fegan's test: On standing, the site where the perforators enter the deep fascia bulges and this is marked. Then on lying down, button like depression (crescent like) in the deep fascia is felt at the marked out points which confirms the perforator site.
  • Pratt's test: Esmarch bandage is applied to the leg from below upwards followed by a tourniquet at saphenofemoral junction. After that the bandage is released keeping the tourniquet in the same position to see the “blow outs” as perforators.
  • Morrissey's cough impulse test: The varicose veins are emptied. The leg is elevated and then the patient is asked to cough. If there is saphenofemoral incompetence, expansile impulse is felt at saphenous opening. It is a venous thrill due to vibration caused by turbulent backflow.
  • Ian-Aird test: On standing, proximal segment of long saphenous vein is emptied with two fingers. Pressure from proximal finger is released to see the rapid filling from above which confirms saphenofemoral incompetence.
  • Examination of the abdomen has to be done to look for pelvic tumours, lymph nodes, which may compress over the veins to cause varicosity.
  • Venous segmental disease score (venous clinical scoring system/VCSS) is done based on different symptoms/signs/ulcer activity/compression therapy with 10 parameters with each having 3 scores as mild/moderate/severe.
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Figs 1.412A and B: Tourniquet tests for long saphenous vein and short saphenous vein.
 
Investigations
  • Venous Doppler:
    • With the patient standing, the Doppler probe is placed at saphenofemoral junction and later wherever required. Basically by hearing the changes in sound, venous flow, venous patency, venous reflux can be very well-identified.
    • Doppler test: When a hand held Doppler (continuous wave 8 MHz flow detector) is kept at SFJ, typical audible, 'whoosh signal' >0.5 sec while performing Valsalva manoeuvre is the sign of reflux at SFJ. It is also used at SPJ and at perforators.
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Fig. 1.413: Doppler machine to assess venous system and its problems.
231
Note:
All clinical/phlebological tests mentioned above have been superseded by Doppler test. Doppler test is considered to be a clinical method.
  • Duplex scan:
    • It is a highly reliable U/S Doppler imaging technique (here high resolution B mode ultrasound imaging and Doppler ultrasound is used) which along with direct visualisation of veins, gives the functional and anatomical information, and also colour map. Examination is done in standing, lying down position and also with valsalva manoeuvre. Hand-held Doppler probe is placed over the site and visualised for any block and reversal of flow. DVT is very well-identified by this method.
    • Venous haemodynamic mapping/VHM/Cartography is essential prior to surgery.
Note:
  • Proper venous haemodynamic mapping (VHM) is essential.
  • Saphenous eye (Egyptian eye) at SFJ should be identified in duplex US.
  • Reflux is defined as retrograde blood flow in reverse direction lasting for more than 0.5 seconds.
  • Micky mouse sign’ is the duplex scan transverse B mode image showing great saphenous vein (GSV) and femoral vein medially and femoral artery laterally.
  • Digitally coded free flow (B flow) USG (Professor Feder Lurie of Hawaii) allows simultaneous visualisation of flowing blood/blood cells and surrounding stationary structures to give proper haemodynamic imaging with functioning mechanism of venous valves, valve leaflets and flow across leaflets. This may be the ideal tool of investigation in future.
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Fig. 1.414: Venous haemodynamic mapping (VHM) of the lower limb.
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Figs 1.415A and B: Duplex scan for venous diseases of lower limb should also be done in standing position.
  • Venography:
    • Ascending venography was very common investigation done before Doppler period.
      A tourniquet is applied above the malleoli and vein of dorsal venous arch of foot is cannulated. Water soluble dye injected, 232flows into the deep veins (because of the applied tourniquet). X-rays are taken below and above knee level. Any block in deep veins, its extent, perforator status can be made out by this.
      It is a good reliable investigation for DVT.
      If DVT is present, surgery or sclerotherapy are contraindicated.
    • Descending venogram is done when ascending venogram is not possible and also to visualise incompetent veins. Here contrast material is injected into the femoral vein through a cannula in standing position. X-ray pictures are taken to visualise deep veins and incompetent veins.
  • Plethysmography:
    • It is a noninvasive method which measures volume changes in the leg. It gives functional information on venous volume changes and calf muscle pump insufficiency.
    • Photoplethysmography: Using probe transmission of light through the skin, venous filling of the surface venules which reflects the superficial venous pressure is measured. Initially patient performs dorsiflexion at ankle for 10 times to empty the venules and pressure tracing falls in photoplethysmography. Patient takes rest and refilling occurs. In normal people, it occurs through arterial inflow in 20–30 seconds. In venous incompetence filling also occurs by venous reflux and so refilling time is faster than normal.
      Disadvantage: Site of reflux cannot be localised by this method.
    • Air plethysmography: Patient is initially in supine position with veins emptied by elevation of leg. Air filled plastic pressure bladder (inflatable polyurethane cuff filled with air) is placed on calf to detect volume changes. Minimum volume is recorded. Patient is turned to upright position and venous volume is assessed. Maximum venous volume divided by time required to achieve maximum venous volume gives the venous filling index (VFI). VFI is a measure of reflux. Ejection fraction is volume change measured prior and after single tiptoe manoeuvre which is a measure of calf pump action. Residual venous fraction is an index of overall venous function which is venous volume in the leg after ten toetip manoeuvres divided by venous volume prior to manoeuvre. Increased VFI and diminished ejection fraction in a patient will benefit from surgery.
  • Ambulatory venous pressure (AVP):
    It is an invasive method. Needle inserted into dorsal vein of foot and is connected to transducer to get its pressure which is equivalent to pressure in the deep veins of the calf. Ten tiptoe manoeuvres are done by the patient. With initial rise in pressure, pressure decreases and eventually stabilises with a balance. Pressure now is called as ambulatory venous pressure (AVP). After stopping exercise, veins are allowed to refill with return of pressure to baseline. Time required for pressure to return to 90% of baseline is called as venous refilling time (VRT). Raise in AVP signifies venous hypertension. Patients with AVP more than 80 mmHg has got 80% chances of venous ulcer formation.
  • Arm-foot venous pressure:
    Foot pressure is not more than 4 mmHg above the arm pressure.
  • Varicography:
    Here nonionic, iso-osmolar, nonthrombogenic contrast is injected directly into the variceal vein to get a detailed anatomical mapping of the varicose veins. It is used in recurrent varicose veins.
 
Treatment
  • Conservative treatment:
    • Elastic crepe bandage application from below upwards or use of pressure stockings to the limb—pressure gradiant of 30–40 mmHg is provided.
    • Elevation of the limb—relieves oedema. Two short times, during day and full night, elevation of foot with feet above the level of heart and toes above the level of nose is the method.
    • Unna boots—provide nonelastic compression therapy. It comprises a gauze compression dressings that contain zinc oxide, calamine, and glycerine that helps to prevent further skin break down. It is changed once a week.
    • Pneumatic compression method—provide dynamic sequential compression.
    • These methods reduce the AVP, reduce transcapillary fluid leakage by increasing SC pressure and improve cutaneous microcirculation.
  • Drugs used for varicose veins:
    • Calcium dobesilate—500 mg BD. Calcium dobesilate improves lymph flow; improves macrophage mediated proteolysis; and reduces oedema.
    • Diosmin—450 mg BD.
    • Diosmin 450 mg + Hesperidin 50 mg (DAFLON 500 mg). Mainly used in relieving night cramps but not to improve healing of ulcers.
    • Toxerutin 500 mg BD, TID. Antierythrocyte aggregation agent which improves capillary dynamics.
    • Diosmin is micronized purified flavanoid fraction. It protects venous wall and valve, and it is anti-inflammatory, profibrinolytic, anti-oedema, lymphotropic.
    • Benzopyrones, saponins, plant extracts, Ruscus (venular α 1 adrenergic receptor partial agonist) coumarins are different drugs used.
      Benefits of all these drugs are doubtful.
  • Injection—sclerotherapy:
    • Fegan's technique: By injecting sclerosants into the vein, complete sclerosis of the venous walls can be achieved.
      Indications
      • Uncomplicated perforator incompetence.
      • In the management of smaller varices—reticular veins, thread veins (telangiectasis).
      • Recurrent varices.
      • Isolated varicosities.
      • Aged/unfit patients.
        233
      • A 23 gauge needle is inserted into the vein (3–8 mm sized) and vein is emptied. 0.5–1 ml of sclerosant is injected into the vein and immediately compression is applied on the vein (prevent the entry of blood which may cause thrombosis, which later gets recanalised, further worsening the condition) so as to allow the development of sclerosis and to have proper endothelial apposition.
      • Usually injection is started at the ankle region and then proceeded upwards along the length of the veins at different points. Later pressure bandage is applied for six weeks. Often injections may have to be repeated at 2–4 weeks intervals for 2–4 sessions. Technique is called as macrosclerotherapy.
      • Entrapped blood may require to be evacuated after 14 days which is often essential to prevent recanalisation.
    • Foam sclerotherapy by Tessari:
      • STDS taken in a syringe is passed rapidly into another syringe which contains air to result in formation of foam. 1 ml of STD is mixed with 4 ml of air to make 5 ml of foam which is injected to vein. Total 6 ml maximum of STDS with 30 ml foam can be used. This foam in much larger quantity is injected into the superficial vein. Air get absorbed between foam and endothelial lining is destroyed. Foam minimises thrombosis by pushing the blood out of the site of the vessel where action is needed. Polidocanol/STDS is used for foam sclerotherapy.
      • Advantages: Cheap, technically easy, easily available, OPD procedure, can be repeated many times, anaesthesia is not needed, can be used along with other procedures for varicose veins.
      • Complications: Headache, transient blindness, stroke, air embolism, thrombophlebitis, pain over injected site, pigmentation.
      • Contraindications: Peripheral arterial disease, DVT.
    • Microsclerotherapy:
      Very dilute solution of sclerosing agent like STDS (0.1% of 0.1 ml—dilute) Polidocanol is injected into the thread veins and reticular veins followed by application of compression bandage (30 G needle). Dermal flare will disappear well by this method.
    • Transillumination microsclerotherapy (vein—lite): It is better imaging of the veins using light generated by halogen bulb with high quality fibre illumination over the skin uniformly and passing 30 gauge needle for microsclerotherapy.
      zoom view
      Figs 1.416A to C: Technique making foam and injecting into the vein. 4 ml air with 1 ml STD is mixed vigorously using 3 way stopcock and two 5 ml syringes. Created foam is injected into the vein immediately. Total of 6 ml STD (30 ml foam) can be injected.
  • 234Echosclerotherapy:
    Sclerotherapy is done under duplex ultrasound image guidance.
  • Catheter directed sclerotherapy:
    It is devised at Miami vein clinic with specific catheter for sclerotherapy. This catheter has got side holes all around the specific length for uniform contact of venous wall with the foam. It also has got a balloon at the tip which after inflation blocks the SFJ thus preventing embolization of foam. It has got three external ports one for balloon inflation; one for bladder valve port; one for injection. This technique is under trial.
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Fig. 1.417: Catheter directed sclerotherapy.
Advantages of sclerotherapy
  • It can be done as an outpatient procedure.
  • It does not require anaesthesia.
Disadvantages of sclerotherapy
  • Inadvertent subcutaneous injection can cause skin necrosis or abscess formation.
  • Anaphylaxis, vasovagal shock, allergy.
  • Hyperpigmentation.
  • Thrombophlebitis.
  • Deep venous thrombosis can occur.
  • Inadvertent intra-arterial injection—serious complication.
  • Intravenous haematoma.
  • Temporary ocular disturbances.
  • Skin staining, injection ulcers, persistent local pain.
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Fig. 1.418: Veins should be marked just prior to surgery using marking ink.
Indications for interventional procedures:
  • To relieve Complaints which are relevant like pain, discomfort;
  • to reverse Complications like skin changes, ulcers, bleeding, superficial thrombophlebitis, lipodermatosclerosis;
  • Cosmesis; prophylaxis.
  • Surgery:
    • Trendelenburg operation (Crossectomy)
      It is juxtafemoral flush ligation of long saphenous vein (i.e. flush with femoral vein), after ligating named (superficial circumflex, superficial external pudendal, superficial epigastric vein), deep external pudendal vein and unnamed tributaries. All tributaries should be ligated, otherwise recurrence will occur. Double saphenous vein is the most common anomaly occurring near saphenovenous junction.
    • Stripping of vein
      • Using Myer's stripper vein is stripped off. Stripping from below upwards is technically easier. Immediate application of crepe bandage reduces the chance of bleeding and haematoma formation. Stripping avulses the vein as well as obliterates the tributaries. Babcock's stripper and rigid metal pin stripper can also be used.
      • Two methods of stripping are used: (1) Extraluminal collision technique using Myer's stripper (Acorn head stripper, 73 cm long) is practiced since long time; but it damages the adjacent tissue, causes infection, postoperative pain, discomfort and haematoma along the stripped tract with possibility of revascularisation of the tract haematoma. (2) Invagination technique is better with less damage to adjacent tissue. Codman's stripper is used for invagination technique.
      • Stripping of the short saphenous vein is done from ankle below upwards after passing stripper from above downwards. It obliterates the mid calf perforator vein which is the common reason for recurrences.
      • Complications of stripping: Saphenous neuralgia (1–7%) 235due to saphenous nerve injury/avulsion; numbness and tingling along femoral nerve distribution; haematoma; infection; ulceration; recurrence of the disease is common (30%) which is not due to any technical default but due to progression of disease itself by neo-angiogenesis and re-vascularisation.
Note:
  • Striping of LSV up to knee level reduces the need for re-intervention for recurrent varicose veins; stripping up to the ankle will not benefit additionally but may increase the chance of saphenous nerve injury. So stripping is not at all done in lower part of the leg for LSV.
  • Stripping of the vein is more effective than just ligation of the vein at the SFJ/SPJ.
  • Stripping of SSV reduces the recurrence but may damage sural nerve.
  • ‘Inverting or invaginating stripping’ using rigid Oesch pin stripper is better as postoperative pain and haematoma is less common and also tissue damage. Vein should be very firmly fixed to the end of the stripper and pulled out to cause the inverting of the vein.
  • Stripping of short saphenous vein is more beneficial than just ligation at saphenopopliteal junction. It is done from above downwards using a rigid stripper to avoid injury to sural nerve.
  • Subfascial ligation of Cockett and Dodd (1938):
    • Perforators are marked out by Fegan's method. Perforators are ligated deep to the deep fascia through incisions in anteromedial side of the leg.
  • Ligation of short saphenous vein at saphenopopliteal junction. It is done in prone position with horizontal incision. Variations in SP junction are common. But stripping is better.
  • Linton's vertical approach (1938)—subfascial ligation of perforators.
  • Stab avulsion of varicose vein and perforators: Avulsion is done using mosquito forceps or avulsion hooks-hook phlebectomy. It is popular method, also used along with other minimal invasive techniques like EVLA, RFA. Multiple incisions are made and veins are carefully and gently avulsed/teased to clear it. Postoperative compression bandage is a must.
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Figs 1.419A and B: Photo of Myer's stripper with Olive tips and also diagrammatic look of the same.
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Fig. 1.420: Incision for juxtafemoral flush ligation of long saphenous vein (Trendelenburg operation).
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Figs 1.421A and B:
236
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Figs 1.421A to C: Saphenofemoral junction and its ligation. Tributaries are well seen.
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Figs 1.422A to C:
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Figs 1.422A to D: Long saphenous vein stripping. Note the stripped vein. Stripping is better than just ligation at the junction.
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Figs 1.423A and B: A. Cockett and Dood subfascial ligation of perforators using multiple small horizontal incisions. B. Linton's vertical approach for subfascial perforator ligation in the leg.
237
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Fig. 1.424: Typical perforator ligation.
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Figs 1.425A and B: Avulsion of the perforator using hook or mosquito forceps through a small skin incision-stab avulsion.
  • Minimally invasive methods:
    1. Subfascial endoscopic perforator ligation surgery (SEPS)
      • A special telescope is introduced deep to deep fascia through a single small vertical incision at proximal leg selecting healthy skin. Potential space between muscle and deep fascia with loose areolar tissue is easy to dissect using endoscope. Technique is done under tourniquet 300 mmHg pressure. Endoscope is advanced down along the medial border of the tibia. Perforators travelling in subfascial plane are identified and fulgurated using bipolar cautery or clips can be applied into the perforators. It is recommended in chronic venous insufficiency (CVI). But its limitation is difficulty in getting ‘lift off’ skin in cases with severe lipodermatosclerosis to identify the perforators.
    2. Radiofrequency ablation (RFA) method (VNUS closure method) (VNUS medical technologies Inc; Sunnyvale, CA, USA) (by Goldman 2000):
      This procedure is done under general or regional anaesthesia. A RFA catheter is passed into long/ short saphenous vein near saphenofemoral or sapheno-popliteal junction under guidance. 85°C temperature is used for longer period of time to cause endothelial damage, collagen denaturation and venous constriction. 7 French catheter is used and 7 cm segment vein is ablated sequentially. Phlebectomy is done while withdrawing the catheter. Wall of the vein is destroyed through its full thickness. Vein forms a cord, which gets dissolved by macrophages and immune cells.
      CELON RFITT—Radio Frequency Induced Thermal Therapy (2007) is newer type.
      zoom view
      Fig. 1.426: Subfascial endoscopic perforator ligation surgery (SEPS).
    3. Trivex method:
      Under subcutaneous illumination and local anaesthesia, a large quantity of fluid is injected percutaneously to identify the superficial veins under. Tumescent anaesthesia created causes hydrodissection. Trivex resector and illuminator are placed under the skin. Resector gently extracts veins by suction and morcellation. Further stages of tumescence flushes all blood and delivers vasoconstriction solutions. Solution is passed through 18 gauze needle to clear all blood underneath. Method is cosmetically acceptable; removes all sized veins; achieves good pain relief; with minimal complications like bruising, induration which gets resorbed eventually; and can be used when there are venous ulcers.
    4. Endovenous laser ablation (EVLA):
      It is done as an outpatient procedure or as day-care surgery. Patient lies supine with diseased leg flexed, hip externally rotated and knee flexed. With aseptic precaution, under U/S guidance LSV is cannulated guide wire is passed beyond SFJ and 5- French catheter is passed over guide wire and tip is placed 1 cm distal to the junction. 200 ml of 0.1% lignocaine (crystalloid with local anaesthetic) is infiltrated along the length of the LSV. Laser fibre is inserted up to the tip of the catheter and catheter is withdrawn for 2 cm and laser fibre protrudes for 2 cm. Laser fibre is fired step by step using diode laser (810–1470 nm diode laser energy), one mm withdrawal in 2 seconds. Once procedure is over catheter is removed 238and pressure bandage is applied for 2 weeks. Heat produced (729–1000°C at tip) by the laser produces steam bubbles with thermal damage of endothelium leading into occlusion of the vein. Laser energy acts on the blood within the vein rather directly through the wall and heats the blood and in turn heats the vein wall. Drawback of laser therapy is inability to create flush occlusion allowing tributaries to open up to cause possible recurrence.
      Complications of EVLA: Pain; ecchymosis, haematoma, skin burns, difficulty in cannulating the unsuitable vein if selected; DVT; sensory disturbances, infection.
      Note:
      EVLA has got 95% efficacy. Tumescent anaesthesia is prepared by mixing 500 ml of normal saline, 30 ml of xylocaine 1% with adrenaline, 10–30 ml of 8.4% sodium bicarbonate. It is injected using long needle along the length adjacent to vein to cause tamponade and to prevent heat burn on the surface.
    5. Other methods:
      • Transilluminated phlebectomy is done by passing transilluminating light under the skin and passing a rotating blade through another small incision. Veins are grasped and removed by rotating movements.
      • Ambulatory phlebectomy is done through tiny small incisions using special phlebectomy instruments.
      • Electrodessication using weak electric current through a fine needle directly into the spider veins (telangiectasis) is also used.
Note:
Contraindication for surgery is deep vein thrombosis (DVT).
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Figs 1.427A and B:
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Figs 1.427A to D: Endovenous laser ablation (EVLA) for varicose veins.
 
VENOUS ULCER (Gravitational ulcer)
It is the complication of varicose veins or deep vein thrombosis.
 
Pathogenesis of Venous Ulcer
Varicose veins or DVT which are recanalised, even-tually causes chronic venous hypertension around ankle
Causes haemosiderin deposition in the subcuta-neous plane from lysed RBC's
Eczema
Dermatitis
239Lipodermatosclerosis
Fibrosis
Anoxia
Ulceration
Ambulatory venous hypertension is the prime cause of venous ulcer formation. Venous hypertension may be gravitational which is due to hydrostatic pressure by weight of blood column from the right atrium (hydrostatic reflux) which is maximum at foot and ankle OR dynamic which is due to muscular contraction across the incompetent perforator with a high pressure up to 200 mmHg (hydrodynamic reflux). There is a peculiar recycling of blood from deep veins → femoral vein → spillage of blood across incompetent SFJ into LSV/GSV → passage of same blood across perforators into the deep veins to reach femoral vein → again to enter the LSV as spillage.
White cell trapping' theory and ‘fibrin cuff’ theory; release of free radicals; increased matrix metalloproteinases (MMPs); abnormal fibroblast activity; inhibition of growth factors; are other causes of venous ulcer formation.
  • Area where venous ulcer commonly develops, is around and above the medial malleoli because of presence of large number of perforators which transmit pressure changes directly into superficial system. This area is called as Gaiter's zone. It can also be on both malleoli.
  • Ulcer is often large, nonhealing, tender, recurrent with secondary infection. Vertical group of inguinal lymph nodes are usually enlarged and tender.
  • Often it leads to scarring, ankylosis, Marjolin's ulcer formation. Slough from the ulcer bed may give way causing venous haemorrhage.
  • Periostitis is common which also prevents ulcer from healing.
    zoom view
    Fig. 1.428: Venous ulcers around both ankles (bilateral).
    zoom view
    Fig. 1.429: Gaiter's zone. It is handbreadth area around malleoli where complications of venous disease occurs. Word gaiter (French) is a leather/cloth covering for lower leg and ankle.
    zoom view
    Fig. 1.430: Champagne bottle sign/inverted beer bottle sign is seen in lipodermatosclerosis due to prominent calf with narrow ankle, contracted skin and subcutaneous tissue. Sign is often observed in DVT also.
  • Most of the venous ulcers have surrounding lipodermatosclerosis. Lipodermatosclerosis is pigmentation, thickening, chronic inflammation and induration of the skin in calf and around ankle.
    240
    zoom view
    Fig. 1.431: Marjolin's ulcer in a chronic venous ulcer.
  • Due to regular walking on toes so as to relieve the pain causes contraction and extra-articular fibrosis of achilles tendon. Proper exercise is the remedy for—talipes equinovarus.
    Note:
    70–80% of leg ulcers are venous ulcers.
 
Investigations
  • Discharge from the ulcer for culture and sensitivity.
  • X-ray of the area to look for periostitis.
  • Biopsy from the ulcer edge to rule out Marjolin's ulcer.
  • Investigations to rule out other causes of leg ulcers like arterial; neurological; diabetes; sickle cell disease and other haemolytic diseases.
  • Erythrocyte sedimentation rate; C-reactive protein, peripheral smear; red cell counts.
  • Doppler—venous and often arterial.
 
Treatment
  • Bisgaard method of treating venous ulcer:
    • Measures to reduce oedema, increase venous drainage, so as to promote ulcer healing.
      • Elevation.
      • Massage of the indurated area and whole calf.
      • Passive and active exercise.
    • Care of ulcer by regular cleaning with povidone iodine, H2O2.
    • Dressing with EUSOL.
    • Four layer bandage (45 mmHg pressure) technique to achieve high compression pressure. It is changed once a week.
    • Antibiotics depending on culture and sensitivity of the discharge.
    • Once ulcer bed granulates well, split skin graft (SSG) is placed (Thiersch Graft), or pinch graft.
  • Specific treatment for varicose veins should be under-taken—Trendelenburg operation, stripping of veins, perforator ligation.
  • Fifty percent of venous ulcer occurs as a result of recanalisation of DVT, and the leg is commonly called as postphlebitic limb (leg). It presents with all compli-cations of venous diseases like eczema, ulceration, lipodermatosclerosis and venous ulcers. Here surgery for superficial varicose veins are contraindicated. Venous valve repair (Kistner's valvuloplasty) or valve transplantation or drugs like Stanazolol, which reduces the fibrous tissue thereby increasing the oxygenation are beneficial.
    zoom view
    Fig. 1.432: Skin graft is done over a venous ulcer once ulcer has shown healthy granulation tissue.
(EUSOL is Edinburgh University solution of lime containing boric acid, sodium hypochlorite, calcium hydroxide.)
Note:
  • Present concept is to treat the ulcer first by compression bandage; regular dressing; skin grafting. Once ulcer has healed definitive procedure for varicose veins is done. Studies show that rapidity of healing of ulcer perse is not dependent on the surgery for varicose veins.
  • Recurrence rate of venous ulcer after proper therapy is 30%. Reulcer formation is more in post-phlebitic/ thrombotic limb.
241
 
COMPRESSION THERAPY FOR VARICOSE VEINS
  • Compression reduces the venous wall tension; prevents reflux; controls the venous over-distension.
  • Compression diverts the blood towards deep veins through perforating veins; prevents the outward flow of blood in perforator incompetence; improves the efficacy of calf muscle pump. Compression reduces the oedema and improves the venous and lymphatic drainage; improves venous elasticity; improves the microcirculation and more important is it prevents further damage of the venous wall.
  • Compression may be elastic/inelastic/combination of elastic and inelastic (Unna boot)/multilayered (four layered) compression system which can provide sustained high compression for several days—usually up to a week/intermittent pneumatic compression. Unna boot is three-layered paste gauze compression dressing containing calamine, zinc oxide, glycerin, sorbitol, gelatin and aluminium silicate which has mainly inelastic inner component with partly elastic outer layer wrap.
  • Recommended pressure in mild varicose veins, pregnancy and postoperative period is 20 mmHg; in symptomatic varicose veins and after sclerotherapy is 30 mmHg; in venous ulcer and post-phlebitic leg it is 40–45 mmHg; in phlebolymphoedema (venous oedema with lymphatic oedema which is more dangerous) it is more than 45 mmHg.
  • Skin maceration, excoriation, dryness, infection, ulceration and failure are the complications of compression therapy.
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Fig. 1.433: Compression stockings should be worn in varicose vein disease even after intervention to reduce the chances of recurrence.
 
THROMBOPHLEBITIS
It is the inflammation of veins, usually of superficial, veins due to different causes. It is actually superficial vein thrombosis (SVT) with inflammation (slight).
 
Types
  1. Acute: Due to IV cannulation, trauma, minor infections, hypercoagulability.
  2. Recurrent.
  3. Spontaneous: Polycythaemia vera, polyarteritis, Buerger's disease.
  4. Thrombophlebitis migrans (Trousseau's sign, 1876): It is spontaneous migrating thrombophlebitis seen in visceral malignancy like pancreas, stomach.
  5. Mondor's disease.
It can be—SVT with varicose veins (V-SVT) or SVT without varicose veins (NV-SVT). It can also be—primary or secondary.
Duplex ultrasound Doppler of both limbs is a must.
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Fig. 1.434: Superficial thrombophlebitis with clot and infection.
242
 
Clinical Features
  • Pain, redness, tenderness, cord like thickening of veins, fever.
  • It can be seen either in upper limb or lower limb.
 
Complications
  • Destruction of venous valves resulting in varicose veins.
  • DVT, embolism, infection.
 
Treatment
  • Elevation.
  • Anti-inflammatory drugs, antibiotics.
  • Application of crepe bandage—compression therapy.
  • Anticoagulation—LMWH for SVT >3 cm in length.
 
KLIPPEL-TRENAUNAY SYNDROME
It is a nonfamilial mesodermal anomaly with skin naevus, varicose veins, soft tissue and bone hypertrophy. Deep veins are often aplastic. It is usually managed with compression bandages. If patient is undergoing surgery for some other condition, then LMWH should be started. Condition itself occasionally can be treated with EVLA for varicose veins if only deep veins are normal; bone length discrepancy correction of leg is done.
Parkes-Weber syndrome is a differential diagnosis. PW syndrome presents with varicose veins, multiple AV fistulas, chronic venous hypertension, high output cardiac failure and ulceration.
 
ANTICOAGULANTS
These are the agents used to prevent and treat thrombosis and thromboembolic events.
 
HEPARIN (UNFRACTIONATED/UFH)
  • It is a natural anticoagulant, a mucopolysaccharide.
  • It prevents clotting of blood both in vivo and in vitro by acting on all three stages of coagulation. It prolongs clotting time and activated thromboplastin time in specific (by 1.5–2.0 times the control).
  • Heparin also causes hyperkalaemia, thrombocytopenia, osteoporosis.
  • Commercial heparin is derived from lung and intestinal mucosa of pigs and cattle.
  • The onset of action is immediate after administration, lasting for 4 hours.
  • It is metabolised in the liver by heparinase.
  • It does not cross placental barrier and is not secreted in breast milk.
 
Indications
  • As prophylaxis in major surgeries, postoperative period, puerperium.
  • As therapy in DVT.
 
Dose
  • For prophylaxis: 5,000 units/subcutaneously 8th hourly.
  • For therapy: 10,000 units/IV 6th or 8th hourly. Later changed to subcutaneous dose.
  • In severe cases, 5,000 units to 20,000 units is given daily through IV infusion at a rate of 1,000 units per hour. Daily dose should not exceed 25,000 units.
Heparin should not be given intramuscularly and should not be combined with streptokinase or urokinase. Heparin is not given orally.
Heparin administration should always be monitored with APTT.
 
Complications
Allergy, bleeding, thrombocytopenia.
Note
Danaparoid is an antifactor Xa, heparinoid, is an anticoagulant used in patients where heparin is contraindicated.
 
LOW MOLECULAR WEIGHT HEPARIN (LMWH)
It is a commercially prepared heparin with a molecular weight of 4,000 to 6,500.
  • Enoxaparin.
  • Dalteparin.
  • Parnaparin.
  • Reviparin.
  • Fraxiparine.
Heparin antagonist: 50 mg of 1% protamine sulphate solution is given slow intravenous. 1 gm reverses 100 units of heparin. It is given only after doing activated thromboplastin time. Overdosing or infusion without indication may itself precipitate bleeding.
 
ORAL ANTICOAGULANTS
They are given orally and are slow-acting.
 
Types
  • Coumarin derivatives: Bishydroxycoumarin (Dicoumarol): First coumarin drug derived from sweet clover.
    Warfarin sodium: Most common oral anticoagulant used.
  • Indandione derivative: Phenindione, anisindione.
 
Mode of Action of Oral Anticoagulant Therapy
  • By suppressing synthesis of prothrombin, factors VII, IX and X.
  • By inhibiting vitamin K mediated carboxylation of glutamic acid.
  • Oral anticoagulant does not have in vitro action.
  • They are slow-acting, and long-acting.
  • Control of oral anticoagulant therapy is by monitoring prothrombin time.
  • PT comes to normal only 7 days after cessation of the drug.
  • They cross placental barrier and are known to cause teratogenicity when given in 1st trimester.
  • They are secreted in breast milk.
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Indications
  • In DVT after cessation of heparin for maintenance therapy.
  • After valve replacement surgery.
To achieve adequate anticoagulant effect and to prevent thromboembolic episodes the INR has to be maintained within 2–3.
 
Side Effects
  • Bleeding—it may require blood transfusion/FFP or vitamin K injection intramuscular or oral to control.
  • Cutaneous gangrene.
  • Fetal haemorrhage and teratogenicity.
  • Alopecia, urticaria, dermatitis.
  • Drug interactions: with NSAIDs, cimetidine, omeprazole, metronidazole, cotrimoxazole, erythromycins, barbiturates, rifampicin, griseofulvin.
 
WARFARIN
WARFARIN (Wiskonian Alumini Research Foundation + coumARIN derivative) SODIUM is the most common drug used. It has got lesser side effects. It has got cumulative action and so given in tapering dose.
Dose is 5 mg, once a day.
It should be discontinued 7 days before any surgery like tooth extraction and prothrombin time should return to normal level. During surgery, if excess bleeding occurs, fresh frozen plasma may be given.
The effects of warfarin sodium is reversed by injection vitamin K; the dose depends on INR and emergency of reversal (takes 24 times to reverse).
Note
In Vitro Anticoagulants: Oxalates, citrates, EDTA (Ethylene diamine tetra-acetic acid).
Differences between oral anticoagulants and heparin
Oral anticoagulant
Heparin
Slow-acting
Immediate
Long-acting
Short-acting
Only in vivo action
Both in vitro and in vivo action
Monitored by
Prothrombin time
Partial thromboplastin time
Crosses the placental barrier
Does not cross the placenta
Secreted in milk
Not secreted in milk
Administration
Orally
Intravenously/subcutaneously
 
DIRECT THROMBIN INHIBITORS
  • Recombinant hirudin and hirudin analogues—derived from leeches, are direct inhibitors of thrombin.
  • Argatroban, dabigatran, etixilate—synthetic direct thrombin inhibitor.
  • Rivaroxaban—It is direct factor Xa inhibitor. It is given orally once or twice daily as 15–20 mg dose per day. It is given initially 15 mg twice daily, later 20 mg once daily. It shows rapid bioavailability; shows rapid onset of action; coagulation monitoring is not required. Apixaban and edoxaban are other drugs.
 
ANTIPLATELET DRUGS
  • Small dose aspirin—inhibits platelet synthesis of thrombaxane A2.
  • Ticlopidine (125 mg BD)—alters platelet membrane, thereby platelet aggregation.
  • Clopidogrel—action similar to ticlopidine.
  • Dextran—decreases platelet aggregation.
  • Abciximab—glycoprotein IIb/IIIa inhibitors, block platelet aggregation, and platelet adhesion to fibrin.
  • Dipyridamole—xanthine oxidase inhibitor.
 
PULMONARY EMBOLISM
  • It is commonly due to lower limb DVT (15% of lower limb DVT). It can also occur after pelvic vein DVT or upper limb DVT (30% of upper limb DVT).
  • Chest pain, cough, haemoptysis, dyspnoea are the features.
  • Often site of DVT may be asymptomatic. When symptomatic, fever, pain, tense, tender calf, with positive Homan's sign may be evident.
  • Massive embolism causes sudden cardiac arrest and death due to pulmonary artery block. Moderate embolism causes pyramidal wedge-shaped infarcts in lungs.
  • Duplex scan of limb, CT angiogram of thorax, pulmonary angiogram (gold standard), X-ray chest, ventilation perfusion scan, ECG, echocardiography are useful investigations.
  • Treatment is thrombolysis, heparin/LMWH, compression bandage.
  • Occasionally surgical removal of clot from pulmonary artery is done if possible.
  • IVC filter placement is essential in recurrent DVT with anticoagulation, DVT with contraindication for anticoagulation, pulmonary hypertension. Greenfield IVC filter is ideal with 95% patency rate. Complications are—bleeding, haematoma, migration of filter into pulmonary artery, thrombosis at filter level, IVC perforation.
  • 244Retrievable IVC filters are newer method used to prevent long-term filter complications. It is used in young patients who are at risk of DVT and embolism, for short specified period only like-high-risk trauma with orthopaedic injuries, extensive iliofemoral thrombosis, during thrombolytic therapy. Recovery filter, Gunthur-Tulip filter, OptEase filters are used. They are deployed through IJV or femoral vein under angiographic or intravascular US guidance. Recovery and Gunthur-Tulip types are recovered through right IJV. OptEase is recovered from right femoral vein. Complications are same as nonretrievable IVC filters. Retrieval failure, retrieval site thrombosis and embolism are specific complications.
  • DVT prophylaxis is a must in all these patients.
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Fig. 1.435: X-ray showing IVC filter in position.
O. Lymphatics
CHAPTER OUTLINE
  • ❖ Surgical Anatomy
  • ❖ Lymphangiography
  • ❖ Isotope Lymphoscintigraphy
  • ❖ Lymphoedema
  • ❖ Lymphomas
  • ❖ Hodgkin's Lymphoma
  • ❖ Non-Hodgkin's Lymphoma
  • ❖ Mantle Cell Lymphoma
  • ❖ Malt Lymphomas
  • ❖ Burkitt's Lymphoma
  • ❖ Cutaneous T Cell Lymphoma
  • ❖ Chylous Ascites
  • ❖ Chylothorax
  • ❖ Chyluria
  • ❖ Sarcoidosis245
 
SURGICAL ANATOMY
Primordial lymphatic system begins to develop during 6th week of development adjacent to jugular vein as lymph sacs. Peripheral lymphatic systems develop from these primordial lymph sacs. Lymphatic system has three components. Terminal lymphatic capillaries, which have high porosity absorb lymph, macromolecules, cells and microbes from tissues into the system; lymphatic vessels which collect and transport lymph; lymph nodes which are interposed in the lymphatic pathway filter lymph and maintain immunity of the body. Lymphatic vessels run adjacent to main blood vessels reaching the major lymphatic channels. Cisterna chyli is formed in the abdomen, continues as thoracic duct (formed at 9th week of gestation) in the thorax which has got initial main course towards right side of the mediastinum; but later towards left side entering the internal jugular vein at its joining point of the subclavian vein. In the periphery, there is hardly any lymphovenous communications. Lymphovenous communications occur at lymph node level; iliac, subclavian and jugular levels. Lymphatics are absent in epidermis, cornea, CNS, cartilage, tendon and muscle.
Great lymph ducts are—the thoracic duct—single; right lymph duct—single; subclavian, bronchomediastinal and jugular trunks on both sides. These ducts contain valves to prevent backflow.
Cisterna chyli is formed by joining of right and left lumbar lymphatic trunks and intestinal lymphatic duct. Lumbar trunks are short lymph vessels arising from para-aortic lymph glands. It receives lymph from lower limb, pelvis and pelvic viscera, kidney, adrenal and deep lymphatics of abdominal wall. Left lumbar trunk is behind the aorta. Intestinal lymph duct arises from preaortic nodes. It joins the cisterna chyli from front. It receives lymph from stomach, intestines, liver (except most convex surface which drains into right lymph duct), spleen and pancreas. Cisterna chyli is a lymph sac lying in front of the L1 and L2 vertebrae between aorta and crus of the diaphragm. From its upper end it continues as thoracic duct. Thoracic duct passes through the aortic orifice of the diaphragm, runs medial to azygos vein and right of the aorta in posterior mediastinum. In front it is related to oesophagus, diaphragm and pericardium; behind right intercostal arteries, hemiazygos and accessory hemiazygos vein. At the level of 7th thoracic vertebra, it crosses towards left side behind the oesophagus obliquely reaching left side at 5th thoracic vertebral level. It runs upwards between left margin of oesophagus, medial part of left pleura, and behind left subclavian artery. In the neck, it passes in front of vertebral system (vertebral vessels and sympathetic chain) and behind carotid system (Common carotid artery, internal jugular vein, vagus nerve), crossing scalenus anterior, phrenic nerve, transverse cervical and suprascapular arteries ending as a single vessel at the junction of internal jugular vein and subclavian vein with a valve. Tributaries of thoracic duct are—trunk from lateral intercostal nodes from lower six spaces; efferents from posterior mediastinal nodes, lateral intercostal nodes of upper six spaces, left jugular lymph trunk from head and neck region, left subclavian lymph trunk from left upper limb, left bronchomediastinal trunk from left side of the thorax. Single termination of duct is common (77%); but double/triple/quadruple terminations are known to occur. Occasionally it may end in left subclavian vein, left vertebral vein, right internal jugular vein, right subclavian vein. Thoracic duct is 45 cm in length and 5 mm wide (wider at both ends; narrow in the middle).
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Fig. 1.436: Thoracic duct anatomy; cisterna chyli; tributaries of thoracic duct.
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Fig. 1.437: Watershed zones/areas of lymphatic drainage. Vertical sagittal midline; clavicular horizontal line; umbilical line—are used to divide areas into three zones on each side. Above clavicular line drainage occurs to cervical nodes; between clavicular line and umbilical line drainage occurs into axillary nodes; below umbilical line drainage occurs to inguinal lymph nodes. At the level of (lines) drainage can occur to lymph nodes on either side.
Right lymph duct is 2.5 cm in length, formed by right jugular, right subclavian and right bronchomediastinal trunks; runs on the scalenus anterior joining the junction of right internal jugular vein and subclavian vein.
There are about total 450–600 lymph nodes in the body. Around 200 in the neck; around 100 in the thorax; around 50–60 in the axilla; around 250 in the abdomen and pelvis; around 50 in the groin area.
 
Lymphatic Watersheds of Skin
Lymph from the dermis and appendages drain into a plexus in deep fascia which in turn drains into respective lymph nodes. There are six watershed areas in the body for lymphatic drainage. One vertical midline divides into right and left. Two horizontal lines on each side divide the area into three zones. First lies above the line of clavicle; second between line of clavicle and line at umbilical level; third below the level of umbilical line. First drains into head and neck lymph nodes; second drains into axillary nodes; third drains into inguinal/groin nodes. Malignancy drains into their respective nodes depending on the location. Lesion on the line can spread to both territory lymph nodes. In skin and appendageal cancers, deep fascia also should be cleared.
 
Microanatomy of Lymph Node
Lymph node contains three regions—cortex; paracortex and medulla. Cortex contains mainly follicles. It may be rounded lymphocytic aggregations of primary follicles or lymphocytic aggregation with germinal centres of secondary follicles due to antigenic stimulation. It contains B lymphocytes, macrophages, dendritic reticulum cells. Germinal centre is surrounded by small B lymphocytes. Both cortex and medulla are associated with humoral immunity. Proliferation of germinal centres suggests active humoral immunity with antibody production. Central medulla contains mainly lymphatic sinuses, arteries and veins, plasma cell and B lymphocytes. Paracortex is located in a zone between cortex and medulla. It contains T lymphocytes, related to cell mediated immunity. Post-capillary venules with high endothelial cells and lymphocytes in the wall are typical. In cell mediated immunity, paracortex expansion occurs. Afferent lymph vessels enter the node through the capsule. It enters the marginal sinus, communicates with intranodal sinus, merging as efferent lymph vessels which enter the hilum. Intranodal sinus lining is highly phagocytic containing littoral cells and sinus lining histiocytes. Main artery and veins pass through the hilum to enter the medulla, paracortex and inner part of cortex. Superficial cortex is supplied by direct capsular vessels.
 
Function of Lymphatics
Most of the intravascular proteins are daily filtered through lymphatics and returned to the circulation again. Macromolecules (albumin, globulin and fibrinogen) and microbes are also filtered at the nodal level as first immune system. From GIT fat is absorbed directly through lymphatics. Lymph shows centripetal flow. Cholesterol, long chain fatty acids, fat soluble vitamins are transferred through lymphatics into cistern chyli directly from GIT bypassing the liver. Transport is mainly due to intrinsic contractility of the lymphatic vessels which contain valves for effective forward flow. To a lesser extent other factors like muscle contraction, arterial pressure, thoracic pressure, respiratory movements play role. 8 litres of lymph is produced daily; once it reaches to lymph nodes it is concentrated to 4 litres which enters the venous circulation. Protein concentration in lymph is very high (25 grams/litre).
Note:
Lymph drains protein rich fluid; there are no communicating/perforator lymphatics; lymphatics will not regenerate
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Fig. 1.438: Acute lymphangitis leg. Usually regional lymph nodes are enlarged and tender.
 
LYMPHANGIOGRAPHY
 
Indications
  • Congenital lymphoedema like aplasia, hypoplasia, hyperplasia.
  • Lymphomas show reticular pattern. It is also useful to assess the response to treatment.
  • Secondaries in lymph nodes, especially iliac and para-aortic lymph nodes.
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Technique
Patent blue dye or 1 ml isosulphan blue is injected subcutaneously between toes. Dye is taken up by lymphatics which will be visualised clearly. After making incision, one of the lymphatic vessels is dissected and 30 G needle is passed. Ultra-fluid lipiodol which is an oily contrast medium is injected slowly using pressure pump at a rate of 1 ml in 8 minutes (total quantity is 7 ml). Slowly in 24 hours, it passes through the lymphatics and reaches the iliac and para-aortic lymph nodes. Radiographs taken will help to visualise both lymphatic vessels as well as lymph nodes.
Secondaries in lymph nodes causes filling defects. Lymphomas shows enlarged nodes which have foamy or reticular appearance.
 
Disadvantages
  • Technically difficult.
  • Extravasation of dye can occur.
  • Dye may not reach the required area.
  • Time consuming and invasive procedure.
 
ISOTOPE LYMPHOSCINTIGRAPHY
  • Radioactive technetium labelled sulphide colloid particles, or radioiodinated human albumin are injected into the web space using fine needle. These particles are specifically taken up by lymphatics.
  • Using gamma camera, limb and inguinal region is exposed to visualise the lymphatics and inguinal lymph nodes.
  • Radioactivity in inguinal nodes is measured at 30 and 60 minutes. Normal uptake is 0.6–1.6%; if it is <0.3% in 30 minutes it is diagnostic of lymphoedema. If it is >2% it suggests rapid abnormal clearance due to oedema as the result of venous disease.
  • In 3 hours, it reaches the para-aortic lymph nodes, other abdominal lymph nodes and liver.
  • Later thoracic duct also can be visualised. It can be compared to the take up on the other limb.
 
Advantages
  • It is more sensitive.
  • Technically easier and faster compared to lymphangiography.
  • Thoracic duct, other lymph nodes and liver can be visualised.
  • It is the test of choice. It is simple and safe.
  • It has 90% sensitivity; 100% specificity.
 
LYMPHOEDEMA
It is accumulation of fluid (lymph) in extracellular and extravascular fluid compartment, commonly in subcutaneous tissue. It is primarily due to defective lymphatic drainage.
It is increased protein rich interstitial fluid.
 
Classification
Kinmonth classified lymphoedema as:
  • Primary without any identifiable lymphatic disease.
  • Secondary is acquired due to definitive cause. Most common form.
 
Pathophysiology of Lymphoedema
Decreased lymphatic contractility, lymphatic valvular insufficiency, lymphatic obliteration by infection, tumour or surgery causes all effects and pathology of lymphoedema. This leads to lymphatic hypertension and dilatation causing lymph stasis, accumulation of proteins, glycosamines, growth factors, and bacteria. There is more collagen formation, deposition of proteins, fibroblasts, ground substance causing fibrosis in subcutaneous and outside deep fascia. Muscles are normal without any oedema but may get hypertrophied.
Note:
Secondary lymphoedema develops rapidly.
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Fig. 1.439: Right side congenital limphoedema in a girl.
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Fig. 1.440: Early lymphoedema left side—pitting type.
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Fig. 1.441: Late lymphoedema—grade 2.
 
Filariasis
It is caused by a parasite Wuchereria (Brazil) bancrofti (Australia). It was also called as Malabar leg in 1709, by Clarke, Cochin. Female adult worm is longer 7–10 cm than male worm (4 cm). Microfilaria is colourless, translucent, 300 µ length and 10 µ thick. It has head, body and tail. Microfilaria circulates in blood. In India, Asian countries and China, they show nocturnal periodicity (from 10 PM to 4 AM). It is related to night biting habits of the vector, Culex fatigans mosquito and sleeping habits of the host.
Man is the definitive host; animal or reservoir host is not known. Female mosquito is intermediate host (in India and China—Culex fatigans). Development or multiplication of microfilaria will never occur in human blood. Life span of microfilaria in human blood is 3-months. Microfilaria is infective to female mosquito. A density of 15 microfilaria/drop of blood are needed to make it infective.
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Fig. 1.442: Lymphoedema leg extending into the thigh with lymphangitis.
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Figs 1.443A to C: Lymphoedema foot in different patients—severe with vesicles/oedema/skin changes/fissures.
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Life Cycle
Microfilaria from carrier human blood → enters the stomach of female Culex mosquito when it bites human carrying the parasite in blood → ex-sheathing of microfilaria in stomach of mosquito in 6 hours → penetrate the stomach wall → migrate to thoracic muscles of mosquito in 12 hours → metamorphosis into sausage shaped first stage larva in 48 hours → second stage larva in one week → elongated actively motile third stage infective larva in one more week (one microfilaria forms one infective larva; microfilaria never multiplies in mosquito nor in human) → enters the proboscis of mosquito to become infective to human during the mosquito bite; it takes 20 days for microfilaria to develop into infective 3rd stage larva in mosquito [extrinsic incubation period]→ enters human skin while biting → many larvae get destroyed in human skin by immunity, few enters lymphatics → enters regional lymph nodes in inguinal or axillary or abdominal nodes → develop into adult worm in lymph nodes → mating of female and male worms takes place → gravid female worm releases up to 50,000 microfilariae/day into lymph circulation → thoracic duct → subclavian vein → microfilaria in human circulation → infective to female mosquito. Time from 3rd stage infective larva entering human skin and forming adult worm and later releasing microfilaria into blood is called as biological incubation period (12 months); time from 3rd stage infective larva entering human skin to appearance of first clinical feature is called as clinical incubation period (16 months).
 
Effects of Wuchereria Bancrofti Infection
  • Carrier stage having circulating microfilaria but asymptomatic.
  • Immune and allergic reactions by adult worm causing macrophage and lymphocyte infiltration, endothelial hyperplasia, lymphatic vessel wall thickening, lymph stasis, dilatation, further reaction, fibrosis, further blockage, calcification, recurrent streptococcal infection, filarial lymphoedema.
  • Filarial fever, utricaria, pruritus, epididymo-orchitis as acute presentation.
  • Occult filariasis where microfilaria is not demonstrable in blood but identified in lungs (by biopsy confirmation) causing eosinophilia, bronchospasm, nocturnal cough, fever, wheeze, weight loss, arthritis, thrombophlebitis, tenosynovitis.
  • Lymphadenitis, lymphangitis.
  • Lymphangiovarix, lymphorrhagia, lymph scrotum, lymphocele, chyluria, chylous diarrhoea, retroperitoneal lymphangitis, chylous ascites, chylothorax.
  • Blood smear—night time (thick and thin), lymph node biopsy, skin test, eosinophilia, serological tests, DEC provocation test (by giving 100 mg DEC) are different investigations.
Rarely it causes protein losing diarrhoea, chylous ascites, chylothorax, chyluria, lymphorrhoea. Recurrent lymphadenitis occurs in the region which aggravate the condition.
Disease in the limb is confined to skin and subcutaneous tissue, i.e. often, only superficial lymphatics are involved by the disease, deep lymphatics are not. Superficial and deep lymphatics are not communicating with each other (Unlike the veins in the limb where superficial and deep veins are freely communicating with each other).
 
Clinical Features
  • Swelling in the foot, extending progressively in the leg—tree trunk pattern leg.
  • Loss of normal perimalleolar shape—tree trunk pattern leg.
  • Buffalo hump in the dorsum of the foot.
  • Squaring of toes.
  • Skin over the dorsum of foot cannot be pinched because of subcutaneous fibrosis—Stemmer's sign.
  • Initially pitting oedema occurs, which later becomes nonpitting.
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Fig. 1.444: Typical elephantiasis leg with late lymphoedema.
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Figs 1.445A and B: Different lymphoedema pictures. Note the oedema, fissuring, cracks. All these make it more vulnerable for infection.
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Fig. 1.446: Lymphoedema of lower limb developed after ilioinguinal block dissection for nodal secondaries from melanoma.
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Fig. 1.447: Recurrent filarial leg with nodules and ulceration.
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Fig. 1.448: Extensive scrotal lymphoedema of filarial origin. Patient underwent scrotal reduction.
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Figs 1.449: Lymphoedema right forearm. Common causes for upper limb lymphoedema are filarial and post-mastectomy with axillary nodal clearance.
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Figs 1.450A and B: Lymphoedema of penis. It needs reduction and reconstruction otherwise it may cause urinary problem and sexual dysfunction.
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Fig. 1.451: Severe lymphoedema foot with vesicles and thickening.
  • Dull ache/severe pain/burning/bursting/cramps; 50% patients will have pain.
  • Debility/immobility/obesity/muscle wasting.
  • Athlete's foot with joint pain and disability.
  • Eczema, fissuring, papillae formation, ulceration, lymph ooze, elephantiasis are other features.
  • Fever, malaise, headache.
  • Recurrent abscess formation.
  • Psychological and social discomfort causing severe morbidity.
  • Endemic elephantiasis/podoconiosis is common in Africa; seen in barefoot workers; due to destruction of lymphatics by silica derived from soil containing alkaline volcanic rocks.
 
Differential Diagnosis
  • Cardiac causes, hypoproteinaemia, malnutrition, nephrotic syndrome, liver failure.
  • Myxoedema.
  • Trauma.
  • Venous diseases like DVT.
  • Lipodystrophy and lipoidosis (lipoedema). Lipoedema occurs exclusively in females; begins in puberty; bilateral and symmetrical; trunk may be involved; feet are not involved; not pitting; not related to elevation/compression; MRI shows only fat without fluid.
  • Arterial diseases including AV malformations.
  • Gigantism.
  • Drug induced— steroids, estrogens, nifedipine.
  • External compression of veins as caused by abdominal tumours.
 
Complications
  • Skin thickening, abscess and maggot's formation.
  • Recurrent cellulitis, nonhealing ulcers, septicaemia.
  • Lymphangiosarcoma; Stewart Treves syndrome (0.5%, occurs after 10 years), which presents as multiple bluish satellite nodules in the skin of the limb often with ulceration and haemorrhage. Skin/nodule biopsy is confirmative. Chemotherapy, radiotherapy, later even though radical amputation is the treatment, it carries very poor prognosis. This syndrome is usually seen in upper limb after mastectomy.
  • Recurrent streptococcal infection.
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Treatment
 
Conservative
  1. Elevation of the limb, exercise, weight reduction.
  2. Static isometric activities like prolonged standing or carrying weights should be avoided; rhythmic isotonic movements like swimming/massaging should be encouraged.
  3. Diuretics to reduce the oedema is controversial. It more often causes eletrolyte imbalance than being beneficial.
  4. Benzopyrones are protienolytic agents/lympedim. They are coumarin (I, 2 benzopyrones) derivatives with no anticoagulant effect but increase the lymphatic peristalsis and pumping mechanism along with proteolysis.
  5. Daily wearing of below knee stockings.
  6. Avoid trauma and infection.
  7. Intermittent pneumatic compression devices (Pressure >50 mmHg); multilayered lymphoedema bandaging (MLLB)—nonelastic type is preferred method; graded stockings.
  8. Antibiotics—flucloxacillin, erythromycin, long-acting penicillins.
  9. Topical antifungal 1% clotrimazole and systemic griseofulvin 250–1000 mg.
  10. Regular washing and keeping the limb clean is very important.
  11. Diethyl carbamazine citrate (DEC) 100 mg tid for 3 weeks.
  12. Pain relief—by suitable means.
  13. Skin care:
    • Keratolytics like salicylic acid 5%; bland emollient; soft/liquid paraffin.
    • Avoidance of skin sensitisers like some soaps.
    • Topical steroids.
    • Control of allergy.
    • Control of fungal infection by drugs like fluconazole.
    • Three per cent benzoic acid ointment to prevent Athlete's foot.
    • Control of lymphorrhoea.
    • Prevention/control of skin infections.
  14. Complex decongestive therapy is a comprehensive two phase program of elevation, exercise, massaging, and compression wraps. First phase is intensive therapy and second phase is maintenance therapy.
    Compression wraps may be high stretch wraps or low stretch wraps. Low stretch wraps are better accepted. It should be worn initially for 24 hours. Compression wraps are used in initial intensive phase of therapy. Graduated elastic compression garments are used in maintenance phase which provides maximum pressure of 50 mmHg at the distal part with gradual reduction of pressure in proximal portion.
  15. Manual lymphatic drainage is a specialised technique to stimulate the contractility of lymph collecting vessels and enhance fluid and protein transport by gentle, light, superficial massaging of the skin so as to open up new lymphatic vessels. Technique is done first on the opposite normal side; then trunk, same side trunk; same side proximal; same side distal and later same side distal to proximal fashion, so as to redirect the lymph towards functioning lymphatic territories.
 
Surgery
Surgeries for lymphoedema has been classified as:
  1. Excisional
    • Charle's operation.
    • Homan's operation.
  2. Physiological
    • Omentoplasty.
    • Nodovenous shunt (Neibulowitz).
      zoom view
      Fig. 1.452: Charle's excisional surgery. Here after excising lymphoedematous tissue, area is covered with skin graft.
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      Fig. 1.453: Thompson's Swiss-roll operation. Here after removal of lymphoedematous tissue, deep fascia is opened to expose the muscle. Epidermis abraded using skin graft knife. This shaved dermis is buried into the muscle to get communication into the deeper lymphatics.
    • Lymphovenous shunt (O’Brien's).
    • Ileal mucosal patch.
      Here either communication between superficial and deep lymphatics are created or new lymphatic channels are mobilised to the site.
      Omentoplasty (Omental pedicle): As omentum contains plenty of lymphatics, omental transfer with pedicle will facilitate lymph drainage.
  3. Combined: Both excision + creation of communication between superficial and deep lymphatics.
    • Sistrunk operation.
    • Thompson's operation.
    • Kondolean's operation.
  4. Bypass procedure:
    • Handley's (1908) silk threads/nylon threads/perforated polyethylene tubes placement as burial from ankle to mid-abdominal level, kept for one year. Procedure is only of historical interest.
    • Skin bridge across the thigh and abdomen (Gillies).
    • Nodovenous shunt.
    • Lymphovenous shunt using microscope.
    • Ileal mucosal patch (Kinmonth). Segment of ileum with pedicle is isolated and opened to expose the mucosa; mucosa is denuded and this mucosa is placed in the thigh as burial to communicate with lymphatics to drain into abdominal lymphatics across ileum.
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      Fig. 1.454: Diagram showing right side groin nodovenous shunt between inguinal lymph node and long saphenous vein. Left side showing lymphovenous shunts between dilated lymphatics and long saphenous vein. At least 4 lymphatics should be anastomosed using 7 zero/11 zero prolene—using operative microscope.
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      Fig. 1.455: Believe it or not! Severe scrotal lymphoedema reaching almost up to feet; after surgical excision it weighed 40 kg; post-operatively patient went home with – 40 kg weight(Courtesy: Professor Shivananda Prabhu, MS, KMC, Mangaluru).
    • Baumeister lymphatic grafting.
    • Autotransplantation of free lymphatic flap from opposite side—done in post-mastectomy lymphoedema (Trevidic and Cormier).
  5. Limb reduction surgeries:
    • Sistrunk operation: Along with excision of lymphoedematous tissue, window cuts in deep fascia is done, so as to allow communication into normal deep lymphatics.
    • Homan's operation: Excision of lymphoedematous tissue is done after raising skin flaps. Later skin flaps are trimmed to required size and sutured primarily. Medial and lateral sides of the limb are done at separate sittings with 6 months interval.
    • Thompson's operation: Lymphoedematous tissue is excised under the skin flaps. Epidermis and part of the dermis of one of the skin flaps is shaved off using Humby's knife. It is buried under opposite flap, deep to the deep fascia like a swiss roll (Swiss roll operation or buried dermal flap operation).
      Problems here are formation of epidermal cysts and sinus.
    • Kondolean's operation: Along with excision of lymphoedematous tissue, vertical strips of deep fascia is removed so as to open the deep lymphatics which creates communication between superficial and deep lymphatics.
    • Macey's operation: Here skin and subcutaneous tissue are peeled back with deep fascia and split skin grafting is done over the denuded area. Overlying pad of tissue is sutured back temporarily and after 10 days, it is trimmed away.
    • Miller's procedure: It is excision of subcutaneous tissues under the skin flap with deep fascia in two stages. First stage is done over the medial aspect of the limb; second stage done after two months over lateral aspect of the limb.
    • Charle's (1912) operation: Done in severe lymphoedema with elephantiasis. Along with excision of lymphoedematous tissue, skin grafting is done. It reduces the size and weight of the limb. Patient becomes ambulatory. Wound sepsis, graft failure, dermatitis, hyperkeratosis are the complications.
    • Reduction surgeries are done for lymphoedema of scrotum, penis, labia and eyelid.
      In severe type, occasionally amputation may be required.
 
LYMPHOMAS
They are progressive neoplastic condition of lymphoreticular system arising from stem cells.
Lymphomas are the 3rd most common malignancy among children comprising 15% of paediatric cancers.
 
Aetiology
  • Genetic predisposition.
  • Sjogren's syndrome—30 fold increase of NHL.
  • HIV infection.
  • Wiskott—Aldrich syndrome.
  • Ataxia—telangiectasia.
  • Bloom's syndrome.
  • Virus aetiology—Epstein-Barr virus.
  • Celiac sprue—intestinal T cell lymphoma.
  • H. pylori may be associated with MALT lymphoma.
  • Occupation causes—hair dye workers; herbicide exposure.
  • Ionising radiation.
  • Smoking; alcohol consumption; tobacco usage.
  • Lymphomas are more common in western countries than in Asia.
 
Types
  • Hodgkin's lymphoma (HL).
  • Non-Hodgkin's lymphoma (NHL).
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Fig. 456: Lymphoma involving neck nodes. Differential diagnosis could be tuberculous lymphadenitis.
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Figs 1.457A and B: Stage IV lymphoma with neck nodes/sternal swelling/axillary nodes which has ulcerated (ulceration is not common in lymphoma).
 
HODGKIN'S LYMPHOMA (HL)
  • It is the most common type of lymphoma.
  • Infectious mononucleosis, Epstein-Barr virus, HIV infection and genetic monoclonal B cell disorder (90%) may be the aetiologies.
  • Grossly lymph nodes are fleshy, pinkish grey, and rubbery in consistency.
  • Microscopically contains cellular infiltration with lymphocytes, reticulum cells, histiocytes, fibrous tissue and Reed-Sternberg cells: (Reed-Sternberg cells are giant cells with two large mirror image nuclei). Owl eye, 50 µm sized.
 
Clinical Features
  • It is more common in males.
  • It has got bimodal presentation. It is seen in young and adolescents (20–30 years) as well as in elderly (> 50 years).
  • Painless progressive enlargement of lymph nodes. They are smooth, firm, usually discrete (without matting), nontender, typically with India rubber consistency.
  • Pain after alcohol consumption even though is very uncommon (3%) with low sensitivity but when present has got high specificity and is pathognomonic of HL. Pain appears within 3 minutes after alcohol intake in the vicinity of the involved node.
 
Site
  • Cervical lymph nodes most common—82% (lower deep cervical group and in posterior triangle).
  • Others include axillary, mediastinal, inguinal, abdominal.
  • Axial lymphatics are commonly involved.
 
Specific Features
  • Nodular sclerosis is most common type.
  • Consecutive group of lymph nodes are involved.
  • Splenomegaly is very common (45%).
  • Hepatomegaly with jaundice (5%)—jaundice is due to haemolysis or due to diffuse liver involvement.
  • Para-aortic lymph nodes may be enlarged and often palpable as vertically placed mass at or just left of the midline, which does not move with respiration, does not fall forward, nonmobile, resonant, smooth, firm mass often with transmitted pulsation from aorta (secondaries are hard, nodular usually primary from GI, melanoma, testis). Ascites is not a common feature.
  • Pruritus—25%. It may be the only presenting symptom. It is usually seen in nodular sclerosis type.
  • Constitutional symptoms like fever, night sweats, weight loss may be present which signifies stage “B”, which has got poor prognosis. Stage “A” is absence of these symptoms which signifies better prognosis.
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Figs 1.458A and B: Lymphoma in a boy and in an adolescent with neck nodes. Note the diffuse nature. Nodes are usually India rubber consistency.
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Fig. 1.459: Hodgkin's lymphoma in neck region.
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Figs 1.460A and B: Fungating lymphoma in both axilla of a patient.
256
  • Mediastinal lymph node involvement may cause compression features like SVC obstruction. Mediastinal lymphoma is the most common mediastinal malignancy which usually occurs in anterior mediastinum. Occasionally presentation may be difficulty in breathing, chest pain, dysphagia and SVC obstruction (Pemberton's sign may be positive). It may be asymptomatic also. If ratio between maximum transverse diameter of mediastinal mass to maximum transverse intrathoracic diameter (MMR) is more than 0.33 in chest X-ray or more than 0.35 in CT chest, then it carries worst prognosis.
  • Occasionally bone like vertebrae may get involved.
  • Anaemia, pancytopenia, fatigue, bone pain, petechiae with red coloured skin patches, nephrotic syndrome (minimal change disease).
zoom view
Fig. 1.461: Secondaries in neck lymph nodes. It is hard, large probably fixed and nonmobile making it advanced and inoperable.
 
Investigations
  • Blood: Hb%, ESR, peripheral smear, blood urea, serum creatinine. Serum alkaline phosphatase and calcium may elevated.
  • FNAC of lymph nodes. Not very sensitive; but initially done to rule out secondaries or tuberculosis.
  • Excision biopsy of lymph nodes. Full lymph node is excised to retain the architecture of the lymph node. It is important to grade the tumour. It is better to have immunohistochemistry of tumour tissue. As cell mediated immunity is decreased, CD4/CD 8 ratio will be decreased. CD 15, 30, 45 are very useful.
  • Chest X-ray—to look for mediastinal lymph nodes, pleural effusion.
  • Ultrasound abdomen—to look for the involvement of liver, spleen, abdominal lymph nodes.
  • CT scan of mediastinum/chest, abdomen and pelvis is better, ideal and essential. CT is used ideally to stage the disease.
  • MRI and PET scan are very useful to identify extranodal tissue involvement. Gallium scan is less useful.
  • Bone marrow biopsy or aspiration to stage the disease and to see the response to treatment. Usually iliac crest biopsy is done under local anaesthesia. It gives the staging.
  • Chamberlain's mediastinoscopy and biopsy of mediastinal lymph node is done if peripheral nodes are not available for biopsy. Laparoscopy and biopsy of different abdominal lymph nodes is also a good option.
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Fig. 1.462: Staging laparotomy for Hodgkin's lymphoma. Needle and wedge biopsies from liver/nodal biopsies from para-aortic, celiac, mesenteric, iliac nodes/splenectomy/ovarian translocation/iliac crest biopsy are the components of staging laparotomy. This can be very well-achieved through laparoscopy also now. Staging laparotomy is not commonly done now.
 
Treatment for HL
  • Stage I and II:
    • Mainly radiotherapy—external high cobalt RT.
      • Above the diaphragm—“Y” field therapy, covering cervical, axillary, mediastinal lymph nodes. It may cause carcinoma of breast.
      • Below the diaphragm, mantle or inverted “Y” field therapy, covering para-aortic and iliac nodes. It may cause infertility.
    • Chemotherapy is also given.
  • Stage III and IV: Mainly chemotherapy.
 
Treatment for Relapses
  • Autologous stem cell transplantation.
  • High dose chemotherapy.
  • High dose chemotherapy with autologous stem cell transplantation.
  • MOPP/ABV hybrid regime.
  • Single dose vinorelbine (new vinca alkaloid); gemcitabine; immunotherapy; tumour vaccination; gene therapy.
Differences between HL and NHL
HL (more common)
NHL
Age:
Young and elderly
Middle age and elderly
Pattern of involvement:
Symmetrical and consecutive
Asymmetrical
Cervical lymph node:
Commonly involved
Any group can be involved
Splenomegaly:
Common
Not common
Peripheral lymph node involvement (e.g. epitrochlear nodes)
Not common
Common
Treatment:
Mainly radiotherapy
Chemotherapy (MOPP regime)
Mainly chemotherapy
Prognosis:
Better
258Poor
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Figs 1.463A and B: Mediastinal nodes involved in lymphoma as seen in chest X-ray and chest CT scan.
 
Prognosis
  • Stage I and II— 80%.
  • Stage III A— 70%.
  • Stage III B and stage IV— <40%.
 
NON-HODGKIN'S LYMPHOMA (NHL)
  • It occurs in middle aged and elderly. It is more aggressive than HL.
  • It involves asymmetrical group of lymph nodes.
  • General condition is poor.
  • Inner Waldeyer ring, epitrochlear lymph nodes, peripheral lymph nodes are commonly involved.
  • Spleen is not commonly involved.
  • Hepatomegaly is common.
  • Vertebral involvement is common; paraplegia can occur. (40%).
  • Secondary infection, cachexia and immunosuppression is more common.
  • Inner Waldeyer ring and oropharynx lymphoma (NHL-B cell) may be associated with MALT lymphoma of stomach; so gastroscopy is indicated in these patients.
  • Pyoderma gangrenosum may the presentation.
  • Small bowel lymphomas are usually NHL type. Western type is annular, ulcerative multiple B cell type, presents as obstruction, bleeding, weight and appetite loss, perforation. Celiac disease related lymphoma is usually primary T cell type presents with severe unresponsive diarrhoea, PUO, obstructive features. Mediterranean lymphoma of small bowel is seen in North America and Middle East which is associated with alpha chain disease.
  • Sarcoma, carcinomas/secondaries are the differential diagnosis for NHL.
Chemotherapy for Hodgkin's Lymphoma (HL)
Mopp regime (1960) Not used now
ABVD regime (Standard)
Stanford V regime
BEACOPP regime
Mustine (Mechloroethamine)—6 mg/q meter on 1st and 8th day.
Oncovin (Vinca alkaloids)—1.4 mg/sq meter on 1st and 10th day
Procarbazine—100 mg orally daily for 10 days
Prednisolone—45 mg orally daily for 10 days
Adriamycin—30 mg/m2 meter (cardiotoxic)
Bleomycin—10 mg/m2 (pulmonary fibrosis)
Vinbladtine—6 mg/m2 (bone marrow suppression)
DTIC/Dacarbazine 350 mg/m2
Adriamycin (Doxorubicin)
Bleomycin
Vincristine, vinblastine
Mechlorethamine
Etoposide
Prednisolone
Bleomycin
Etoposide
Adriamycin (Doxorubicin)
Cyclophosphamide
Oncovin – Vincristine
Procarbazine
Prednisolone
Note:
MOPP is no longer considered effective regime
Note:
ABVD is becoming more popular, standard and commonly used regime now. It started in Italy, 1970.
It is commonly used in US.
Note:
It involves more intensive schedule with incorporation of radiotherapy.
Not well accepted.
Note:
It is commonly used in Europe; its efficacy is 15% better than ABVD; but it is costly; it needs granulocyte stimulating factor to control adverse effect; secondary leukaemia is slightly higher here
Note: Gonadal dysfunction and growth retardation is the long-term adverse effects in childhood HL due to treatment (RT and CT).
259
Rappaport classification
Working classification
  • Nodular
  • Low grade
  • Diffuse
  • Intermediate grade
  • High grade
 
Treatment
Mainly chemotherapy
Various regimens available include:
  • CHOP regime is used–Cyclophosphamide; Hydroxydaunorubicin; Oncovin; Prednisolone. This is the standard regime commonly used.
    • R CHOP regime is adding Rituximab when lymphoma is B cell type.
    • R-CHOEP regime is when Etoposide is added.
    • Side effects are–haemorrhagic cystitis (Mesna is given); alopecia; nausea and vomiting; neutropenia; severe sepsis.
  • ABVD—Adriamycin, Bleomycin, Vincristine, Dacar-bazine.
  • ABVP—Adriamycin, Bleomycin, Vincristine, Prednisolone.
  • Combinations of above.
  • Rituximab may be used with chemotherapy regimes.
  • Role of radiotherapy in NHL: When vertebra is involved.
  • Prognosis is poor compared to HL.
 
MANTLE CELL LYMPHOMA
  • It is a type of NHL under B cell subtype comprising 6% of NHL. It is aggressive type of NHL.
  • It is due to CD5 positive antigen-naive pre-germinal center B cell within the mantle zone that surrounds normal germinal center follicles. MCL cells generally over-express cyclin D1.
  • It is an acquired genetic disorder; MCL is neither communicable nor inheritable.
  • Types are—nodular or diffuse pattern with two main cytologic variants: typical or blastic (aggressive).
  • Common in old people; presenting with lymphadenopathy, fever, weight loss, night sweats, splenomegaly often other visceral organ involvement.
  • Investigations are – lymph node biopsy with immunohistochemistry (CD5; CD10; CD23; cyclin D1); CT chest, abdomen, pelvis; bone marrow biopsy; PET scan; cell proliferation index (Ki-67). The Mantle Cell Lymphoma International Prognostic Index (MIPI) was derived to classify as low, intermediate and high-risk group patients. Beta-2 microglobulin is another risk factor in MCL used primarily for transplant patients.
  • Treatment: Chemotherapy, immune-based therapy, radioimmunotherapy and new biologic agents are used. R Maxi CHOP alternating with R-HDAC is used as chemotherapy (see table below). Fludarabine is also can be used additionally. Total body irradiation with stem cell transplantation is also useful. Immunotherapy using rituximab is used in combination; it may be combined with radioactive molecules to have radioimmunotherapy. Targeted therapy using ibrutinib, temsirolimus, bortezomib, also used.
  • Prognosis: MCL carries poor prognosis. Mean survival is 3 years.
 
MALT LYMPHOMA (MALTOMA)
  • It is lymphoma arising from mucosa associated lymphoid tissue; it is actually extranodal marginal zone B cell lymphoma of gut mucosa associated lymphoid tissue. It is usually primary GI lymphoma (4% of gastric lymphoma); of non-Hodgkin's B cell type.
  • Commonest site is stomach. Helicobacter pylori infection is the causative agent commonly.
  • It can be low grade or high grade.
    • Low grade occurs in chronic gastritis patient with Helicobacter infection. Diffuse mucosal thickening with ulceration is seen. Anti-helicobacter therapy is very useful in this type.
    • High grade is aggressive one. It presents with features similar to gastric carcinoma often with smooth, firm gastric mass in epigastric region.
Regime and drugs for NHL
Drugs
Standard R-CHOP 14 or R-CHOP 21 regime
R-Maxi—CHOP regime
Mode of administration
Number of days
Rituximab
375 mg/m2
375 mg/m2
Intravenous infusion
Day 1
Cyclophosphamide
750 mg/m2
1200 mg/m2
Intravenous infusion
Day 1
Hydroxydaunorubicin
50 mg/m2
75 mg/m2
Intravenous infusion
Day 1
Oncovin
1.4 mg/m2
2 mg (max dose)
Intravenous infusion
Day 1
Prednisolone
40 mg/m2
100 mg/m2
Orally qid
Days 1–5
R – Maxi – CHOP is used in Mantle cell lymphoma as 21 days interval regime alternating with R-HDAC (Rituximab with high dose cytarabine). In other NHL excluding aggressive forms, R-CHOP standard dose is first line therapy.
  • 260Dawson's criteria for primary GI lymphoma (NHL)— No palpable superficial lymph nodes; no thoracic lymph nodes in CT scan; normal WBC count and bone marrow; predominant bowel pathology; liver, spleen are normal.
  • Systemic features like fever, night sweats, and weight loss can occur in 50% cases. Bleeding with haematemesis with obstruction is not uncommon. Locoregional lymph nodes (only) may get involved.
  • Endoscopic biopsy is essential to diagnose. Endosonography, bone marrow biopsy, CT scan of chest, abdomen and pelvis is a must to confirm primary GI/gastric lymphoma and to identify or to rule out extragastric lymph node NHL.
  • Ann Arbor staging system is commonly used but is inadequate. Lugano staging system is widely accepted one—Early: Single primary lesion or multiple noncontiguous primary lesions confined to GI tract with or without nodal involvement; Advanced: Disseminated extranodal spread or supradiaphragmatic spread.
  • Treatment: First line treatment— Primary chemotherapy with anti-helicobacter pylori regime, often with RT is the standard treatment. Palliative gastrectomy in case of bleeding, perforation and obstruction is done. Radical gastrectomy is done in diseases which are confined to stomach only to in selected individuals (limited role).
    • Early stage (Lugano) with +ve H. pyloriH. pylori eradication therapy is used; Early stage with – ve H. pylori or with H. pylori therapy failure, local RT is used often with chemotherapy as single or multiple agents.
    • Advanced stage (Lugano) is treated with H. pylori regime with immunotherapy (Rituximab with fludarabine) and chemotherapy (oral cyclophosphamide or oral chlorambucil; IV cladribine, bortezomib).
 
BURKITT'S LYMPHOMA (Malignant Lymphoma of Africa)
  • It is common in South Africa and New Guinea.
  • Epstien-Barr virus may be the aetiological agent. It is common in children.
  • It is associated with infectious mononucleosis.
  • It is common in malaria endemic area.
  • The tumour is multifocal, rapidly growing, painless.
  • Different groups of lymph nodes can also be affected.
 
Microscopy
Primitive lymphoid cells with large clear histiocytes—starry night (starry sky) pattern.
 
Sites
  • It is common in jaw—either lower or upper.
  • Abdominal presentation and renal involvement is common (75%).
  • Renal involvement often may be bilateral.
  • In females, ovaries are commonly affected.
 
Types
  1. Endemic (African)—commonly occurs in jaw.
  2. Nonendemic (sporadic)—commonly occurs in abdomen.
  3. Aggressive lymphoma—occurring in HIV patients.
 
Investigation
  • FNAC and biopsy confirms the diagnosis.
  • Jaw X-ray shows osteolytic lesions.
  • Ultrasound abdomen is done to look for involvement of kidneys.
  • Blood urea and serum creatinine estimation is done.
 
Treatment
  • Radiotherapy.
  • Chemotherapy: Cyclophosphamide, methotrexate, orthomelphalan.
  • Surgery is usually not indicated unless it is localised or in case of involvement of ovaries.
Prognosis is good.
 
CUTANEOUS T CELL LYMPHOMA
  • Cutaneous T cell lymphoma comprises mycosis fungoides, Sezzary syndrome, reticulum cell sarcoma of skin and other cutaneous lymphocytic dysplasias. Mycosis fungoides is the most common among them.
  • Cutaneous T cell lymphoma can be indolent (commonly mycosis fungoides); aggressive (Sezzary syndrome); provisional (granulomatous/panninculitis like T cell lymphoma).
  • Initial macular patch/plaque phase slowly changes into tumour phase with painful, pruritic erythroderma often with visceral spread. Alopecia mucinosa and follicular mucinosis are common in mycosis fungoides. Lymph nodes may get involved. Tumour cells in peripheral smear are also important in deciding therapy and prognosis.
  • Multiple skin biopsies/peripheral smear/node biopsy/immunohistochemistry/pheo or genotyping are important investigations.
  • Prognosis depends on extent of skin involvement (more than 10% body surface area carries poor prognosis)/nodal spread/blood spread.
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Figs 1.464A and B: Cutaneous T cell lymphoma.
  • 261Treatment: Localised external beam radiotherapy; topical chemotherapy (bexarotene gel/carmustine ointment); phototherapy; total skin electron beam therapy; extracorporeal photochemotherapy. Bexarotene is a type of retinoid.
  • Sezary syndrome is a type of cutaneous T cell lymphoma with skin lesions with special Sezary cells having cribriform nucleus. It is often associated with leukaemias. It is treated like any other cutaneous T cell lymphoma.
 
CHYLOUS ASCITES
It is collection of lymph in the peritoneal cavity. It is due to obstruction of intestinal lymphatics and subsequent leak.
 
Causes
  • Most common cause is—congenital lymphatic abnormality in children (megalymphatics with lymphoedema) and in adults lymph node malignancy, either primary or secondary.
  • Filarial lymphoedema causing obstruction.
  • Malignancy either nodal secondaries or nodal primary causing obstruction.
  • Tuberculosis causing blockage of lymph drainage and rupture and leak into the peritoneal cavity.
  • Post-surgical cause.
 
Features
  • Ascites, often massive.
  • Severe malnutrition and protein deficiency.
  • Features specific to the cause.
  • Triglycerides >110 mg/dl in ascitic fluid is diagnostic.
  • Ascitic fluid aspiration is chalky white in colour and it shows chylomicrons. It should be studied for fat globules, proteins, AFB and malignant cells.
  • Laparoscopy and biopsy is necessary when lymphoma/secondaries are suspected.
  • CT scan and CT guided biopsy may be needed.
  • Lymphangiography to find out the site of leak.
 
Treatment
  • Control of infection.
  • Antituberculous and antifilarial drugs.
  • Fat free, protein rich diet.
  • Nutritional support—TPN/enteral.
  • Medium chain triglycerides can be given as it directly gets absorbed into the blood rather into the lymphatics.
  • Repeated tapping, peritoneovenous shunts are often required.
  • Surgical ligation of leaking lymphatic duct.
 
CHYLOTHORAX
  • It is accumulation of lymph in the pleural cavity.
  • It is common on right side because of long course of thoracic duct towards right side.
 
Causes
  • Injury due to trauma/surgeries in neck or chest. Surgical trauma is the most common cause— may be oesophageal surgeries, pneumonectomy, cervical sympathectomy, neck dissections or aortic surgeries.
  • Tuberculosis, lymphoma or secondaries in the mediastinum.
  • Carcinoma lung or oesophagus.
 
Features
  • Chest pain, dyspnoea, pleural effusion.
  • Protein loss and malnutrition
  • Pleural tap will show chalky white fluid rich in chylomicrons. Triglycerides more than 110 mg/dl in the pleural fluid.
  • Chest X-ray, CT chest are needed.
 
Treatment
  • ICT placement.
  • Fat free protein rich diet.
  • Antibiotics therapy for the cause.
  • Often pleurodesis using bleomycin, talc, tetracycline or pleural stripping is needed.
  • Thoracic duct ligation is beneficial in traumatic/iatrogenic cases.
  • Through thoracoscopic approach, ligation of the thoracic duct is done if leak persists beyond one week. If oral cream is given to the patient 6 hours before surgery, leaking site will be better identified. Thoracic duct is ligated above and below the leak either through thoracoscopy or thoracotomy.
  • ICT drainage, oral diet of medium chain triglycerides which is absorbed directly into blood not through lymphatics; with TPN, is the usual earlier way of management.
 
CHYLURIA
  • It is passage of milky white chylous urine, which is aggravated after fatty meal.
  • It may be due to obstruction of intestinal lymphatic vessels leading to high lymphatic pressure causing diversion of lymph into renal lymphatics or it often may be due to rupture of intestinal lymphatics into renal pelvis or ureter leading into a lymphourinary fistula.
  • The most common cause is filarial (2% of filarial cases): Other causes are tumour, tuberculosis, malaria and ascariasis infestation.
  • Urinary infection, protein loss is common.
  • It mimics bacterial/tuberculous pyuria or phosphaturia.
  • Clot colic due to lymph clot in urinary system may be the presentation.
  • Urine study, culture, IVU, lymphangiography, U/S abdomen is needed.
  • Treatment is low fat, protein rich diet, antibiotics, DEC, plenty of oral fluid intake, ligation of dilated lymphatics through laparotomy or sclerosing the lymph vessels.
  • Condition causes severe psychological and nutritional problem.
262
 
SARCOIDOSIS
It is a differential diagnosis for lymph node mass. It is basically a granulomatous condition of unknown cause with bilateral hilar lymphadenopathy; with involvement of lungs, liver, spleen, lymph nodes, lacrimal glands, parotid glands, CNS, hypercalciuria, acute onset of erythema nodosum in the skin. Fever and loss of weight are not common. It shows noncaseating epithelioid granuloma with positive Kveim-Siltzbach skin test (80%); high levels of serum angiotensin converting enzyme (SAGE). Investigations needed are—CT chest; mediastinoscopy; nodal biopsy; slit lamp examination of eye; often abnormal immunoglobulins in the circulation. It is treated by corticosteroids with good response. It should be differentiated from other causes of lymphadenopathy especially Hodgkin's lymphoma.
Note:
For topics tuberculous lymphadenitis and lymph node secondaries please refer chapter ‘Neck’.
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Figs 1.465A and B: Gross feature of sarcoidosis of spleen(Courtesy: Dr Arunkumar, Mch, gastroenterologist).
263P. Peripheral Nerves
The power of moving in every part of the body by means of the muscles which obey the will, or by means of others the actions of which are involuntary; the various perceptions by the five external senses; and lastly those mental powers named memory, imagination, attention, and judgement, together with the passions of the mind; all these seem to be exercised by the ministry of the nerves; and are impaired, disturbed, or destroyed, in proportion to any injury done to the brain, the spinal marrow, and nerves, not only by their peculiar diseases, of which we know little, but by contusions, wounds, ulcers, and distortions, and by many poisons of the intoxicating kind.
—William Heberden, 1802
CHAPTER OUTLINE
  • ❖ Peripheral Nerve Injuries
  • ❖ Tinel's sign
  • ❖ Brachial Plexus Injuries
  • ❖ Causalgia
  • ❖ Median Nerve Injury
  • ❖ Carpal Tunnel Syndrome
  • ❖ Ulnar Nerve Injury
  • ❖ Claw Hand
  • ❖ Radial Nerve Injury
  • ❖ Common Peroneal Nerve Injury
  • ❖ Foot Drop
  • ❖ Medial Popliteal Nerve Injury
  • ❖ Axillary Nerve Injury
  • ❖ Long Thoracic Nerve Injury
  • ❖ Meralgia Paraesthetica
 
PERIPHERAL NERVE INJURIES
zoom view
Fig. 1.466: Cross-section of a nerve.
 
Classification
 
Seddon's Classification
  • Neuropraxia: It is temporary physiological paralysis of nerve conduction. Here recovery is complete. There is no reaction of degeneration.
  • Axonotmesis: It is division of nerve fibres or axons with intact nerve sheath. There is reaction of degeneration distally with near complete recovery. Patient can present with sensory loss, paralysis of muscles or causalgia.
    zoom view
    Fig. 1.467: Dermatomes.
  • Neurotmesis: Here complete division of nerve fibres with sheath occurs. Degeneration occurs proximally up to the first node of Ranvier as well as distal to the injury. Recovery is incomplete even after nerve suturing. There is complete loss of motor and sensory functions with loss of reflexes. If the nerve is mixed type other than pure motor or sensory recovery is still poorer.
    Injuries may be incised or lacerated or crushed one.
    Cut end of the nerve forms proximally neuroma and distally glioma.
264Neuromas may be:
  • True neuroma or false neuroma.
  • End neuroma or side neuroma.
 
Clinical Features
  • Loss of sensory, motor, autonomous and reflex functions.
  • Secondary changes in the skin and joint.
Primary nerve suturing is done if it is a clean incised wound.
Secondary nerve suturing is done after 3 weeks if it is a crushed wound.
 
Management
  • Associated injuries like fracture, vessel injury, injuries in other systems should be looked for.
  • Assessment of nerve injury is done by checking sensation, muscle power, reflexes.
  • Nerve conduction studies.
  • Investigations relevant for associated injuries.
  • Exploration of the wound.
Debridement of the area is done. If injury is incised one, then nerve is sutured with 8-0 to 10-0 nonabsorbable interrupted sutures (polypropylene).
 
Types of Nerve Suturing
Usually microscope or loup is used for nerve suturing.
  1. Epineurorrhaphy: Only epineurium is sutured using interrupted sutures.
  2. Epi-perineurorrhaphy: Initially perineural sheath and then epineurium is sutured.
    Nerve suturing can be:
    • Primary repair: It is done immediately after injury. Nerve ends are minimally trimmed very close using a blade. All fascicles of the nerve are oriented correctly. Two stay sutures are placed to keep the orientation properly. Usually epineural suturing is done using 8-0 polypropylene interrupted sutures. It needs magnification. 6–8 sutures are placed for large peripheral nerve like median or ulnar nerve. For small nerve like digital nerve, only 2–3 sutures are placed.
    • Secondary repair: It is done at a later period. It is done in a preexisting scar tissue. Here first nerve ends, both proximal and distal are identified, carefully dissected adequately. Proximal neuroma and distal glioma are trimmed for 1 cm to expose the normal fascicles of the nerve ends. Often guide sutures of silk may be present which were placed earlier during exploration of the trauma. Once nerve ends are clean, it is sutured alike primary suturing with stay sutures, with proper alignment of fascicles, followed by epineural suturing. Here as epineurium is thicker, suturing is easier.
Note
  • If nerve is lacerated, then marker stitches (using silk) are placed at the cut end site to identify the nerve for suturing at a later period.
  • If nerve suturing fails or if could not be done, then tendon transfer is done at a later period after 4–6 months.
  • Incomplete injury usually does not require any suturing.
Prognostic factors in healing of the nerve injury:
  • Higher the lesion worse the prognosis.
  • More the gap between the cut ends worse the prognosis.
  • Associated injuries alter the prognosis.
  • Children do better with nerve injury.
  • Type of the injury also decides the prognosis.
The rate of growth of nerves after peripheral nerve suturing is 1 mm/day.
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Fig. 1.468: Primary nerve repair.
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Fig. 1.469: Secondary nerve repair.
265
 
TINEL'S SIGN
It is the clinical sign (prognostic indicator) used to assess the level of regeneration. It is elicited 3 weeks after the nerve injury (Regeneration begins after the completion of nerve degeneration).
Tapping over the course of the nerve is done from distal to proximal to elicit a sensation of “pins and needles” or hyperaesthesia.
If sensation is felt at the site as well as distally along the distribution of the nerve, that means good recovery can be expected. If sensation is felt only at the site of tapping, then result is equivocal. If no sensation is felt it means no recovery.
 
BRACHIAL PLEXUS INJURIES
It can be:
  • Supraclavicular injury
65%
  • Infraclavicular injury
25%
  • Combined
10%
It can also be:
  • Upper plexus injury.
  • Lower plexus injury.
It can be:
 
Investigations
  • Nerve conduction studies.
  • CT/MRI.
  • Electromyogram.
  • X-ray cervical spine and part.
 
Treatment
  • Conservative, nerve repair.
  • Tendon transfer, physiotherapy.
Osteotomy of coracoid process proximal to the attachment of pectoralis minor, short head of biceps and coracobrachialis is done to improve abduction—Sever's operation.
zoom view
Fig. 1.470: Brachial plexus anatomy.
 
CAUSALGIA
It is severe burning pain and hyperaesthesia in the distribution of a peripheral nerve due to incomplete injury to the nerve.
 
Sites
  • Common in upper limb.
  • Commonly seen in median nerve, also often in brachial plexus injuries. In the lower limb it is seen in sciatic nerve or tibial nerve injuries.
Features of upper and lower plexus injuries
Upper plexus injury (Erb-Duchenne paralysis)
Lower plexus injury (Klumpke's paralysis)
1.
It is due to depression of shoulder by trauma
1.
Forcible hyperabduction of shoulder causes this injury
2.
After difficult labour in newborn
2.
In newborn it result due to difficult breech delivery
3.
Here C5 and C6 roots are injured
3.
Here C8 and T1 are injured
4.
Muscles affected are deltoid, biceps brachioradialis and supinator
4.
Intrinsic muscles of the hand are involved
5.
Effects are:
5.
Effects are:
a. Elbow will be extended, pronated and upper limb is internally rotated (Policeman receiving tip)
a. Combined median and ulnar claw hand
b. Sensory deficit over the lateral aspect of arm and upper part of the lateral forearm
b. Horner's syndrome
c. Sensory deficit over the medial aspect of forearm, hand, and medial 1½ finger
266
 
Pathology
Incomplete nerve injury produces abnormal impulse towards sensory nerve ending causing vasomotor instability and pain.
 
Features
  • Hyperaesthesia with severe disabling and burning pain.
  • Skin becomes red, shiny and glossy which sweats profusely—Weir-Mitchell's skin.
  • Eventually skin becomes atrophic, cyanotic, cold and blotchy.
  • Skin is less sensitive to heat, cold, and pin prick, but hypersensitive to touch and tender to pressure.
  • Nails are rigid, brittle with change in colour.
  • Investigation: Nerve conduction studies.
  • Treatment:
    • Anti-inflammatory drugs, steroids, physiotherapy.
    • IV guanethidine regionally.
    • If not improved, sympathectomy—cervical for upper limb, lumbar for lower limb.
 
MEDIAN NERVE INJURY
  • Median nerve arises from lateral (C5, 6, 7) and medial cord (C8 and T1) of the brachial plexus. It is initially lateral to the axillary artery and becomes medial in the lower part of the arm and in the cubital fossa. It passes through the pronator teres, descends in relation to flexor muscles and enters the palm through the carpal tunnel at the wrist.
  • It supplies pronator teres, flexor carpi radialis, palmaris longus and flexor digitorum superficialis. Anterior interosseous branch of the median nerve supplies pronator teres, lateral half of the flexor digitorum profundus, flexor pollicis longus and pronator quadratus.
  • In the wrist, it supplies abductor pollicis brevis, flexor pollicis and opponens pollicis of thenar eminence and lateral two lumbricals. It gives sensory supply to lateral three and half fingers of the hand.
 
Clinical Features of Median Nerve Palsy
In high median nerve palsy
  • Wasting of the thenar eminence. Loss of sensation on lateral three and half fingers.
  • Ochsner's clasping test shows pointing index because of the inactivity of lateral two divisions of the profundus.
  • Ape or Simian thumb deformity” is due to overaction of the adductor pollicis which is supplied by the deep branch of ulnar nerve. As all other thenar muscles are paralysed, thumb comes in the same plane of the metacarpals.
  • Pen test”: In median nerve injury, pen held in front of the hand cannot be touched by thumb as abduction is not possible due to paralysis of the abductor pollicis brevis.
In low median nerve palsy profundus is not paralysed and so pointing index is not seen.
 
Investigations
  • Nerve conduction studies.
  • X-ray of the part in case of fracture.
  • Electromyogram.
 
Treatment
  • Nerve suturing or nerve graft.
  • Tendon transfer.
  • Treat the cause like carpal tunnel syndrome.
 
CARPAL TUNNEL SYNDROME
  • It is the compression neuropathy of median nerve in the carpus, deep to flexor retinaculum.
  • Flexor retinaculum (transverse carpal ligament) maintains the concavity of wrist and extends laterally from trapezium and scaphoid to pisiform and hook of the hamate medially.
Carpal tunnel is formed by carpal bones behind and flexor retinaculum in front. It contains median nerve and long flexor tendons of fingers and thumb. Ulnar nerve lies superficially, not in the carpal tunnel.
Median nerve gets compressed if space of the carpal tunnel gets reduced.
 
Causes
  • Lunate dislocation, malunited Colle's fracture.
  • Radiocarpal arthritis, flexor tendon tenosynovitis.
  • Myxoedema, acromegaly, pregnancy.
 
Clinical Features
  • Common in females.
  • Tingling, numbness, paraesthesia and burning sensation in the lateral three and half fingers supplied by median nerve. Burning sensation gets aggravated at night.
  • Ape thumb deformity, wasting of thenar muscles, weakness of opponens pollicis and abductor pollicis brevis, i.e. features of low median nerve palsy.
  • When BP cuff is inflated patient feels the typical pain in the fingers.
  • Tapping the median nerve at the distal end of forearm with the wrist held in extension aggravates the symptoms.
  • Condition is often bilateral.
  • Phalen's Test (Wrist flexion test): Flexion of the wrist causes exacerbation of the symptoms within 1 minute and the symptoms will disappear as the wrist is straightened.
 
Differential Diagnosis
  • Cervical spondylosis.
  • Cervical rib syndrome.
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Figs 1.471A and B: Anatomy of the carpal tunnel and flexor retinaculum.
 
Diagnosis
  • Nerve conduction studies.
  • X-ray/MRI neck.
 
Treatment
  • Surgical decompression of median nerve by cutting both superficial and deep part of flexor retinaculum completely, by 'S' shaped incision.
  • Surgery is usually done under local anaesthesia. General or brachial block can be used. Tourniquet is commonly used. Vertical crease incision is made in the proximal part of the palm with convexity of the incision towards the ulnar side.
  • Skin incision is deepened. Palmar cutaneous branch of the median nerve should be preserved. Incision is deepened to identify the flexor retinaculum. Entire length, both superficial and deep parts 268should be cut properly. It is cut towards ulnar side of the wound. Only skin is sutured using interrupted nonabsorbable 3 zero polypropylene or polyethylene sutures.
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    Fig. 1.472: Incision for carpal tunnel syndrome.
  • Complications are incomplete fasciotomy and recurrence, nerve injury.
  • Using small proximal incision, endoscopy can be passed to visualise and cut the entire flexor retinaculum—minimal access surgery.
  • Postoperatively good physiotherapy is required.
  • Condition is permanently curable.
 
ULNAR NERVE INJURY
  • After arising from the medial cord of the brachial plexus (C8 and T1), it runs on the medial aspect of the axillary artery up to middle of the arm. Then it enters the posterior compartment in relation to triceps muscle. After passing behind the medial epicondyle and through two heads of flexor carpi ulnaris, it runs in front of the flexor digitorum profundus (FDP) in the forearm. It reaches the hand in front of the flexor retinaculum through “Guyon's canal”. Here it divides into superficial and deep branches.
  • Ulnar nerve supplies flexor carpi ulnaris, medial half of flexor digitorum profundus, all muscles of the hypothenar eminence (palmaris brevis, abductor digiti minimi, opponens digiti minimi, flexor digiti minimi), adductor pollicis of the thenar eminence and all interossei of the hand. It also gives sensory supply to medial part of the hand, medial one and half fingers.
 
Clinical Features
  • Claw hand deformity.
  • Weakness of all the muscles supplied by the ulnar nerve.
  • Card test”: A card is placed between the two fingers of the patient to grasp. As the palmar interossei are weak, patient cannot grasp [palmar interossei are adductors of the fingers (PAD)].
  • Abduction of fingers are checked [dorsal interossei are abductors (DAB)].
  • Froment's sign: A book is placed to grasp between fingers and thumb of the patient. Normally thumb will be straight because of the action of adductor pollicis muscle. As it is paralysed in ulnar palsy, grasp is achieved by the action of flexor pollicis longus and there will be flexed thumb.
  • Loss of sensation over medial one and half fingers and hand.
 
Investigations
  • Nerve conduction studies.
  • Electromyogram.
 
Treatment
  • Nerve suturing or nerve grafting.
  • Tendon transfer.
Intrinsic minus deformity: It is due to loss of intrinsic muscle power, i.e claw hand.
Intrinsic plus deformity: It is due to muscle contracture and fibrosis.
Ulnar paradox: In ulnar palsy, higher the lesion, lesser the deformity, lower the lesion more the deformity. In higher lesion, FDP is also paralysed. In lower lesion FDP is intact and so FDP causes more flexion (overaction) and so aggravates the claw hand.
 
CLAW HAND
  • It is the hyperextension of the metacarpophalangeal joint with flexion of the interphalangeal joints of the hand.
  • Extension of MCP joint is due to unopposed action of extensor digitorum.
  • Flexion of MCP joint and extension of interphalangeal joints are by extensor hood of interossei and lumbricals. So extensor hood is functioning mainly by ulnar nerve and also by median nerve. In ulnar or median nerve palsies, these actions are paralysed and so patient develops claw hand.
  • It is actually intrinsic minus deformity.
 
Clinical Features
  • Typical claw hand.
  • Loss of sensation along the distribution of the nerve.
  • Inability to grasp card between the fingers.
  • While holding the book between the thumb and fingers, thumb will be flexed in ulnar claw hand (positive Froment's test).
 
Types
  • Ulnar claw hand: Only medial two fingers are involved.
    • Low ulnar palsy: Here lesion is in the wrist (at Guyon's canal). Here deformity is more because of the over-action of the FDP.
    • High ulnar palsy: Here FDP is also paralysed and over-action is not there. So lesser deformity occurs.
    Ulnar paradox: Higher the lesion lesser the deformity, lower the lesion more the deformity.
  • Median claw hand: Only lateral two fingers are involved. It is less common.
  • Combined median and ulnar claw hand: Here all four fingers of the hand are involved.
 
Investigations
  • Electromyogram.
  • Nerve conduction studies.
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Figs 1.473A and B: Ulnar claw hand with hyperextension of metacarpophalangeal joints and flexion of proximal and distal inter-phalangeal joints in medial two fingers due to ulnar nerve palsy.
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Figs 1.474A and B: Combined claw hand involving all fingers due to both ulnar and median nerve injuries.
 
Treatment
  • Paul Brand's operation: Extensor carpi radialis longus or brevis (ERCB) is transferred with a graft to the extensor hood through the lumbrical canal. Graft is taken from palmaris longus or plantaris muscle.
  • Stye-Bunnell's operation: Flexor digitorum superficialis of index finger is used (only in ulnar claw hand) to transfer to extensor hood.
  • Fowler's operation: Extensor digitorum is used to transfer to extensor hood.
  • Riordan operation: Flexor carpi radialis is used for tendon transfer.
  • Anterior transpositioning of the ulnar nerve in case of tardy ulnar palsy.
 
RADIAL NERVE INJURY
  • Radial nerve is derived from the posterior cord of the brachial plexus (C5, 6, 7, 8 and T1). It descends behind the axillary artery in front of the sub-scapularis, latissimus dorsi and teres major. It passes through the medial and lateral heads of the triceps muscle, winds round the humerus through the radial groove and enters the forearm in front of the lateral epicondyle in relation to brachio-radialis, brachialis and extensor carpi radialis longus muscles.
  • In the arm it supplies triceps, anconeus, brachio-radialis, extensor carpi radialis longus and part of brachialis. It gives posterior and lower lateral cutaneous nerves of the arm and posterior cutaneous nerve of the forearm.
  • Superficial branch of the radial nerve from the elbow runs in the forearm in relation to supinator and brachioradialis and ends by forming five digital nerves which gives sensory supply to lateral three and half fingers on the dorsal aspect—except skin over the distal phalanges.
  • Deep branch also called as posterior interosseous nerve winds round the radius supplying supinator and extensor carpi radialis brevis. It gives three short branches to extensor digitorum, extensor digiti minimi and extensor carpi ulnaris. It also gives two long branches—one to abductor pollicis longus and extensor pollicis brevis; another to extensor pollicis longus and extensor indicis.
 
Clinical Features
  • Wrist drop because of inability of extending the wrist.
  • Inability to extend metacarpophalangeal joint, but extensions of the interphalangeal joints are normal.
  • 270Inability to extend the forearm.
  • Inability to extend the thumb.
  • Flexion of the elbow against resistance with forearm in mid-prone position is difficult because of the weakness of the brachioradialis muscle.
  • Loss of sensation in back of the arm, forearm, hand and lateral three and half fingers.
Posterior interosseous nerve is purely motor and so sensation is intact when it gets injured. It causes only dropped fingers.
 
Investigations
  • X-ray of the part.
  • Nerve conduction studies.
 
Treatment
  • Nerve suturing or nerve graft.
  • Tendon transfer.
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Fig. 1.475: Wrist drop—due to radial nerve palsy.
 
COMMON PERONEAL NERVE INJURY
This nerve supplies the extensor and peroneal group of muscles and sensory supply to the skin over the front and lateral aspect of the leg and dorsum of the foot.
 
Clinical Features
  • Foot drop with high stepping gait.
  • Talipes equinovarus deformity.
  • Loss of sensation on the lateral side of the leg and dorsum of the foot.
 
Management
  • Treating the foot drop.
  • MCR chappals.
 
FOOT DROP
Inability to dorsiflex and evert the foot due to paralysis of the peroneal and extensor group of muscles, as a result of common peroneal nerve injury.
 
Clinical Features
  • High stepping gait.
  • Loss of sensation over lateral and dorsum of the foot.
 
Treatment
Tendon transfer using tibialis posterior muscle. Tendon of the muscle is detached from its navicular insertion and with a tendon graft (from plantaris) it is transferred to cuboid and cuneiform bones to get dorsiflexion and eversion.
  1. Ober's procedure.
  2. Barr's procedure.
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Fig. 1.476: Foot drop with claw toes. It is due to peroneal nerve injury (Lateral popliteal nerve).
 
MEDIAL POPLITEAL NERVE INJURY
It supplies the soleus, gastrocnemius, popliteus, plantaris, tibialis posterior, flexor digitorum longus and flexor hallucis longus.
Medial popliteal nerve is rarely involved by any disease process. Trauma can cause medial popliteal nerve palsy.
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AXILLARY NERVE INJURY
Axillary nerve supplies the deltoid and teres minor muscle and also sensory supply to the skin over the upper lateral aspect of the arm.
Axillary nerve is affected in:
  • Fracture neck of the humerus.
  • Dislocation of humeral head.
  • Following IM injection into the deltoid.
Clinically there will be loss of abduction of the shoulder and anaesthesia of the skin over the lateral part of the arm.
 
LONG THORACIC NERVE INJURY (Nerve of Bell)
  • It supplies serratus anterior muscle. It arises from C5, 6, 7 cervical roots.
  • The nerve is injured commonly in malignancy, during breast, axillary or chest wall surgeries.
  • Clinically, when outstretched (elbow extended) arm is pushed against the wall, the inferior angle of the scapula will become prominent (Winging of the scapula).
 
MERALGIA PARAESTHETICA
(Meralgia – Greek – thigh)
  • It is entrapment neuropathy of lateral cutaneous nerve of thigh. Nerve gets compressed while passing through the inguinal ligament. It arises from posterior divisions of lumbar plexus (L2, 3); runs over the quadrates lumborum and iliacus muscles; emerges behind the lateral part of the inguinal ligament; divides into anterior and posterior branches, supplying skin over anterolateral part of the thigh and anterior part of the gluteal region.
  • It causes hyperaesthesia, tingling over upper lateral aspect of the thigh along the distribution of the nerve. Symptoms get worsened on standing or walking; it is relived by sitting.
  • It mimics disc prolapse or Hansen's disease or neuropathies.
  • It is treated by reassurance; carbamazepine; steroids. Often release of inguinal ligament fibres that are compressing the nerve is needed.
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Fig. 1.477: Lumbar plexus showing origin of lateral cutaneous nerve of thigh.
272Q. Neoplasm
CHAPTER OUTLINE
  • ❖ Definition
  • ❖ Dysplasia
  • ❖ Carcinoma In Situ
  • ❖ Aetiologic Factors
  • ❖ Spread of Malignant Tumours
  • ❖ Grading of Tumour
  • ❖ Staging of the Tumour
  • ❖ Paraneoplastic Syndromes
  • ❖ Investigations for Neoplasm
  • ❖ Management Strategy for Cancers
 
DEFINITION
Willis defined neoplasm as “it is an abnormal mass of tissue, the growth of which exceeds and is uncoordinated with that of the normal tissues and persists in the same excessive manner even after cessation of the stimuli.”
 
Classifications
Benign
Malignant
Well-differentiated
Lack of differentiation
Structures are typical of tissue/cell of origin
Atypical structure with anaplasia
Smooth, slow, progressive rate of growth
Erratic, rapid growth
Normal mitotic figures
Abnormal mitotic activity
Well localised and capsulated
Not localised. Not capsulated
Do not infiltrate surrounding normal tissues
Infiltrate the surrounding tissues
No metastasis
Metastasise through lymphatics or blood
Curable
May not be completely curable
Few benign tumours after a long time may turn into malignancy
Treatment is simple
Treatment is complex and complicated
No recurrence
Recurrence can occur
Sarcoma
Carcinoma
Arising from mesenchymal tissues
Arising from epithelial cells derived from any of the three germ layers
‘Sar’ means flesh (Greek), Oma means tumour
Carc means crab like
Smooth, firm or hard swelling
Hard, proliferative, with everted edge
Warm and vascular with dilated veins over the surface
Spreads mainly through blood commonly to lungs, e.g. liposarcoma, fibrosarcoma,
Spreads through lymphatics as well as blood, e.g. squamous cell carcinoma, renal cell carcinoma, adenocarcinoma
 
Components
Parenchyma: It contains proliferating neoplastic cells.
Stroma: It contains supporting connective tissues and blood vessels.
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Fig. 1.478: Soft tissue sarcoma thigh. Note the dilated vassels on the surface.
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Fig. 1.479: Carcinoma heel region. Note the everted edge with proliferative cauliflower like look.
 
DYSPLASIA
It means “disordered growth”. There is loss in the uniformity of the cells with pleomorphism and hyperchromatism, as well as loss in their architectural orientation.
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Fig. 1.480: Squamous cell carcinoma scalp. Note the everted edge. It is ulceroproliferative lesion.
 
CARCINOMA IN SITU
Here dysplasia involves the entire thickness of the epithelium, and is preinvasive. Basement membrane is intact in carcinoma in situ.
 
AETIOLOGIC FACTORS
 
Age
It is more common in elderly. But it is variable.
Tumour suppressor gene p53 plays important role in prevention of the cancers. Its function is prevention of replication of damaged DNA. If damaged DNA replicates there is high chances of abnormal mitotic activity and cancer transformation of the tissue. Loss or reduction of ability/function of p53 suppressor gene can lead into cancers. Common cancers associated with p53 loss are cancers of breast, colorectum, retina, bone, brain, soft tissues, blood and familial related type.
 
SPREAD OF MALIGNANT TUMOURS
  1. Local spread: Into adjacent structures like soft tissues, vessels, bone.
  2. Lymphatic spread
    • By permeation: Here malignant cells proliferate through lymphatic vessels up to lymph node level. For example, in carcinoma breast malignant cells permeate into axillary lymph nodes.
    • By embolisation: Here cells get dislodged from lymphatic vessels and freely travel to spread into further level of lymph nodes. In carcinoma breast by embolisation, spread occurs from axillary lymph node to supraclavicular lymph node.
    • Retrograde lymphatic spread occurs once lymph vessel get blocked by malignant infiltration. In carcinoma breast retrograde spread occurs to opposite breast, opposite axilla, or to mediastinum. In melanoma, through dermal lymphatics and retrograde spread ‘in transit nodules’ occur in the skin.
  3. Blood spread
    • Occurs through veins, as veins are thin-walled and infiltration is easier (Arteries contain elastic fibres in their wall, which resist malignant infiltration).
    • Blood spread is commonly to lungs, bone (upper end of femur and humerus, ribs, skull), liver, brain, adrenals and other organs.
      • Both by permeation (e.g. in renal cell carcinoma permeation through renal vein is common) and by embolisation (in other malignancies).
      • In carcinoma prostate, due to increased pressure and venous blockade, retrograde venous spread occurs through vertebral venous plexus which causes osteoblastic secondaries in pelvic bones and vertebrae.
  4. Seedling: For example
    • From lower lip cancer to upper lip as kiss cancer.
    • Recurrence in the scar after surgery for malignancy, e.g. deposition of malignancy in the scar of SPC from bladder tumour.
    • Seedling in the peritoneal cavity from abdominal malignancy is common causing intractable ascites.
  5. Transcoelomic spread:
    • Spillage or dislodge of malignant cells occurs from primary site resulting in seedling on other organ, e.g. in carcinoma stomach secondaries in ovary (Krukenberg tumour) occurs due to transcoelomic spread. Here cells get deposited on the raw surface of ovary during ovulation (So it occurs in menstruating age group only).
 
GRADING OF TUMOUR
  • It signifies aggressiveness of tumour.
  • It is based on differentiation of tumour cells and mitotic activity.
 
Special Features of Malignant Cells
  • Independent and autonomous nature without any control or check.
  • Normal telomeric shortening is altered. Normal cell divides for 40–60 times. Later telomere gets shortened and cell division stops. It is altered in malignancy with infinite cell division.
  • Reduced cellular apoptosis. Normal cell has capacity to die once its function is over. It is normal programmed death of a cell. It is activated by tumour suppressor gene p53. If this gene loses its function, tumour will form.
  • Tumour has got capacity to create and construct blood supply called as angiogenic capacity.
  • Malignant cells invade through the basement membrane and spread through blood and lymphatics. It is through secretion of special enzymes, increased interstitial pressure, capacity to have motility, release of collagenases/proteases/integrins.
  • Spread occurs by proliferation and permeation as well as embolisation.
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Fig. 1.481: Secondaries in neck. FNAC is the investigation to diagnose.
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Fig. 1.482: Carcinoma ovary specimen. It was malignant teratomas of ovary. Other ovary was normal. So chemotherapy is used as an adjuvant. Patient was 23 years young female.
  • Creation of instability and alteration of existing tissue function (not obeying normal tissue function of that particular site).
  • Gompertzian growth—rapid growth of a tumour occurs prior to its clinically detectable stage. Once it becomes clinically detectable which needs thirty generation of cell divisions (1 mm tumour is 109 cells), its growth slows down later. This late slow growth is due to decreased oxygen to tumour/by competition between host cells and tumour cells and also between tumour cells themselves.
  • Tumour mutation occurs at different generation of divisions stabilising the tumour further.
 
STAGING OF THE TUMOUR
It is based on the size of the primary tumour, nodal spread and blood spread. It is called as ‘TNM’ staging. ‘TNM’ staging is more relevant than grading in managing and predicting prognosis.
 
PARANEOPLASTIC SYNDROMES
  • Certain symptom complexes which are not specifically explained by the tumour, but are relevant, often problematic and life-threatening are called as paraneoplastic syndromes.
  • Incidence: Seen in 10% of patients.
 
INVESTIGATIONS FOR NEOPLASM
 
I. BIOPSY
‘Bio’ means life or tissue. Opsis means vision or microscopy.
Biopsy means study of tissues using microscopy.
OR life by vision
OR vision for life (to save life).
  • Biopsy is sent in 10% formaldehyde solution. In special occasions like, to assess receptors/to do histochemistry, biopsy is sent in low temperature; in normal saline or in specialised ingredients. Tissues are kept in formalin for 24 hours and then taken for ‘cut up’ by
    Paraneoplastic syndromes
    Syndrome
    Cause
    Type of tumour
    Cushing's syndrome ACTH
    or ACTH like
    substance
    Small cell carcinoma lung
    Neural tumour
    Pancreatic tumour
    Syndrome of inappropriate
    ADH
    Small cell carcinoma lung
    ADH secretion
    Brain tumour
    Carcinoid syndrome
    Serotonin, bradykinin
    Bronchial adenoma
    Gastric and pancreatic carcinoma
    Hypoglycaemia
    Insulin
    Fibrosarcoma
    Insulin like substance
    Hepatoma
    Hypercalcaemia
    PTH related peptide
    Renal cell carcinoma
    Carcinoma breast, SCC lung
    Ovarian carcinoma, leukaemia
    Polycythaemia
    Erythropoietin
    Renal cell carcinoma, hepatoma
    Cerebellar haemangioma
    Myasthenia
    Immunologic
    Lung cancer
    Acanthosis nigricans
    Epidermal growth factor
    Lung cancer, uterine cancer, gastric carcinoma
    Dermatomyositis
    Immunologic
    Lung carcinoma, breast carcinoma
    Clubbing and hypertrophic
    Ca lung
    Osteoarthropathy of fingers
    Migrating thrombophlebitis
    Tumour product mucin
    Ca pancreas, lung
    (Trousseau phenomenon)
    It activates clotting
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    Fig. 1.483: Ethmoidal sinus tumour. Biopsy and CT scan is needed to confirm and assess the extent.
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    Fig. 1.484: Carcinoma tongue is more common in lateral margin. Incision biopsy from the margin is done here.
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    Fig. 1.485: Typical malignant cachexia observed in GIT malignancies. It is totally malnourished incapacitated situation.
    pathologists. Sections are done after making tissue blocks using microtome up to 5 microns thickness. These sections are placed on a slide for staining with haematoxylin and eosin. This is studied under microscopy by pathologist to give the report. Detailed history, findings, markings of the specimen should be done by the surgeon prior to sending the specimen. Bone specimens are decalcified in hydrochloric acid for 7–21 days before sectioning and staining. So its report will be delayed usually.
  • Inadequate sampling and improper reports may be due to—limited tissue sent; tissues are nonviable; too superficial biopsy done; cautery use on the tissues; crushing effect on the tissues (gentle meticulous biopsy is important without rough handling and without over use of cautery on the required tissues).
  • Specimens are kept for 6 weeks. Blocks are kept for 30 years. Slides are kept for 10 years.
  • Risk of false positivity in malignancy should be remembered. It is probably due to contamination, interchanged specimens, wrong interpretation, ulceration, etc. Re-biopsy/reinterpretation/repeat sectioning may be needed in such situations.
  • Often additional methods like deeper sections; extra blocks; special stains are needed. Special stains are PAS (Periodic Acid Schiff) for glycogen, mucin and fungi; D (diastase) PAS for mucin; Perls Prussian blue for iron in haemochromatosis; reticulin for fibrous tissue; elastin stains for fibrosis; congo red for amyloid; Ziehl-Neelsen for mycobacteria; Grocott for fungi; Giemsa stain for protozoa; Warthin-Starry stain for spirochaetes.
 
Incision Biopsy
  • It is taken from the edge of the lesion as in ulcer, not from the centre as there is necrosis.
  • Usually two biopsies are taken in ulcerative lesion from the edge—edge/wedge biopsy (edge is a line which limits two parts; wedge is an area at two meeting parts like thick to thin, etc.
  • Incision biopsy is contraindicated in a case of melanoma where excision biopsy is preferred.
  • In secondaries in lymph nodes, FNAC is preferred. If it fails to give information, incision biopsy is done.
Note:
Biopsy taken from the centre of the lesion is only in post-radiation ulcer and syphilitic gumma. Because of irradiation there is no blood supply in the margin and tumour proliferates in the centre of the lesion.
 
Excision Biopsy
In small lesions excision biopsy is done, e.g. lymph node biopsy is done in case of lymphoma.
 
Trucut Biopsy
It is done using a specialised device wherein gun with trucut tip is inserted into the surface tissue/organ and gun is fired to close the
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Figs 1.486A and B: Carcinoma cheek—advanced. It needs incision biopsy/orthopantomogram X-ray/CT of the part.
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Fig. 1.487: Secondaries in skull—solitary.
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Fig. 1.488: Carcinoma breast. Note the dilated veins on the surface. FNAC should be done to confirm the diagnosis.
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Fig. 1.489: Soft tissue tumour of buttock. It could be sarcoma.
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Fig. 1.490: CT head showing secondaries in the brain.
278
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Fig. 1.491: Contrast MRI of spinal column showing extradural schwannoma.
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Fig. 1.492: CT scan picture of retroperitoneal leiomyosarcoma.
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Fig. 1.493: Alopecia (hair loss) is common after chemotherapy for cancers.
punching tip of the needle to catch and cut adequate tissue. It is done in prostate, breast and surface tumours. It cannot be done to deeper tissues or tissues which are close to major vessels/structures.
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Fig. 1.494: Trucut biopsy gun used for trucut biopsy. It gives histological diagnosis; it is also helpful to assess histochemistry.
 
FNAC (Fine Needle Aspiration Cytology)
It is cytological study of tumour cells to find out the disease and also to confirm whether it is malignant or not.
Procedure: It is done using 23 or 24 gauge needle fixed to specialised syringes which creates negative pressure for aspiration and contents are smeared on the slides. Dry slides as well as slides fixed with 100% methanol are used for study.
  • It is done in parotid, thyroid, lymph node, breast and all other surface lesions.
  • In follicular carcinoma of thyroid it is not very useful, as angioinvasion and capsular invasion which are specific cannot be detected.
  • In lymph nodes it is useful for detecting secondaries and tuberculosis.
  • U/S guided or CT guided FNAC are popular at present—especially when it is done from liver, lungs, kidneys, etc. (from deeper structures/organs).
It is absolutely contraindicated in testicular tumour. Because tough tunica albugenia usually prevents tumour spread and once it get disrupted by FNAC, spread can occur.
Cytological study is done after Papanicolaou stain; Giemsa staining or Romanowsky staining.
Note:
  • In 1934, Martin and Ellis did FNAC using 18 G needle with syringe with local anaesthesia use.
  • Kline and Neal in 1973 did syringe needle aspiration using 18 G needle making dry smears.
  • In 1982, A John Webb detailed standard FNAC using 21 G needle. Needle is passed obliquely into the lesion; constant suction is applied using Comeco syringe or braced thumb method. With suction persisting needle is moved in 4 directions. Suction is gently released and needle is withdrawn. Needle is detached from syringe to draw air which is reattached to withdrawn needle to blow the content over a dry slide.
  • In 1987, A Zajdello et al fine needle sampling of the tissue in question without aspiration. 25 G needle is used without a syringe. Needle is moved in various directions to detach the cells by sharp end of the needle; by capillary force, cells are conducted into the needle lumen. Air filled syringe is attached to needle to express cells into a glass slide. Trauma to tissue is said to be less; and feel of tissue consistency is better through held needle. It is called as Fine Needle Sampling Without Aspiration / Fine Needle Non-aspirating Cytology (FNNAC)/Fine Needle Capillary Sampling (FNCS; as capillary action causes conduction of cells into needle).
  • US guided/MRI guided/CT guided/Mammographic guided FNAC are available now which are more precise versions of localization of lesions to be aspirated.
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Fig. 1.495: Fine needle aspiration cytology (FNAC) of thyroid. It is also done in breast, lymph node and other swellings. It is not done for testicular tumour.
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Fig. 1.496: FNAC vacuum creator with loaded syringe [FNAC gun; Cameco syringe (Sweden) holder].(Courtesy: Dr Krishna Upadhya, MD, Nandikoor Laboratory, Mangaluru)
  • Ether with alcohol in equal proportion is used for wet fixation to stain Papanicolaou or H & E stains. Grace in 1994 used modified ultra Pap stain 3 changes – by rehydration of air dried smears using normal saline to cause RBC haemolysis to restore cell transparency; by using mixture of 4% formaldehyde and 65% ethanol to reduce fixation time from minutes to few seconds; by using Richard Allen Haematoxylin 2 and cyto stain. Total time of staining in this modification is 90 minutes.
 
Advantages
  • Very sensitive.
  • Done on OP basis.
  • Least invasive, safer, fast and cheaper.
  • Anaesthesia is not required.
  • Tumour dissemination through the track is not present (except in testicular tumour where it is not done).
  • Presently DNA study of the cell can detect very early malignancy.
 
Disadvantages
  • Negative result cannot rule out malignancy.
  • Tissue study is not possible.
  • Further studies not amenable.
Note:
FNNAC—Fine Needle Non-aspirating Cytology is done in some tissues (in some centres). Here needle is passed into the tissue and material collected from the needle (without any aspiration) is studied for cytological analysis.
 
Frozen Section Biopsy
Frozen section is done whenever biopsy report is needed at the earliest. It is usually done in a pathology set up existing adjacent to the operation theatre. An unfixed fresh tissue is frozen (using CO2) in a metal and sections are made and stained. It is technically difficult; processing and staining is of inferior quality and often it is difficult to give accurate results. But advantage is it is quick and surgeon can decide the further steps of procedure in same sitting like nodal clearance/type of resection to be done, etc.
  • It is done in carcinoma breast or in follicular carcinoma of thyroid when FNAC fails.
  • During surgery after resection of the tumour to look for (on table) the clearance in the margin and depth and also to study the lymph nodes for their positivity.
 
II. IMMUNOHISTOCHEMISTRY
It is detection of specific antigen using an antibody. Antibody labelled with a dye, binds to antigen in a section of tissue causing specific colours like brown, and determines its presence and distribution in the tissues. It is safe, specific and quick.
It is used in:
  • Neoplasia
    • To confirm, to find differentiation, to detect metastases; to plan type of therapy.
    • To categorise leukaemias or lymphomas; either of ‘T’ cell or of ‘B’ cell type.
    • To find out site of origin of metastatic tumours, e.g. by doing prostate specific antigen in prostate cancer or doing thyroglobulin in thyroid carcinomas or clear cells in the lung in metastatic renal cell carcinoma.
    • Detection of receptors or molecules, e.g. estrogen receptors [ER] in breast cancer. ER positive has got better prognosis. Presence of onco-protein product c—erbB2 in breast cancer signifies poor prognosis.
    • Gastrointestinal stromal tumour (GIST) can be treated with imatinib if it shows CD 117 expression.
    • Endocrine tumours are assessed on ki67 proliferative index.
    • Cytokeratin marker for epithelial tumours like carcinoma; S100 and actin for glandular malignancy; S100 for melanoma; CD31 and CD34 for vascular malignancy; CA 125 for ovarian tumours; PSA for carcinoma prostate; CD3 and CD20 for lymphoma.
  • Infections
    • Detection of specific antibodies to the antigens of certain specific infective agents like Epstein-Barr virus, cytomegalovirus, human herpes virus 8, herpes simplex virus, etc.
  • To identify abnormal accumulation of various proteins like α'-1-antitrypsin; deposition of amyloid.
  • Assessment of immunoglobulins.
  • Screening for mutations.
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III. TUMOUR MARKERS
  • Tumour markers are biochemical indicators of presence of a tumour. They are not used for primary pathological diagnosis.
  • They are of prognostic value.
  • Presence of tumour marker signifies recurrence or residual tumour.
 
IV. OTHER METHODS
 
Electron Microscopy
  • It is visualisation of tissue in very high magnification of 1000 × 500 000 in difficult deciding cases. But it is time consuming and expensive.
 
In Situ Hybridisation
  • It is determination of presence or absence of a specific gene and its location in a fresh/fixed tissue sections using an oligonucleotide probe, targeting at specific DNA or RNA sequence.
 
Polymerase Chain Reaction (PCR)
DNA is amplified using this special method and detected by technique like electrophoresis. PCR can be done on blood or nontissue samples. It is highly sensitive, fast and safe. Disadvantages are—expensive and risk of DNA contamination.
 
Uses
  • Detection of mutations in congenital conditions like von Hippel-Lindau disease (vHL gene); haemochromatosis (HFE gene); colorectal carcinoma (APC gene).
  • Gene rearrangements in different conditions like lymphoma or other diseases can be detected by PCR (clonality).
  • Assessment of loss of heterozygosity in tumours like oligodendroglioma (1p, 16q).
  • PCR study for infections like tuberculosis.
 
Fluorescent In Situ Hybridization (FISH)
  • It is a type of cytogenetic study (study of chromosomes) that can be done in fixed or fresh tissues. RNA or DNA probes are prepared which are tagged with fluorophores targeted on specific cells or chemicals.
  • It is used in haematological malignancies, genetic evaluation like trisomy 23; oligospermia; cancer study, leukaemias, and in many syndromes.
  • It is used in assessing the remission and prognosis.
  • It is safe and quack.
 
MANAGEMENT STRATEGY FOR CANCERS
  • Diagnosis is confirmed by biopsy from primary usually.
  • Evaluations for staging—metastatic work up.
  • Approaches for primary—surgery/radiotherapy/chemotherapy.
  • Approaches for secondary.
  • Palliation in advanced stage—palliation of distressing symptoms.
Tumour markers
Category 1
Hormonal:
Human chorionic gonadotrophin (HCG)
— Trophoblastic tumour, nonseminomatous testicular tumour
Calcitonin
— Medullary carcinoma of thyroid
Catecholamines and VMA
— Pheochromocytoma
Ectopic hormones
— In tumours of paraneoplastic syndromes
Category 2
Isoenzymes:
Prostatic acid phosphatase
— Carcinoma prostate
Neuron specific enolase
— Small cell carcinoma lung, neuroblastoma
Category 3
Oncofetal antigens:
Alpha fetoprotein
— Liver cancer, nonseminomatous germ cell tumour
Carcinoembryonic antigen (CEA)
— Carcinoma colon (common). Carcinoma pancreas, lung, stomach and breast
Category 4
Mucin and other proteins:
CA—125 (Carbohydrate antigen)
— Ovarian cancer
CA—15-3
— Breast cancer
CA—19-9
— Pancreatic and colon cancer
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Fig. 1.497: Advanced aggressive malignancy face may be carcinoma or sarcoma.
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Fig. 1.498: Advanced fungating carcinoma of breast.
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Fig. 1.499: Recurrent secondaries in neck after radical neck dissection.
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Fig. 1.500: Secondaries in ovaries—Krukenberg tumour.
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Fig. 1.501: Malignant primary nerve sheath tumour (MPNST).
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Fig. 1.502: Anal canal carcinoma (SCC).
282R. Skin Tumours
CHAPTER OUTLINE
  • ❖ Anatomy
  • ❖ Classification of Skin Tumours
  • ❖ Skin Adnexal Tumours
  • ❖ Dermatofibroma
  • ❖ Dermatofibrosarcoma Protuberans
  • ❖ Keratoacanthoma
  • ❖ Rhinophyma
  • ❖ Seborrhoeic Keratosis
  • ❖ Squamous Cell Carcinoma
  • ❖ Marjolin's Ulcer (1828)
  • ❖ Basal Cell Carcinoma
  • ❖ Turban Tumour
  • ❖ Naevi
  • ❖ Melanoma
 
ANATOMY
Skin is the largest organ in the body with surface area of up to 18,000 sq cms and having 15% of body weight. Its functions are—protective barrier to deeper tissues from infections, chemicals, other agents like heat, solar rays, etc; thermoregulation; fluid, electrolyte, acid and base balance maintenance; perception.
 
Epidermis
  • Epidermis is avascular.
  • Epidermis is 5% of the total skin. It is thickest (0.5–1 mm) in palm, sole, back and buttocks. It is thinnest in eyelids (0.05–0.09 mm).
  • Epidermis has got 5 layers—stratum corneum; granulosum; spinosum; basale and basement membrane. Epidermis contains keratinocytes (maintains homeostasis, secretes cytokines); melanocytes (secretes melanin); Langerhans cells (antigen presenting cells which migrate to regional lymph nodes to reach immune system).
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Fig. 1.503: Skin anatomy.
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Fig. 1.504: Extensive infective destruction of the eyelids, face exposing bone and deeper structures. Maggots are seen on the surface. It mimics carcinoma but it was of infective origin. Phagedena is infective destruction without proliferation. It often mimics malignancy.
 
Dermis
  • It contains collagen fibres, elastic fibres, capillaries, venules, arterioles, lymphatics, nerves, erector pilorum muscle, sweat glands (eccrine, apocrine), sebaceous glands. Merkel cells, Meissner and Pacinian corpuscles are receptors in dermis. Dermis constitutes 95% of the skin. Dermis is 15–40 times thicker than epidermis.
  • 283Dermis constitutes papillary and reticular dermis. Dermis contains type I and II collagen. Main adnexal structures of the skin are–sweat glands, sebaceous glands, hair follicles with their germinal centres. The apocrine glands are located in axilla and anogenital regions. Sebaceous glands secrete sebum to keep the skin soft and oily. The ducts open at the hair follicles and at the skin surface. Pilosebaceous unit contains hair follicle and sebaceous gland.
 
CLASSIFICATION OF SKIN TUMOURS
 
Benign
 
Epidermal
  • Seborrhoeic keratosis.
  • Trichilemmal tumour.
  • Sebaceous adenoma.
  • Sebaceous epithelioma.
  • Hydrocystoma, syringoma, spiradenoma.
 
Dermal tumour
  • Neurofibroma.
  • Dermatofibroma.
 
Malignant
  • Squamous cell carcinoma.
  • Basal cell carcinoma.
  • Melanoma.
  • Malignant skin adnexal tumour.
  • Secondaries in the skin. Sister Joseph nodules around umbilicus.
  • Skin cancers (SC) are also classified as melanotic (MSC) or nonmelanotic (NMSC). NMSC are commonest. Patient who had BCC/SCC has higher risk to develop 2nd new skin cancer (35% in 3 years; 50% in 5 years). NMSC can be low risk or high risk groups. Lesion more than 2 cm in trunk and limbs; more than 1 cm in forehead and neck; more than 6 mm in central face; poorly defined margin; recurrent type; moderate or poor differentiation; perineural/vascular invasion; presence of immunosuppression; previous RT— are high risk lesions.
Note:
  • Multiple sebaceous adenomas with visceral malignancy are called as Torre-Muir syndrome.
  • Secondaries in skin can occur like Sister Mary Joseph nodules around the umbilicus. (Sister Mary Joseph was Superintendent Nurse in St Mary's hospital, 1856–1939).
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Figs 1.505A and B: (A) Abdominal wall cutaneous secondaries; primary is from carcinoma stomach; (B) Sister Mary Joseph secondary nodule in umbilicus.
 
SKIN ADNEXAL TUMOURS
 
Classification
  • Eccrine gland tumours: Syringoma, hidradenoma, syringo-cystadenoma.
  • Hair tumours: Trichoepithelioma, tricholemmoma.
  • It may be benign or malignant.
 
Features
  • They are tumours arising from accessory skin structures like sebaceous glands, sweat glands, hair follicles.
  • It is not uncommon.
  • It presents as protruding well-localised swelling in the skin.
  • Trichoepithelioma is usually seen in nasolabial fold; mimics BCC; presents as small cutaneous nodule.
  • Tricholemmoma is also called as naevus sebaceous of Jadassohn. It is a hamartoma from hair follicle which can turn into BCC in 10% of cases.
  • Adenoma sebaceum is seen in tuberous sclerosis as red papules in face which appears below 10 years. It is often called as Bourneville's disease.
  • Calcifying epithelioma of Malherbe/pilomatrixoma is benign hair matrix cell tumour seen below the age of 10 years, containing basaloid and eosinophilic ghost cells with calcification.
  • Malignant skin adnexal tumour forms a nodular, hard, indurated swelling in the skin, often with involvement of regional lymph nodes which are hard and nodular.
  • It mimics squamous cell carcinoma of skin.
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Fig. 1.506: Skin adnexal tumour (benign) in the face.
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Fig. 1.507: Skin adnexal tumour (malignant) turned out to be of hair follicle origin.
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Figs 1.508A and B: Skin adnexal tumour—preauricular region; (B) Skin adnexal tumour. Vascularity is increased and it is malignant.
  • Differential diagnosis
    • Squamous cell carcinoma of skin.
    • Dermatofibrosarcoma protuberans.
  • Diagnosis
    • Biopsy—excision or incision type.
    • FNAC of lymph node.
  • Treatment
    • Benign tumour—excision.
    • For malignant tumour—wide excision and regional lymph node block dissection when required.
Prognosis is good. It is better than squamous cell carcinoma.
Note:
  • Merkel cell carcinoma is aggressive malignant condition arising from neuroendocrine receptor cells of the skin (dermis) which mimics histologically oat cell carcinoma. It is common in white elderly females (4 : 1) may be due to UV rays. Treatment is wide excision with radiotherapy.
  • Adenocarcinoma arising from the apocrine glands of skin is called as extramammary Paget's disease of skin (intraepidermal adenocarcinoma) commonly observed in perianal region.
    —It can occur in genitalia or in axilla (more apocrine glands). In 25% of cases, the condition is associated with an underlying in situ or invasive carcinoma. Presentation is like red plaque/white/depigmented areas/crusts/scales mimicking dermatitis, eczema, fungal infections. Condition is often associated with GI or urinary malignancies (40%). Biopsy of lesion, CT evaluation for other malignancies, wide local excision and radiotherapy—are the management principles.
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Fig. 1.509: Malignant skin tumour with ulceration of the skin over chest wall. Axillary nodes were enlarged in this patient.
 
DERMATOFIBROMA (Sclerosing Angioma or Subepithelial Benign Nodular Fibrosis)
  • It is a benign tumour arising from skin from dermal dendritic cells.
  • It is formation of firm, single or multiple nodules occurring commonly in extremities (limbs).
  • It can be red, brownish yellow (due to lipid), or bluish black (due to haemosiderin).
    Histologically, spindle cells are arranged in ‘mat like’ or ‘cart-wheel’ pattern.
  • It is also called as dermal histiocytoma.
  • Treatment: Excision.
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Fig. 1.510: Dermatofibroma in leg.
 
DERMATOFIBROSARCOMA PROTUBERANS
  • It is a low grade fibrosarcoma which grows slowly but persistently. It arises from dermal fibroblasts.
  • Occurs in head and neck, limbs, abdominal wall and back–Trunk is commonest site (50%).
  • It is not a rare entity, often attains a large size with multiple, nodular, hard, swelling with often involvement of lymph nodes. Malignant spindle cells are seen histologically.
  • Rarely it spreads into lungs through blood.
  • It mimics squamous cell carcinoma of skin and skin adnexal tumour.
  • Positive for CD34 and ring chromosome.
  • With melanin pigmentation it is called as Bednar's tumour.
 
Diagnosis
  • Biopsy of the lesion.
  • Chest X-ray, CT scan.
  • FNAC of the lymph node.
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Figs 1.511A and B: Dermatofibrosarcoma.
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Fig. 1.512: Dermatofibrosarcoma protuberans.
 
Treatment
  • Wide excision and follow up.
  • Recurrence is common—50%.
  • Prognosis is good.
 
KERATOACANTHOMA (MOLLUSCUM SEBACEUM)
  • It is an overgrowth and subsequent spontaneous regression of pilosebaceous glands with proliferation of squamous cells protruding out of the duct which are common in adult males (3:1) and places where more sebaceous glands are found.
  • Causes: Human papilloma virus; genetic; immunosuppression; UV rays, trauma are considered.
  • It presents as a rapidly growing, painless, single swelling in the skin with central brown area.
  • It grows usually for 4 weeks and later shows spontaneous regression in 4 months. It is a pseudomalignancy.
  • During regression phase, central area separates from the lesion leaving a deeply seated scar.
  • Eventhough it is usually benign, 6% of cases may be invasive squamous cell carcinoma and often called as keratoacanthoma variant.
  • Commonly keratoacanthoma is solitary, but rarely can be multiple, giant or generalised.
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Fig. 1.513A:
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Figs 1.513A and B: Typical keratoacanthoma with central brownish area. It is self-limiting disease.
 
Features
  • Mobile, hard, painless, nontender, lump with a central brownish volcano like area. It is common in face. It can be recurrent in lips and fingers.
  • Lymph nodes are not enlarged.
  • Differential diagnosis: Squamous cell carcinoma.
  • Treatment: Excision. The tissue is sent for histopathological study.
 
RHINOPHYMA (Potato Nose) (Bottle Nose)
  • It is a glandular form of acne rosacea causing immense thickening of distal part of skin of nose with visible openings of sebaceous follicles. Nose is bluish red in colour with dilated capillaries.
  • It is due to hypertrophy and adenomatous changes in sebaceous glands.
  • Male to female ratio is 12:1. Three per cent cases may have occult BCC in it. But rhinophyma itself will not cause BCC.
  • Treatment: Excision of excess tissue and reconstruction.
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Figs 1.514: Rhinophyma. Typical look and site.
 
SEBORRHOEIC KERATOSIS (Seborrhoeic Wart, Basal Cell Papilloma)
It is a benign overgrowth of the basal layer of epidermis with excess of small darkly stained basal cells, which protrudes from the surface of the epidermis to give oily appearance.
 
Features
  • It is common in elderly. Common sites are the back, face, neck.
  • It grows slowly with widening in area without altering in thickness.
  • It often gets infected but uncommon to bleed on touch.
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    Figs 1.515A to C: Seborrhoeic keratosis in face, ear and in periumbilical region. It is not a premalignant condition.
  • It is pigmented due to melanin and so mimics naevus or melanoma.
  • It is common Caucasians. It is familial—autosomal dominant gene related.
  • Often when it falls off, it leaves a pale pink patch on the skin with visible small surface capillaries.
  • It is not a premalignant condition
    Note:
    Solar keratosis is a premalignant condition.
  • It is hard and stiffer than normal skin.
  • Lymph nodes are not involved.
  • It does not occur in palms and soles.
  • It can be picked off from the skin.
  • 287‘Stuck on’ appearance is characteristic.
  • Differential diagnosis: Melanoma, pigmented BCC, naevus,
  • Treatment:
    • Excision cures the condition.
    • Shave excision or curettage can be done.
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Fig. 1.516: Bowen's disease (John T Bowen, 1912).
 
SQUAMOUS CELL CARCINOMA (Epithelioma)
  • It occurs in premalignant conditions like Bowen's disease, Paget's disease, leukoplakia, chronic scars, chemically induced chronic irritation, radiodermatitis, senile keratosis, e.g. Kangri cancer in Kashmir, Chimney scrotal cancer, Kang cancer of Tibetans.
  • It arises from squamous layer of the skin. Usually it occurs in a pre-existing predisposing lesion; occasionally can develop in de novo skin.
  • It can be grossly proliferative/ulcerative/ulceroproliferative/red plaque like. Proliferative type is cauliflower like.
  • It expresses cytokeratins one and ten.
  • It is the 2nd (20%) most common skin cancer.
  • It is common in males.
  • Exposure to UV B rays (ultraviolet rays are A, B, C types) causes SCC by direct carcinogenic effects on keratinocytes, unrepaired mutations, decreased immune surveillance response, inhibition of tumour rejection, mutation of p53 suppressor gene (seen in 90% SCC).
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Fig. 1.517: Squamous cell carcinoma eyelid. Note the involvement.
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Fig. 1.518: Squamous cell carcinoma on the labia.
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Common Sites are:
  • Dorsum of hand, limbs, face, and skin of abdominal wall SCC can occur in external genitalia, mucocutaneous junction, oral cavity, respiratory system, oesophagus, gall-bladder, in urinary bladder as metaplasia from transitional cell lining.
 
Clinical Features
  • An ulcerative or ulceroproliferative or proliferative lesion.
  • Raised and eve rted edge.
  • Indurated base and edge.
  • Bloody discharge from the lesion.
  • Regional lymph nodes are commonly involved, which are hard, nodular, initially mobile but eventually fixed to underlying structures.
  • Usually blood spread does not occur.
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Figs 1.519A and B: Squamous cell carcinoma foot—ulceroproliferative lesion with fungating inguinal node secondaries. It is an advanced disease. Opposite inguinal nodes are also significantly enlarged.
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Figs 1.520A and B: Recurrent SCC in amputated stump. Note the enlarged significant lymph nodes in the groin.
 
Variants
  • Marjolin's ulcer which occurs in chronic scar is a type of squamous cell carcinoma without lymph node spread.
  • Verrucous carcinoma is a squamous cell carcinoma, commonly occurring in mucous membrane or muco-cutaneous junction without lymph node spread. It is dry, exophytic, warty, indurated growth. It has good prognosis. It is a curable malignancy.
  • A rare multiple self-healing SCC is observed usually in face as familial autosomal dominant (Ch 9q) disease in Western Scotland-Ferguson-Smith syndrome.
  • SCC often associated with BCC also.
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Figs 1.521A and B: Carcinoma cuniculatum—in heel and under great toe which is a low grade verrucous type of SCC.
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Fig. 1.522: Verrucous carcinoma of penis. It is an exophytic, dry, warty, locally malignant lesion (Squamous cell carcinoma).
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Fig. 1.523: Squamous cell carcinoma and BCC in face of a patient.
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Histology
  • Malignant whorls of squamous cells with epithelial or keratin pearls are characteristic feature.
  • Spindle cells, invasion, deep and peripheral margin clearance.
 
Differential Diagnosis
  • BCC.
  • Melanoma.
  • Keratoacanthoma.
  • Skin adnexal tumours.
  • Actinic keratosis.
  • Pyogenic granuloma.
 
Investigations
  • Wedge biopsy from the edge.
  • FNAC from lymph node.
  • USG/CT scan to identify nodal disease; MRI to identify local extension is useful.
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Figs 1.524: Squamous cell carcinoma in the forearm and foot. It is proliferative cauliflower like lesion. Wedge biopsy has to be done.
TNM staging for skin cancer other than melanoma
Tumour
Node
Metastasis
T0 no tumour found
N0—No nodes
M0—No distant spread
T is Tumour in situ
N1—Regional nodes ++
M1—Distant spread ++
T1 Tumour < 2 cm
T2 Tumour 2-5 cm
G1—Low grade
T3 Tumour > 5 cm
G2—Moderate grade
T4 Spread to cartilage, muscle or bone
G3—High grade
 
Treatment
  • Radiotherapy using radiation needles, moulds, etc. is given.
  • Wide excision, 2 cm clearance followed by skin grafting or flaps.
    (Presently for tumour less than 2 cm, 4 mm clearance and for tumour more than 2 cm, 1 cm clearance is sufficient). Wide excision should show clearance both at margin as well as in the depth. If muscle, fascia, cartilage are involved, it should be cleared. Reconstruction is usually done by primary split skin grafting (SSG/Thiersch). Delayed skin grafting also can be done once wound granulates well. Often flaps of different types may be needed depending on the site of lesion.
  • Amputation with one joint above.
  • For lymph nodes, block dissection of the regional lymph nodes is done.
  • Curative radiotherapy (RT) is also useful in tumours which are not adherent to deeper planes or cartilage as SCC is radiosensitive. It is also useful in recurrent SCC and in patients who are not fit for surgery. A dose of 6000 cGy units over 6 weeks; 200 units/day is used. Recurrence after RT is treated by surgical wide excision.
  • In advanced cases with fixed lymph nodes, palliative external radiotherapy is given to palliate pain, fungation and bleeding.
  • Chemotherapy is given using methotrexate, vincristine, bleomycin.
  • Field therapy using cryo probe or topical fluorouracil or electrodessication.
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MARJOLIN'S ULCER (1828)
  • It is a well-differentiated squamous cell carcinoma which occurs in chronic scars like burn scar, scar of venous ulcer.
  • As it develops in a scar due to chronic irritation and there are no lymphatics in scar tissue, it will not spread to lymph nodes.
  • As scar is relatively avascular it grows slowly. As scar does not contain nerves, it is painless.
  • Once it reaches the normal skin it may behave like any other squamous cell carcinoma, i.e. it will spread to lymph nodes. It occurs in unstable scar of long duration.
 
Clinical Features
  • History of pre-existing venous ulcer or burn scar.
  • Indurated, painless, nontender, ulcer with raised and everted edge.
  • Biopsy from the edge confirms the diagnosis.
 
Treatment
  • Wide excision.
  • In case of large ulcer, amputation is required.
  • Radiotherapy should not be given as it may turn into poorly differentiated squamous cell carcinoma.
    It is a curable malignancy.
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Fig. 1.525: Marjolin's ulcer foot in a pre-existing burns scar. It is a well-differentiated squamous cell carcinoma occurring in an unstable scar of long duration.
 
BASAL CELL CARCINOMA (Rodent Ulcer)
It is a low grade, locally invasive, carcinoma arising from basal layer of skin (or adnexal basal layer of hair follicle) or muco-cutaneous junction. It does not arise from mucosa.
  • It is the commonest (70%) malignant skin tumour.
  • It is more common in white-skinned people than blacks.
  • Common in places where exposure to UV light is more (Australia).
  • Other causes are—arsenics, coal tar, aromatic hydrocarbons, skin tumour syndromes.
  • It is common in males, common in middle-aged and elderly.
  • Common site is face—above the line drawn between angle of mouth and ear lobule (90%)—Onghren's line.
  • It is called as tear cancer because it is commonly seen in area where tears roll down.
  • Often it can occur in muco-cutaneous junctions.
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    Fig. 1.526: Note the common site of BCC—in the face above the line drawn between angle of mouth and ear lobule—Onghren‘s line.
  • Basal cell naevus syndrome (Gorlin syndrome) with BCC; medulloblastoma; bifid ribs.
  • It is only locally malignant. It does not spread through lymphatics nor through the blood. But it erodes deeply into local tissues including cartilages, bones causing extensive local destruction. Hence the name rodent ulcer”.
 
Types
  1. Nodular—common in face.
  2. Cystic/nodulocystic.
  3. Ulcerative.
  4. Multiple, often associated with syndromes and other malignancies.
  5. Pigmented BCC—mimics melanoma.
  6. Geographical or field fire or forest fire BCC is wide area involvement with central scabbing and peripheral active proliferating edge.
  7. Basi-squamous—behaves like squamous cell carcinoma which spread into lymph nodes. BCC which has not been treated for long time can turn into Basisquamous carcinoma.
Note:
Nodulocystic and noduloulcerative is the commonest form (70–90%).
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Figs 1.527A and B: (A) BCC in perianal region. It is nodular type. Wide excision is required; (B) Nodular BCC in the nose (Common in face).
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Fig. 1.528: Sebaceous epidermal naevus. It is common in females, often extensive, begins in childhood. It needs surgical excision and skin grafting. It has got 10% chances of turning into BCC.
 
Clinicopathological Types
  1. Superficial type—small buds of tumour masses.
  2. Morpheic type—dense stroma with basal cells and type IV collagen; spreads rapidly; sclerosing BCC.
  3. Fibroepithelioma type of Pinkus shows elongated cords of basaloid cells with mesh work.
It contains outer palisading columnar cells with central polyhedral cells but no prickle cells or keratinisation.
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Fig. 1.529: BCC lesions in different places (multiple).
 
Clinical Features
  • Ulcer on the face in a middle-aged man which is nontender, dry, slowly growing, nonmobile, with raised and beaded edge with central scab, often with central depression or umbilication.
  • Site of beading signifies the area of active proliferating cells. In between beaded areas dormant nonactive cells are present.
  • No lymph node or blood spread occurs. Due to large sized tumour cells/tumour cluster, it does not spread through lymphatics.
  • BCC can be low risk or high-risk.
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Figs 1.530A to C: Basal cell carcinoma in different locations. Note the nodularity and ulceration. Note the beaded edge.
 
Differential Diagnosis
  1. Squamous cell carcinoma.
  2. Melanoma.
  3. Keratoacanthoma.
  4. Seborrhoeic keratosis.
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Investigations
Wedge biopsy, X-ray of the part, CT scan.
 
Treatment
  • It is radiosensitive. If lesion is away from vital structure (like away from eyes), then curative radiotherapy can be given. Radiotherapy is not given, once it erodes cartilage or bone. RT is not given to BCC of ear and close to lacrimal canaliculi.
  • Surgery:
    • Wide excision (1 cm clearance) with skin grafting, primary suturing or flap (Z plasty, rhomboid flap, rotation flap) is the procedure of choice.
    • Laser surgery, photodynamic therapy, 5 fluorouracil local application.
    • Cryosurgery.
    • MOHS (Microscopically Oriented Histographic Surgery) (Federic E Mohs, American Surgeon) is useful to get a clearance margin and in conditions like BCC close to eyes, nose or ear, to preserve more tissues. MOHS is becoming popular in BCC/dermatofibrosarcoma protuberans/melanoma. Procedure is done by dermatological surgeon along with a histotechnician/histologist. Under local anaesthesia, a saucerised excision of the primary tumour is done and quadrants of the specimen are mapped with different colours. Specimen is sectioned by histotechnician from margin and depth, and it is stained using eosin and haematoxylin. It is studied by MOHS surgeon or histologist. Residual tumour from relevant mapped area is excised and procedure is repeated until clear margin and clear depth are achieved. Clearance must be complete and proper in BCC otherwise there will be very high chance of recurrence (70%).
 
TURBAN TUMOUR
It is a descriptive term wherein entire scalp looks like a turban because of multiple scalp swellings. It can be due to multiple cylindroma; multiple hidradenomas; subcutaneous neurofibromas; nodular multiple basal cell carcinoma.
  • Multiple cylindroma is usually considered disease under this term. Cylindroma is a variant of eccrine spiradenoma (skin adnexal tumor). Multiple firm pinkish nodules in the scalp are the presentation in multiple cylindroma. They are rare, often locally malignant, grows slowly over the span of many years to cover entire scalp with reddish lobulated lesion.
  • Hidradenoma is a rare benign sweat gland tumour. Multiple tumours commonly look like a turban in the scalp. They are painless, disfiguring, cosmetically problematic, soft, boggy, non-fluctuant, non-compressible cutaneous swellings; commonly observed in middle age group.
  • Multiple sebaceous cysts over the scalp mimic the same.
  • Management is initial biopsy to find out the cause; then wide excision with skin grafting.
 
NAEVI
  • It is a hamartomata of melanocytes due to excessive stimulation.
  • It may present during birth or appear later in life.
 
Types
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Fig. 1.531: Different types of naevi.
  1. Hairy mole is a mole with a hair growing on its surface.
    zoom view
    Fig. 1.532: Hairy naevus.
  2. Nonhairy mole.
  3. Blue naevus. It is seen in children. It is located deep in the dermis, hence appears blue. It is common in buttock (Mongolian spot), hand, feet.
  4. Junctional naevus. It lies centred in the junctional layer (basal layer) of the epidermis as clusters. It is immature, unstable and premalignant. Microscopically there is proliferation of melanocytes at the epidermal junction. Features of malignant transformation are—change in the size, colour, bleeding, ulceration, crusting, satellite spots.
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    zoom view
    Fig. 1.533: Junctional naevus.
  5. Compound naevus. It is combination of intradermal and junctional naevus. Intradermal part is inactive but junctional part is potentially malignant.
    zoom view
    Fig. 1.534: Compound naevus.
  6. Juvenile melanoma (Spitz naevus) (It is a misnomer). It appears as junctional like mole before puberty. It is seen in children on face. They present as brownish red nodular lesion which needs always excision.
  7. Hutchinson's freckle. It is seen in elderly with large area of dark pigmentation. In the macular stage it is smooth and brown. In the tumour stage it is dark and irregular. It can turn into melanoma commonly.
  8. Halo naevus: Halo of depigmentation around the pigmented naevus. This halo is due to antibody response to melanocytes. Halo naevus is often seen along with vitiligo. Similar halo may develop around a malignant melanoma lesion.
  9. Intradermal naevus: Cluster of dermal melanocytes is seen without junctional component. Common in face.
    zoom view
    Fig. 1.535: Intradermal naevus.
  10. Spindle cell naevus: It is dense, black pigmented lesion containing spindle cells and atypical melanocytes at dermo-epidermal junction; seen in females on high with malignant potential.
  11. Naevus spilus: It is hyperpigmented speckles throughout, also called as speckled lentiginous naevus. Malignant potential is rare.
  12. Naevus of Ota is dermal melanocytic hamartoma seen in distribution area of trigeminal nerve (ophthalmic /maxillary). It is seen in oriental and African race adolescent females (thigh) with a hormonal influence.
  13. Naevus of Ito is similar lesion occurring in shoulder region.
  14. Dysplastic naevus is proliferation of atypical melanocytes from epidermal basal layer having variegated irregular look; it is usually >5 mm in size; can be familial; 10% cases may turn into superficial spreading melanoma.
  15. Congenital naevus: It is present since birth.
    zoom view
    Fig. 1.536: Congenital naevus.
Note:
  • Giant naevus is naevus more than 1% of body surface area or more than 20 cm in size. Giant congenital pigmented naevus (GCPN) often shows dermatomal distribution. Pigment cells spread from epidermis to fat and muscle often. It may turn into melanoma (5% risk). Such melanomas are usually axial; is usually associated with retroperitoneal / intracranial melanosis. Curettage, dermabrasion, laser, excision and SSG are the treatment options.
    zoom view
    Fig. 1.537: Giant congenital naevus(Courtesy: Dr MuraliKeshav, MD, Pediatrician, KMC Mangaluru).
  • Mongolian spot is a blue brown/grey pigmented macular area which is seen in sacral region during birth and after initial intense pigmentation regresses fully in 7 years.
  • Normal number of melanocytes releasing abnormally higher number of melanin granules is called as freckle/ephilis.
 
Treatment
Excision. Always should be sent for histopathology.
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MELANOMA
  • It is a malignant tumour arising from epidermal melanocyte which is most aggressive cutaneous malignant tumour.
  • It is of neural crest (ectodermal) origin.
  • It is 20 times more commonly seen in whites than blacks.
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Fig. 1.538: Large nodular melanoma in the sole.
  • Its incidence is equal in both sexes.
  • Its incidence is increasing over the years.
  • Five per cent of skin cancers are melanomas.
  • It is most common in Queensland, Australia. Auckland, New Zealand.
 
Sites
  • In females, leg is the commonest site.
  • In males, the front or back of the trunk.
  • In the Bantu tribe, sole is the commonest site.
Other sites:
Eyes (iris, ciliary body, choroids), mucocutaneous junction (anorectal region, genitalia), head and neck (meninges, oropharynx, nasopharynx, paranasal sinuses).
 
Risk Factors
  • Exposure to sunlight (exposure to UV light; more common in white-skinned—20 times).
  • Ethnic factors, socioeconomic status (high society), lifestyle, climate.
  • Albinism.
  • Xeroderma pigmentosa – RR is 1000 (By Kaposi in 1874): It is an autosomal recessive (Ch 9q) disease with defect in DNA excision repair mechanism causing formation of aberrant nucleotide causing ultraviolet rays' intolerance, erythema, pigmentation, photophobia, premature skin ageing, multiple malignancies with 60% mortality at the age of 20.
    zoom view
    Fig. 1.539: Xeroderma pigmentosa with BCC in the nose. Such patients are prone for other skin malignancy like melanoma also. There is defective DNA excision repair.
  • Junctional naevus.
  • Familial dysplastic naevus syndrome.
  • Sporadic dysplastic naevi. 10% risk.
  • Large congenital naevi (larger than 20 cm).
  • Family history of melanoma (10% through chromosomes 1p, 6q, 7 and 9). They often present with multiple primary melanomas; associated with dysplastic naevus.
  • History of earlier skin cancers other than melanoma.
  • Patients who are on immunosuppressive drugs or after renal transplantation or NHL (RR - 30).
 
Classifications
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Relation of Tumour Thickness to Nodal Spread—Based on AJCC Classification
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Fig. 1.540: Clark's level.
 
Differential Diagnosis (Other Pigmented Lesions of the Skin)
  • Seborrhoeic keratosis, dermatofibroma
  • Pigmented BCC, pigmented SCC
  • Naevus, sebaceous epidermal naevus
  • Kaposi's sarcoma, mycosis fungoides
  • Cutaneous haemangioma
  • Certain skin adnexal tumours
  • Solar keratosis
  • Pyogenic granuloma
  • Cutaneous angiosarcoma
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Fig. 1.541: Extensive pigmented lesion of the skin.
 
Clinical Types
  1. Superficial spreading:
    • Most common. 70%. Occurs in any part of the body with variegated irregular look. It has more radial growth and better prognosis. It commonly arises from a pre-existing naevus. In men, common in back; in women in leg.
      zoom view
      Fig. 1.542: Superficial spreading melanoma (70%).
  2. Nodular melanoma: 12–25%.
    • More aggressive. It is common in younger age group, occurring in any part of the body. It has more vertical growth. Common in mucosa and mucocutaneous junction; uniform; nodular; more vertical growth; nodal spread is common; has got poor prognosis. It usually appears as de novo. Common in men; common in trunk, head and neck.
      zoom view
      Fig. 1.543: Nodular malignant melanoma.
  3. Lentigo maligna melanoma:
    • 7–15%. Less common, least malignant. Occurs in old age and common in face (Hutchinson's melanotic freckle296). It is slow growing, variegated, brown macule/lentigo; common in face/neck/hands; common in elderly women. Lentigo maligna is in situ type.
  4. Acral lentiginous melanoma:
    • 5%. Occurs in palms, soles and subungual region. Common in Japan. It has got a poor prognosis. It is least common. Usually attains large size; nodular type with more vertical growth phase. It is common in Africa and Asia. It is less common in whites. It is often flat, irregular macule. It mimics fungal infection/pyogenic granuloma.
  5. Amelanotic melanoma:
    • This is the worst type. Because of the undifferentiation, tumour cells loose their capacity to synthesise melanin. It presents as rapidly progressive pinkish fleshy tumour. It may mimic soft tissue sarcoma. It needs markers like S100, HMB45 for diagnosis.
  6. Desmoplastic melanoma has high affinity for perineural invasion; is common in head and neck with higher recurrence rate. It is amelanotic melanoma with thicker lesion carrying poor prognosis due to neural invasion.
Note:
  • Subungual melanoma which was earlier thought of acral lentiginous type is now considered as superficial spreading type. It is involvement of nail fold matrix (not nail plate). Triangular, macular, progressively widening pigmentation of nail fold with nail dystrophy is typical—Hutchinson's sign. It should be differentiated from benign racial melanonychia which are dark streaks under the nail. Biopsy of nail matrix should be done here.
  • Ocular melanoma: It is the commonest malignancy arising in eye. It may arise from retina, iris, ciliary body, choroid. It rarely metastasize or only at late stage as it is devoid of lymphatics. Ocular melanoma commonly shows its distant spread to liver. Massive hepatomegaly is typical and is often seen many years after the treatment of primary ocular lesion. Condition is treated with enucleation, radiation, photocoagulation.
  • Clark's concept—Two phases of growth: Initial radial growth phase occurs horizontally, later vertical growth phase occurs with invasion.
 
Clinical Features
  • It can stat in a pre-existing naevus (commonly junctional naevus)—50–60% or as de novo in a normal skin—40-50%.
  • Melanoma is unknown before puberty.
  • Induration is not seen in melanoma
  • Pigmentation with irregular surface and margin with rapid growth.
  • Ulceration, bleeding, itching, change in the colour.
    zoom view
    Fig. 1.544: Melanoma in the sole. Often such pigmentation may be unnoticed.
Note:
When a mole turns malignant, following changes should be observed (Glasgow criteria:
  • Major signs: Change in size (diameter more than 6 mm), shape and colour
  • Other changes:
    • Inflammation, crusting, bleeding, itching
    • Nodularity, ulceration, halo around a mole
    • Satellite lesions
    • Doppler positive pigmented lesions using hand held Doppler (> 1 mm thick lesion)
 
Spread
  • Through lymphatics it spreads to regional lymph nodes either by permeation or by embolisation.
  • In-transit nodules or satellite nodules are seen in the skin between the primary lesion and regional lymph node area, and is due to retrograde spread to dermal lymphatics.
  • Through blood: To lungs, liver (huge liver), brain, skin, bones. Secondaries are typically black.
  • Melanoma in choroid has got better prognosis, because as there are no lymphatics, spread is delayed.
  • Sometimes primary is very small and unnoticed (in anus, subungual region). They present with features of secondaries only.
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Figs 1.545A and B: Primary melanoma with lymph node secondaries in two different individuals. Note the pigmented ulcerated secondaries in one.
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Figs 1.546A and B: (A) ‘In-transit’ nodules in melanoma. They are secondary depositions in dermal lymphatics; (B) Satellite nodule in melanoma occurs within 2 cm of primary. Note the primary in the heel and satellite nodule adjacent to it.
Note:
  • Infiltration into deep fascia by melanoma is rare in initial stages as deep fascia acts as a strong barrier.
  • Melanoma can also occur in places other than skin like tongue, mucous membrane or genitalia.
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Fig. 1.547: Melanoma in tongue.
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Figs 1.548A and B: Melanoma in vagina—in mucocutaneous junction. On table and excised specimen of melanoma.
 
Staging of Malignant Melanoma (It is older staging system)
IA:
Thickness less than 0.75 mm.
IB:
Thickness between 0.76 to 1.5 mm.
IIA:
Thickness between 1.51 to 4.0 mm.
IIB:
Thickness more than 4.0 mm.
IIIA:
Any of the above + nodes less than 3 cm.
IIIB:
Any of the above + nodes more than 3 cm.
IV:
Any of the above + any node + M1 (distant spread).
 
Investigations
  • No incision biopsy. It can cause early blood spread.
  • Excision biopsy of primary. It is done with 2 mm margin with deeper fatty tissue. One should avoid using cautery and avoid crushing the tissues as much as possible. Instead of excision biopsy, punch biopsy is done in case of large primary tumour very close to pinna, eye, nose. Punch biopsy assesses the depth/thickness of the lesion. Punch should be done at the most elevated part of the lesion to get proper depth.
  • FNAC of lymph node.
  • US abdomen to look for liver secondaries (usually huge hepatomegaly occurs).
  • Chest X-ray to look for secondaries in lung (“cannon ball” appearance). HRCT of chest is ideal.
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Newer TNM staging (2010) for melanoma
Tumour
Node
T0 No tumour
N0 No nodes
T is In situ tumour
N1a—one node micrometastasis
T1a <1 mm level II, III no ulceration, mitoses < 1 mm2
N1b—one node macrometastasis
T1b <1 mm, level IV with ulceration, mitoses > 1 mm2
N2a—2 or 3 nodes micrometastasis
T2a 1–2 mm no ulceration
N2b—2 or 3 nodes macrometastasis
T2b 1–2 mm with ulceration
N2c—no nodes but satellite or in transit lesions
T3a 2–4 mm no ulceration
N3–4 or more nodes; nodes with satellite or in transits
T3b 2–4 mm with ulceration
Stage 0 – T is N0M0
T4a >4 mm no ulceration
Stage IA – T1a N0M0; IB – T1b/T2aN0M0
T4b >4 mm with ulceration
Stage IIA – T2b/T3aN0M0; IIB – T3b/T4aN0M0; IIC – T4bN0M0
M—Metastasis
Stage IIIA – T1-4aN1a/N2aM0; IIIB – T1-4bN1a/N2aM0, T1-4aN1bN2bM0, T1-4a/bN2cM0; IIIC – T1-4bN1b/N2bM0, any TN3M0
M0—no blood spread
Stage IV – Any T, Any N, M0
M1a—Skin, subcutaneous tissue, distant node
M1b—Lung spread
M1c—Other viscera or distant spread and increase in LDH
  • Relevant other methods depending on site and spread, e.g. CT scan of head, chest, abdomen, pelvis.
  • Urine for melanuria signifies advanced disease.
  • Sentinel lymph node biopsy (SLNB).
  • Tumour markers—LDH; Melan – A; S 100; tyrosinase; HMB 45 are the tumour markers used. Human melanoma black 45 (HMB 45) is a monoclonal antibody against specific antigen (Pmel 17) present in melanocytic tumours. HMB 45 has got 92% sensitivity.
  • MRI of the area; PET scan to detect the spread—in seleted patients only.
 
Treatment
Surgery is the main treatment.
 
For primary:
  1. Handley's wide local excision (WLE) is wide excision with clearance of margin as well as depth. Clearance margin used in olden days is 3–5 cm.
    Tumour thickness in mm
    Wide Local Excision (WLE) margin in cm
    <1 mm
    1 cm
    1–2 mm
    2 cm
    >2 mm
    3 cm
    Present recommendation is— in situ melanoma needs 0.5 cm clearance; melanoma < 1 mm thickness needs 1.0 cm clearance; 1–2 mm thickness needs 1–2 (1.5) cm clearance; 2 cm/3 cm clearance is sufficient for >2.0 mm thickness. Procedure can be done under regional or local anaesthesia. Evidence says that more than 2 cm clearance will not show any additional advantage in treating primary tumour.
    If Primary closure or SSG or local flaps are used to cover the defect.
  2. If primary area is wide and deep, then amputation with one joint above is done.
  3. In fingers and toes, disarticulation is required.
  4. Melanoma in anal canal may require abdominoperineal resection.
  5. Enucleation in case of melanoma in eye.
  6. Melanoma in pregnancy is treated with termination of pregnancy and specific therapy for melanoma. Pregnancy should be postponed for 2 years.
 
For lymph node secondaries:
  1. In a clinically palpable lymph node, FNAC of lymph node is done. In case of spread, then regional block dissection, i.e. ilioinguinal or axillary or neck is done. Once FNAC shows positive lymph node 5-year survival rate reduces to 50%.
  2. In a fixed lymph node, only chemotherapy is the treatment because it is inoperable.
  3. Lymphatic mapping and sentinel node biopsy (Dr Donald Morton, 1970): Radioactive colloid is injected around primary site and lymphoscintigraphy is done using hand held gamma camera to visualise the micrometastasis in the nodal field. If there are micrometastasis, then regional block dissection (therapeutic LND) is done.
    SLN (sentinel lymph node) can be identified in 95% or more of groin and axillary nodes and in 85% cases of head and neck melanomas. Often both blue dye and technetium sulfur colloid is used together to identify the SLN. SLNB is useful for melanoma with thickness more than 1 mm depth. Less than 1 mm thickness is considered as low-risk for metastases; between 1-4 mm thickness is considered as intermediate-risk for metastases mainly of nodal spread; more than 4 mm thickness will be considered as high-risk for both nodal as well as blood spread. SLNB is the investigation of choice for staging in intermediate thickness melanoma.
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Figs 1.549A and B: Widely excised melanoma specimen from heel. Cut section of widely excised specimen of melanoma from heel shows the depth of the tumour.
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Fig. 1.550: Wide excision and skin grafting done for melanoma.
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Fig. 1.551: Wide excision of melanoma from the heel. Note the clearance margin and depth of dissection.
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Figs 1.552A and B: Melanoma secondaries in groin nodes after block dissection. Black lesions are observed in cut section.
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Fig. 1.553: Disarticulation of lateral two toes for interdigital melanoma.
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Figs 1.554: Secondaries in inguinal lymph nodes from primary melanoma sole-on table finding. Pigmented nodes are observed.
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  1. Prophylactic regional block dissection which was previously advocated is now controversial. But still used in many centres. Elective lymph node dissection (ELND) is done when tumour thickness is 1–4 mm.
  2. Management in unknown primary (2%) presenting as nodal secondaries is by nodal radical dissection at the region with adjuvant chemotherapy. They have better prognosis than with known primary. Patient should be monitored and evaluated to identify the primary site during every follow up. Once primary is identified it is treated accordingly depending on its location.
 
For Loco Regional Recurrent Melanoma:
  • Local recurrence is one which recurs within 5 cm radius of the primary tumour in skin or subcutaneous tissues. Risk of local recurrence is 0.2% if primary tumour is less than 0.75 mm; 2% if it is between 0.75–1.5 mm; 6% if it is 1.5–4 mm; 12% if it is more than 4 mm.
    • Isolated limb perfusion (Creech et al, New Orleans, 1958) using cytotoxic agents like Melphalan (M for M), interleukin 2, tumour necrosis factor (TNF). Concentration used here is 15–25 times more than that is used for systemic therapy. Melphalan dose is 10 mg/l perfusion solution in leg (13 mg/l in arm).
      Melphalan is injected at high temperature of 41°C with a pump and oxygenator through cannulas in femoral artery and vein with a proximal tourniquet in situ. Hyperthermia and oxygenation increase the metabolic activity of tumour cells to make it more vulnerable to melphalan. Procedure controls the local disease well with preserving the functioning limb. Complications like DVT, bleeding, sepsis can occur. It is used in local recurrence or ‘In- transit’ deposits.
      It shows 80% response rate with 15% complete response; but only of short period.
    • Laser ablation of multiple small cutaneous lesions.
    • Isolated limb infusion (Thompson, 1993): Vascular catheters are passed and placed across femoral artery and vein through opposite femoral vessels or through arm vessels. The limb is warmed; patient is anaesthetised 2 hours later and also heparinised; papaverine is injected into arterial catheter and tourniquet is applied in the thigh/arm. Melphalan 7.5 mg/l, actinomycin D 75 µg/l in 400 ml saline (10 mg and 100 µg/l in 300 ml NS in upper limb) is infused into the isolated limb for 6 minutes which is pumped around the limb repeatedly for 30 minutes with a hypoxia in limb; drugs are washed out using a Hartmann's solution; tourniquet is removed and normal circulation is regained with removal of vascular catheters. Protamine is given to reverse heparin action.
 
For Distant Spread
  • Brain, lung and liver are the most common sites; skin, bone, GI are less common sites. But melanoma is one of the commonest tumours to spread to intramural GIT to present as intussusception.
  • Distant spread when found or suspected, CT scan of head, chest, abdomen and pelvis are needed. PET scan and tumour markers are very useful.
    • Chemotherapy and immunotherapy is the main treatment.
    • Isolated lung or liver metastasis can be resected.
    • Radiotherapy is useful for bone and brain secondaries. Stereotactic program using gamma knife is better for brain secondaries.
 
Chemotherapy for Melanoma
Indications:
  1. Secondaries in lungs, liver, bones.
  2. After surgery for melanoma. Usually it is given intravenously.
Drugs are:
  1. DTIC: Diethyl triamine iminocarboxamide.
  2. Melphalan (Phenyl alanine mustard) (Melphalan for melanoma).
  3. Carboplatin, vindesine.
  4. CVD regime—is cisplatin, vinblastine and dacarbazine.
 
Immunotherapy/Biological Therapy
  • It is done using specific tumour antibodies, BCG, levamisole, Corynebacterium parvum, alpha interferon, interleukins and tumour vaccines is tried with some success rate up to 40% in advanced melanomas.
  • Biochemotherapy is combination of CVD with interferon α and interleukin 2.
  • Interferon α is a cytokine which is antiangiogenic and stimulator of natural killer NK cells. Dose is 20 mU/m2 IV 3 times a week for 4 weeks then maintenance dose of 10 mU/m2 subcutaneously 3 times a week for one year. Severe myelodepression and fulminant liver necrosis are the toxicity and so often dose is reduced to 3 mU/m2 three times weekly for 2 years.
  • GM2 ganglioside based vaccine (stimulates production of IgM antibodies), Melacine (contains melanoma cell lysates) and cancerVax are three vaccines under trial at present.
  • Ipilimumab is a monoclonal antibody that boosts the body's immune response against melanoma cells.
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Endolymphatic therapy
  • It can be done to control disease in the nodes using radioactive I131 or P32 with ultrafluid lipiodol along with lymphangiography.
 
Targeted therapy
  • Signal transduction inhibitor therapy—Vemurafenib, dabrafenib, and trametinib are signal transduction inhibitors; oncolytic virus therapy; monoclonal antibody therapy—are different targeted therapies.
Note:
  • There is not much role for radiotherapy.
  • Radiotherapy is beneficial only in secondaries in brain and bones.
zoom view
Fig. 1.555: Melanoma involving face extensively with destruction. Note the maggots over the surface of tumour. Melanoma is most aggressive cutaneous malignancy.
 
Prognosis for Melanoma
  • It is not good since it is a very aggressive tumour.
  • Old age has worse prognosis.
  • Females show better prognosis.
  • Extremity melanoma has better prognosis than head and neck.
Prognostic factors—overall poor
Staging as prognostic factor
  • Tumour thickness—very important factor
Stage I: >90% prognosis
Stage II: 70%
  • Nodal spread—once regional nodes are positive, 85% of patients will have occult distant spread. Number of positive nodes is also important
Stage III: 35%
Stage IV: <2%
  • Ulceration—poor
  • Angiogenesis, vascular invasion—poor
  • In-transit nodules—poor
  • Vertical growth—poor prognosis
  • Metastatic disease—poor
  • Staging
  • Mitotic activity
 
Follow-up After Therapy in Melanoma
  • In stage I and II disease after treatment, follow-up is done at 6 months interval for 3 years. It is done by clinical examination, LDH assay, USG abdomen and chest X-ray.
  • In stage III disease, PET scan CT of head, chest and abdomen are indicated.
302S. Sarcomas
CHAPTER OUTLINE
  • ❖ Sarcoma
  • ❖ Liposarcoma
  • ❖ Fibrosarcoma
  • ❖ Malignant Fibrous Histiocytoma
  • ❖ Leiomyosarcoma
  • ❖ Rhabdomyosarcoma
  • ❖ Chondrosarcoma
  • ❖ Haemangiosarcoma
  • ❖ Lymphangiosarcoma
  • ❖ Synovial Sarcoma
  • ❖ Malignant Peripheral Nerve Sheath Tumour
  • ❖ Kaposi's Sarcoma
 
SARCOMA
Sarcomas can arise from bone or soft tissue. Osteosarcoma is the commonest of all sarcomas. Soft tissue sarcoma (STS) which is arising from mesenchyma is the one which will be discussed in this chapter. STS are aggressive tumours which needs multimodality therapeutic approach.
Sarcoma occurs in younger age group compared to carcinoma with fish fleshy gross look with haemorrhage and necrosis. It shows rapid growth, with tendency to show early blood spread. Lymphatic spread is rare even though few sarcomas can spread through lymphatics along with blood spread. Blood spread commonly occurs to lung but liver, skin, brain can also get involved.
Soft tissue is the tissue that connect, surround and support the skeletal system which is non-epithelial, extra-skeletal tissue excluding reticuloendothelial system, glial tissue but it also includes peripheral nervous tissue by convention. Embryologically it is mainly from mesoderm but few from neuroectoderm.
STS are named based on their tissue which it resembles. Liposarcoma—fat; fibrosaroma—fibroblast; malignant fibrous histiocytoma—mesenchyma/histiocytes; leiomyosarcoma—smooth muscle; rhabdomyosarcoma—skeletal muscle; chondrosarcoma—chondroblast; angiosarcoma—blood vessels.
 
Features
  • Sarcomas are much lesser in incidence compared to carcinomas.
  • It occurs in younger age group compared to carcinomas.
  • They can arise from bone (osteosarcoma) or from any soft tissues (soft tissue sarcomas) (Mesenchymal tissue).
  • They are much more aggressive compared to carcinomas.
  • They are rapidly growing tumours with fleshy appearance.
  • They are not encapsulated but often are having pseudocapsule.
  • They spread through blood especially to lungs often also to other organs.
  • Lymphatic spread is not common with certain exceptions.
  • Main method of treatment is surgery, i.e. wide excision, amputation.
  • In inoperable cases debulking is the accepted method of treatment.
  • Chemotherapy is the adjuvant therapy.
  • Commonest sarcoma of bone is osteosarcoma
Note:
Commonest malignancy of bone is secondaries.
  • Commonest soft tissue sarcoma is liposarcoma / malignant fibrous histiocytoma (MFH – 25%) overall; in the extremities both MFH and liposarcoma; in the retroperitoneum it is liposarcoma.
  • Commonest visceral (GIT) sarcoma is leiomyosarcoma.
  • In genitourinary system leiomyosarcoma is commonest in adults and rhabdomyosarcoma in paediatric age group; in uterus leiomyosarcoma; in myocardium angiosarcoma; in hand and foot synovial sarcoma; in skin Kaposi's sarcoma; in head and neck region angiosarcoma.
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Fig. 1.556: Soft tissue sarcoma foot. Note the vascularity.
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Fig. 1.557: Osteosarcoma of the upper end of humerus in an adolescent boy.
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Fig. 1.558: Osteosarcoma upper tibia. Note the size of the tumour and ulceration. It is very vascular.
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Figs 1.559A and B: X-ray pictures of osteosarcoma in tibia and femur.
Note:
  • Many liposarcomas arise at sites devoid of adipose tissue. Most rhabdomyosarcomas arise in locations that lack voluntary muscle.
  • 40% of soft tissue sarcomas are more than 10 cm in size at the time of presentation; 30% are 5-10 cm and 30% are less than 5 cm.
 
Incidence of STS
In adults
  • MFH and liposarcoma—35–45%.
  • Rhabdomyosarcoma—10%.
  • Leiomyosarcoma—9–15%.
  • Synovial sarcoma—7%.
  • Malignant peripheral nerve sheath tumour (MPNST)—6%.
  • Fibrosarcoma—5%.
In children
  • Rhabdomyosarcoma, neuroblastoma are common tumours.
 
Clinical Features of Soft Tissue Sarcoma
  • Painless swelling of short duration with progressive increase in size—soft tissue mass. Thirty percent of patients may present as pain during first evaluation.
  • Compression of adjacent structures
  • Smooth, firm/hard, warm and vascular
  • Features of secondaries in lung—cough, haemoptysis and chest pain. Lung is the commonest site of secondary.
  • Secondaries in liver as a principal site especially in visceral STS.
  • There are no reliable findings to distinguish benign from malignant swellings.
  • One has to maintain a high index of suspicion in any soft tissue mass deep-to-deep fascia, any soft tissue mass > 5 cm, any new enlarging or symptomatic soft tissue mass.
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Figs 1.560A and B: Soft tissue sarcoma upper chest wall. Note the vascularity and extent.
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Investigations
 
Tissue diagnosis
  • Incision biopsy is the most reliable method of diagnosis. It provides adequate tissue sample.
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Fig. 1.561: Incision for biopsy in STS should be longitudinal so that it can be included in future surgical wide excision. Never place transverse incision for biopsy.
  • Trucut biopsy/core needle biopsy is an acceptable first diagnostic step as it is technically easier, not costly, with fewer complications. But it is not useful in visceral STS. Again if it is inadequate one should not be hesitant to go for incision biopsy at the earliest. It is done using 14 gauge needle; often US / CT guide is used.
  • Excision biopsy is done only if the tumor size is < 3 cm which is cutaneous or subcutaneous wherein wide local re-excision is possible. Otherwise excision biopsy should be avoided as it may contaminate the tumour bed and restricts the therapeutic options.
Note:
FNAC is of less value in STS. It is significant only if it positive. It is useful in local or distant recurrences in documented sarcoma patients, or to evaluate nodal status if enlarged. CT guided FNAC is useful for retroperitoneal/intra-abdominal sarcomas.
 
Assessment of the extent of tumour
Imaging in STS provides a 3–dimensional extent of the tumour and helps in accurate planning of surgical procedure. But it does not reliably distinguish between a benign and malignant process. It assesses macroscopic and not microscopic extent of the disease. Imaging is essential for metastatic work up.
  • MRI is the investigation of choice as it determines the vascularity, relation to vessel and fascial planes (extent and invasion). Advantages of MRI are—imaging of choice in STS, excellent soft tissue delineation, without radiation, multiplanar imaging possible. Images of skip metastases are possible. Disadvantages of MRI are—cost, bone involvement is poorly delineated, claustrophobia, not possible in presence of metal implants and pacemakers.
  • CT scan also can be used to see the extent and invasion but not equivalent to MRI. CT scan helps in identifying presence and extent of the soft tissue mass, status of the adjacent structures, with mandatory contrast enhancement isodense masses, vasculature are better delineated. SPECT—3 dimensional reconstruction feasible. Advantages of CT are—easy availability, relatively cost effective, best to demonstrate bony involvement, useful for guided biopsies. Disadvantages of CT are—cross-sectional imaging, ionizing radiation, inferior soft tissue detail.
  • US is less sensitive investigation. It is useful in extremity lesions to assess vascular system. It is initial/first investigation done in GI leiomyosarcoma/retroperitoneal sarcoma. It is useful for serial studies, guided trucut biopsy.
    zoom view
    Fig. 1.562: MRI of STS leg.
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    zoom view
    Fig. 1.563: MRI picture of the soft tissue tumour thigh encasing vessels partially and eroding the bone. Patient needed high level, above-knee amputation.
    zoom view
    Fig. 1.564: CT picture of retroperitoneal leiomyosarcoma.
  • X-ray of part is not necessary; it is only used in initial phases to differentiate STS from bony lesion.
  • Angiogram is traditionally used to delineate adjacent vasculature. It is upstaged by CECT/MRA. It is not necessary to do regularly in all cases but when there is a need for accurate assessment of vasculature it is ideal. It is used in intra-arterial chemotherapy for unresectable tumours.
  • CT abdomen is better in GI/retroperitoneal sarcomas.
 
Evaluation of Metastatic Disease
  • Chest X-ray is done to look for secondaries.
  • CT chest is ideal to see early lung secondaries. It is done in all deep seated, high grade and tumour more than 5 cm in size.
  • US abdomen is sufficient to check liver secondaries. But CT abdomen may be better choice. Often CT pelvis is also added.
  • PET scan or Integrated PET scan (with CT) is often useful to identify metastatic diseases.
 
Other Investigations
  • Radionuclide scintigraphy (Gallium-67).
  • -p-MRS (p-Magnetic Resonance Spectroscopy) and FDG (Fluor-2-Deoxy Glucose) PET are done to assess the metabolic activity of tumour.
  • Immunohistochemistry and FISH (fluorescence in situ hybridization).
  • Tumour markers.
  • Haematocrit, peripheral smear, ESR, serum alkaline phosphatase, serum creatinine.
 
Staging
Staging of the soft tissue tumour is done depending on the tumour size, nodal status, metastasis and histological grading of the tumour (GTNM staging).
TNM staging of soft tissue sarcoma
Grade (G)
Tumour (T)
Gx Cannot be assessed
Tx Cannot be assessed
G1 Well-differentiated
T0 No primary
G2 Moderately differentiated
T1 Size < 5 cm or 5 cm (maximum dimension)
G3 Poorly differentiated
T1a: Superficial
T1b: Deep tumour
G4—is now not used
T2 Size > 5 cm
G is assessed by differentiation; mitoses; necrosis through scores
T2a: Superficial
T2b: Deep tumour
Regional lymph nodes (N)
Distant spread (M)
Nx Nodes cannot be assessed
Mx Cannot be assessed
N0 No nodes
M0 No distant spread
N1 Nodes present
M1 Distant spread present
Note: Superficial tumour is outside the superficial fascia. Deep tumour is deep to superficial fascia or any tumour invading the superficial fascia.
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Note:
  • STS is an aggressive, invasive, destructive growth with high recurrence and distant metastases rate. Tumour shows fish flesh cut appearance.
  • Basis used for classification of STS—STS being highly heterogeneous group of tumour is classified based on adult tissue it resembles; i.e the type of tissue formed rather than from the type of origin.
  • Grade is the single most important factor in staging. It denotes the “biological aggressiveness” of the sarcoma. It predicts the likelihood of metastases.
  • Nodal metastases are rare in STS (3%). It has the poor prognosis.
  • M1 is – Distant metastases.
 
Treatment
 
Principles of treatment
  • Surgery is the main treatment modality. Amputation rate for STS has come down drastically from 50% in 1960 to 5% at present. It is also because of proper adjuvant radiotherapy following function/limb sparing complete excision, application of microvascular surgeries. Neoadjuvant chemotherapy, perioperative/postoperative RT also play a major role.
  • In low grade tumour without any spread—functional/limb sparing complete wide excision is sufficient without any adjuvant therapy. If microscopic margin is positive for tumour then postoperative External Beam RT (EBRT) is given.
  • In high grade tumour <5 cm size, function sparing wide excision with more than 1 cm clearance margin is sufficient. If clearance margin is less than 1 cm or shows microscopic positive margin, then perioperative brachytherapy OR postoperative EBRT is given.
  • In high grade tumour which is between 5–10 cm size, function/limb sparing complete wide excision with perioperative brachytherapy OR postoperative EBRT is given.
  • In high grade tumour more than 10 cm in size, initially neoadjuvant chemotherapy; then functional/limb sparing complete wide excision with postoperative brachytherapy and EBRT should be given.
  • All limbs should be conserved if possible but with curative intent.
 
Surgery
Enneking classification of surgical procedures
  • Intralesional excision—done inside pseudocapsule very high recurrence 100%—not used.
  • Marginal excision—en bloc resections through the reactive zone—high recurrence rate 70%
  • Wide excision means en bloc resection done through normal tissues beyond the reactive zone; it means if the margin is less than 5 cm; tumour is never visualised during surgery; it has local recurrence rate of 30%. Wide margin is classified as adequate if margin is at least beyond 1cm outside the reactive zone or inadequate if margin is within 1 cm.
  • Radical excision—if the margin is more than 5 cm outside the reactive zone. It is like compartment excision with very low recurrence rate.
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Fig. 1.565: Different surgical approaches for STS.
Other procedures
  • Compartmental excision; function/limb sparing.
  • Vascular resections with vascular reconstruction.
  • Amputation.
Note:
Limb sparing; function preserving; margin free wide excision—is the new trend.
A thin barrier is considered to be a 2 cm thickness of normal tissue; a thick barrier is 3 cm thickness; and joint cartilage is said to be equivalent to a 5 cm thickness margin. A surgical margin that is outside a barrier, with normal tissue between the barrier and the reactive zone of the tumour, is considered to be curative.
  • Wide local excision with clearance of 2 cm (minimum need is 1 cm) or more with preservation of function is needed. Depth clearance is also important. 3–5 cm clearance even though was practiced in olden days, is not necessary (Figs 1.583A to E).
  • Compartment resection is a radical limb saving procedure. Here muscle group of one compartment (anterior, posterior or medial) is resected entirely from its origin to insertion with the tumour. It is done only when tumour is intracompartmental. It is not suitable when tumour is extracompartmental or many compartments are involved or encased to major neurovascular bundle.
    Basis for compartmental excision is—STS rarely penetrate anatomical barriers unless it is very advanced.
  • Amputation is done in large tumours of upper or lower limbs.
    • Radical amputation is done as disease has not spread systemically which should be confirmed by CT chest, abdomen and pelvis. In metastatic disease there is no need to do amputation as long-term survival is not possible except if primary is fungating and distressing.
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Figs 1.566A to E: Surgical approach to a deep-seated sarcoma in leg—deep to gastrocnemius and soleus.
Tumor site
Level of amputation
Foot
Below knee
Leg
Above knee
Thigh-middle and lower third
Hip disarticulation
Thigh proximal third
Hemipelvectomy
Buttock
Hemipelvectomy
Hand and wrist
Below elbow
Forearm
Above elbow
Distal arm and elbow
Shoulder disarticulation
Axilla and shoulder girdle
Forequarter amputation
  • Debulking surgery is useful in large advanced tumours like retroperitoneal sarcomas.
 
Radiotherapy
  • Preoperative radiotherapy followed by wide excision—neoadjuvant RT.
  • Postoperative radiotherapy is commonly used because of less tumour burden and less wound problems. Titanium clips are placed during surgery at high-risk areas to identify the site to concentrate proper RT.
    • Brachytherapy is very effective in local control of the tumour. Initially precise mapping of the area is done in the operation theatre. Loading catheters are placed in surgical field peroperatively. Later these catheters are loaded with iridium 192. Dose is 45 Gy to tunbour bed for 6 days.
    • Permanent radioactive sources can also be placed to the area.
    • Postoperative external beam radiotherapy (EBRT)—it is quiet effective and used in high grade tumour more than 5 cm often with brachytherapy. Dose is 70 Gy-25 fractions.
  • Palliative external radiotherapy can be given to prevent bleeding, fungation and to reduce pain in advanced cases. It is also used in secondaries in brain, bone.
  • Primary radiotherapy alone (radical) is of less beneficial in soft tissue sarcoma, but now it is used with more favorable results.
 
Chemotherapy
  • Chemotherapy drugsVAC (Vincristine, Adriamycin, Cyclophosphamide) are commonly used. Other drugs ifosfamide, dacarbazine are used in combination with above drugs. Mesna is used as a protection for haemorrhagic cystitis. Chemotherapy is used when tumour is more than 5 cm or high grade.
  • Usually postoperative chemotherapy is given. MAID regime is used especially in recurrent STS. Mesna, Adriamycin, Ifosfamide, Dacarbazine drugs (MAID regime) are used. Its response rate is 50%. But survival benefit is controversial.
  • Neoadjuvant chemotherapy is used to make the primary tumour better operable. It makes eventual surgery better; provides early treatment for micrometastasis; gives idea about the response for chemotherapy. Drugs used are adriamycin and ifosfamide.
  • Isolated limb perfusion using cytotoxic drugs and tumour necrosis factor with hyperthermia is also often used.
  • Chemoradiation is a good alternate adjuvant therapy used.
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Distant Spread
  • Pulmonary metastasis can be treated with wedge resection, segmentectomy, lobectomy, pneumonectomy. Surgery is done only when primary is well-controlled. Radiotherapy and chemotherapy are also tried. More than three number metastases in lung signify poor prognosis.
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Figs 1.567A and B: Recurrent chest wall tumour, could be secondaries, as patient was earlier amputated for soft tissue tumour hand (forearm amputation). X-ray of the same patient shows large tumour mass.
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Figs 1.568A and B: Recurrent soft tissue sarcoma over scapular region and forearm in two different patients. Old surgical scar is seen.
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Fig. 1.569: Recurrent soft tissue tumour thigh. Note the scar of old surgery.
 
LIPOSARCOMA
  • It is the commonest type of soft tissue sarcoma arising from the fat cells (of primitive mesenchymal cells).
  • Lipoma as a precursor tumour for liposarcoma which was thought earlier is disproved/not accepted now.
  • It is 20% of all soft tissue sarcomas.
 
Common Sites
  1. Thigh—commonest site.
  2. Retroperitoneum.
  3. Back.
  4. Shoulder.
 
Types
  1. Well-differentiated—common between 50–70 years age group; common in extremities (75%); metastasis is rare.
  2. Dedifferentiated—common between 50–70 years age group; common in retroperitoneum (75%); metastasis is high.
  3. Myxoid—common at 25- 45 years age; common in extremities (75%); high rate of metastasis.
  4. Round cell type—common at 25–45 years age; common in extremities (75%); high rate of metastasis.
  5. Pleomorphic (5%)—poor prognosis.
 
Features
  • Microscopically, it contains lipoblasts with ‘signet ring’ malignant cells. It is low grade type:
    • Spread is to lungs.
    • Treatment is wide excision or radiotherapy with surgical debulking in places where complete removal of tumour is not possible like in retroperitoneal liposarcoma.
 
FIBROSARCOMA (11%)
  • It can arise from the bone or from soft tissues.
  • It is common between 30-55 years; common in deep soft tissues of lower extremities with intact overlying skin.
  • It is arising from fibroblasts. Intramuscular and inter-muscular fibrous tissue, fascial envelops, aponeurosis and tendons are common origin.
  • Commonest site is thigh.
  • Spindle fibroblasts with ‘herring bone’ pattern are typical on microscopy.
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zoom view
Figs 1.570A to C: (A) Recurrent dermatofibrosarcoma protuberans, (B) Malignant dermatofibrosarcoma left side of the chest wall, (C) Dermatofibrosarcoma.
 
Types
  1. Well-differentiated.
  2. Poorly differentiated.
  3. Dermatofibrosarcoma protuberans. It is common in trunk. DFSP is an intermediate grade fibrohistiocytic tumor with nodular cutaneous mass; common in adult male; common in trunk and proximal extremities having slow growth without deep muscle invasion. Skin is taut, nodular and commonly ulcerated.
  4. Aggressive fibromatoses are variant of fibrosarcoma which are locally malignant in which desmoid tumour is also included.
 
Features
  • Fibrosarcoma is slow growing tumour which attains large size.
  • Clinically, it is smooth, hard, warm, localised tumour.
  • It compresses or infiltrates the adjacent structures like neurovascular bundle.
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MALIGNANT FIBROUS HISTIOCYTOMA (MFH)
  • It is group of malignant soft tissue tumours with a fibrohistiocytic appearance.
  • MFH is one of the most common STS in adult (18–20%).
  • 70% occur in skeletal muscles.
  • Lower extremity is the common site.
  • It presents as solitary, multilobular lesion.
  • It spreads along the fascial planes or between muscle fibres which is the probable reason for local recurrence.
  • Myxoid/giant cell/inflammatory/angiomatoid/pleomorphic are the types. It is common in adults and elderly.
zoom view
Fig. 1.571: Large soft tissue tumour over gluteal region with ulceration and vascularity. It was confirmed as malignant fibrous histiocytoma. Patient was successfully operated.
 
LEIOMYOSARCOMA
  • It arises from smooth muscle. Cut section shows whorled appearance.
  • It constitutes (10–17%) of STS; common after 60 years.
  • Two third occurs in women.
  • It is undetermined grade—aggressive.
  • It is common in retroperitoneum and viscera, but can occur in limbs and skin. Uterus is also common site.
  • Recurrence is common. It has got poor prognosis.
  • It can occur in the piloerector muscle of skin; inferior vena cava; pulmonary artery.
  • Desmin and actin are the most common immunohistochemical stains.
 
RHABDOMYOSARCOMA
  • It arises from striated muscle.
  • It is common in head and neck, upper thigh and arm.
  • It is commonest sarcoma in children.
  • It can occur in retroperitoneum, pelvis and genitourinary tract.
  • It is common in males.
 
Types
  • Pleomorphic—msot common type of rhabdomyosarcoma. It is common in adult, aggressive with poor prognosis.
  • Embryonal—common in infants and children—is seen in viscera like urinary bladder.
  • Botryoidal—slow growing polypoidal—respond well to chemotherapy and radiotherapy.
  • Alveolar—chromosomal translocation is common.
 
Feature
  • It is more aggressive tumour with poorer prognosis (High grade).
  • It also metastasises to lymph nodes.
 
CHONDROSARCOMA
  • It arises from chondroblasts.
  • It attains large size with slow growing nature.
  • Common sites are ribs, flat bones.
zoom view
Figs 1.572A and B: Chondrosarcoma leg lateral aspect. X-ray shows calcified tumour. It was successfully removed as limb salvage procedure.
 
HAEMANGIOSARCOMA
  • It originates from blood vessel endothelium.
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Fig. 1.573: Angiosarcoma.
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Types
  • Malignant haemangioendothelioma.
  • Malignant haemangiopericytoma.
 
LYMPHANGIOSARCOMA
  • It arises from lymph vessel endothelium.
  • It commonly occurs after radical lymph node dissection Stewart-Treves syndrome.
 
SYNOVIAL SARCOMA (7%)
zoom view
Fig. 1.574: Synovial sarcoma.
  • It is the 4th commonest type. It occurs 15–40 years of age.
  • Origin need not be from synovium.
  • 85–90% occurs in lower limb; head, neck and shoulder are the next common site.
  • It is common in thigh, leg, shoulder, hand and foot.
  • Occasionally it can occur in the abdominal wall and retroperitoneum.
  • It is common in young individuals.
  • It occurs adjacent to joint but uncommon to involve the synovial sheath of the joint.
  • It spreads both through blood as well as through lymph nodes (20%).
  • It is very aggressive soft tissue sarcoma (High grade).
  • Calcification with or without ossification is common—10%.
  • Synovial sarcoma may be biphasic or monophasic.
  • It possess specific chromosomal translocation (96–100%) – t(X; 18)(p11.2; q11.2).
 
MALIGNANT PERIPHERAL NERVE SHEATH TUMOUR (MPNST) (3%)
  • It arises from peripheral nerves.
  • It shows differentiation along nerve elements.
  • MPNST replaced older terms—malignant schwannoma, neurofibrosarcoma, neurogenic sarcoma, malignant neurilemmoma.
  • 20–50% arises from neurofibromatosis type 1 (latent period 15–20 years). MPNST is an exception to sarcoma will not arise from benign precursor.
  • Common sites are major/proximal nerve trunks.
 
KAPOSI'S SARCOMA
  • It is malignant blood vessel tumour of multicentric origin arising from vascular smooth muscle or pericytes.
  • It is seen commonly in HIV patients due to immunosuppression.
  • Primary tumour commonly occurs in skin, mucous membrane, lymph nodes or viscera.
  • It is linked with Human Herpes Virus 8 (HHV8) as causative agent.
 
Types
  1. European Kaposi‘s sarcoma: It is common in old age. It is first described by Kaposi in 1862. It mainly involves skin especially lower extremity. Visceral involvement is rare.
  2. African Kaposi‘s sarcoma: It occurs commonly in children and young individual. It involves skin and lymph nodes commonly. It resembles lymphoma.
  3. Transplant associated Kaposi‘s sarcoma: It is due to drug- induced immunosuppression. It involves mainly skin and often regresses once immunosuppression is discontinued.
  4. AIDS associated Kaposi‘s sarcoma: It occurs in 30–40% of AIDS patients. It is common in homosexuals. It has got wide, disseminated involvement with metastases. It is very aggressive. It is often associated with lymphoma and other malignancies.
Note:
Kaposi's sarcoma is not found in transfusion related AIDS.
 
Clinical Features
  • Multiple reddish-blue nodules in the skin with ulceration over the nodule.
  • Lymph node enlargement.
  • Koebner phenomenon is common in areas of trauma.
  • Differential diagnosis:
    • Lymphomas.
    • Cutaneous angiomatoses.
    • Mycobacterial infection of skin.
  • Investigations:
    • Biopsy from the skin lesion.
    • Tests for HIV infection.
  • Treatment:
    • Irradiation.
    • Chemotherapy. Drugs used are adriamycin, bleomycin and vinblastine.
    • Antiretroviral therapy.
    • Interferons.
T. Amputations
“Amputation is one of the meanest yet one of the greatest operations in surgery, i.e. mean—when resorted to where better may be done. Great—as the only step to give comfort and prolong life.”
—Sir William Ferguson
CHAPTER OUTLINE
  • ❖ Amputation
  • ❖ Complications of Amputations
  • ❖ Prosthesis312
 
AMPUTATION
 
Indications
  • Gangrene due to atherosclerosis, embolism, TAO, diabetes, ergots.
  • Trauma: To save life in crush injuries.
  • Neoplasms: Osteosarcomas, Marjolin's ulcer, melanomas.
  • Gas gangrene.
  • Severe sepsis.
  • Occasionally severe elephantiasis, madura foot, when all other methods have failed to help.
  • Dead, dying, devitalised tissues.
  • Severe deformity congenital or acquired.
 
Types
It can be:
  • Non-end bearing/side bearing—Weight is taken up by the joint.
  • End bearing/cone bearing—Weight is taken up by the body.
It can be:
  • Weight bearing.
  • Non-weight bearing.
It can be:
  • Provisional amputation with flap—later final formal amputation my be required.
  • Guillotine amputation which always requires revision formal amputation.
  • Formal amputation—is definitive one.
 
Types of flaps
  • Long posterior flap in below-knee amputation.
  • Equal flaps in above-knee amputation.
 
Ideal Stump
  • Should heal adequately by 1st intention.
  • Should have rounded, gentle contour, with adequate muscle padding.
  • Should have sufficient length to bear prosthesis.
    • For B-K 7.5 (minimum) to 12.5 cm from tibial tuberosity
    • For above and below elbow 20 cm stump.
    • For A-K 23 cm from greater trochanter.
zoom view
Figs 1.575A and B: Different levels of amputation in upper limb and lower limb.
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Fig. 1.576: Little toe amputation for gangrene. Wound has healed well.
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Fig. 1.577: Forefoot amputation.
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Fig. 1.578: Above-knee amputation done for osteosarcoma of the upper end of the tibia. Here equal flaps are used.
  • Should have thin scar which does not interfere with prosthetic function.
  • Should have adequate adjacent joint movement.
  • Should have adequate blood supply.
  • Scar should be in a place where it is not exposed to pressure.
  • Scar should be freely mobile over underlying tissues. Skin and scar should be freely mobile over the underlying bone. It is achieved only if deep fascia is closed properly. Scar and skin should be free to achieve free movement of the prosthesis. Socket of prosthesis with mobile skin creates a piston to bone to move like a joint.
  • Skin should not be infolded.
  • Redundant soft tissue should not be there.
  • Stump should be free from tenderness and conical.
 
Evaluation of the Patients who need Amputation
  • Haematocrit, control of anaemia by transfusing blood/packed cells.
  • Control of infection using antibiotics.
  • Decision of level of amputation by skin temperature, arterial Doppler.
  • Informed consent should be taken.
  • Plan for prosthesis and rehabilitation by physiotherapist and rehabilitation team.
 
Principles in Amputation
  • Adequate blood supply of the flap should be maintained.
  • Proper marking of the skin incision is essential.
  • Tourniquet should not be used if amputation is done for vascular diseases.
  • Proximal part of the flap contains muscle component but distal part should contain only skin and deep fascia.
  • Flap length should be adequate; not short. It should be ideally semicircular not rectangular to get a conical stump.
  • Nerve should be pulled down and cut using a sharp knife and allowed to retract into the soft tissue otherwise neuromas may develop.
  • In crush injury/entrapment injury/sepsis—guillotine amputation is done. Later skin is pulled down by using skin traction, eventually to have better skin coverage.
  • Bone should be cut with beveling and all sharp margins should be rounded.
  • 314Postoperatively regular dressings are done. Patient is mobilised using axillary crutches. After 3 months, once scar has matured and stump has become supple, proper prosthesis is fit. Berlamont first started immediate postoperative fitting of prosthesis to leg for early mobilisation. Plaster pylon is applied to the stump and a prosthetic extension is fit to facilitate partial weight bearing immediately after surgery. It has got more stump complications and so it has not become popular.
    zoom view
    Fig. 1.579: Pylon is plaster cast with walking component used for immediate mobilisation after below-knee amputation.
  • Stumps can be side bearing (sutures are on the side); end bearing/conical (sutures are on the end) or cylindrical.
  • Postoperatively active exercise should be given to the proximal joint so that prosthesis can be fit to it properly.
  • If there is sepsis especially in gangrene limb, flaps should be left open or loosely sutured otherwise flap necrosis occurs.
  • Proper anatomy of muscles and neurovascular bundle around should be known in all amputations.
 
Different Amputations
  • Ray amputation Amputation of toe with head of metatarsal or metacarpals.
  • Transmetatarsal amputation (Gillies')
    Here amputation is done proximal to the neck of the metatarsals, distal to the base.
  • Lisfranc‘s amputation (Tarsometatarsal amputation)
    Here tarsometatarsal joint is disarticulated with a long volar flap. It needs a surgical boot. But there is inevitable development of equinovarus deformity. So stabilisation of midtarsal and ankle joints is needed. In Hey's modification, 2nd metatarsal is cut at base instead of disarticulation.
  • Chopart‘s amputation (Midtarsal amputation)
    Here talonavicular joint and calcaneo-cuboid joints are disarticulated. Tibialis anterior muscle is sutured to drilled talus bone. A long volar flap is used and immobilised for 6 weeks after surgery.
  • Syme's amputation
    • It is removal of the foot with calcaneum and cutting of tibia and fibula just above the ankle joint with retaining heel flap (dividing both malleoli). Heel flap is supplied by medial and lateral calcaneal vessels (branches of posterior tibial artery). Elephant boot is used for the limb after Syme's which is inexpensive. Many patients walk well with Syme's stump without difficulty. It is presently mainly used in trauma (crush injury) and malignancies in distal part of the foot. In vascular diseases, calcaneal vessels may not be adequate to maintain the viability of the flap. While raising the flap, knife should be very close to the calcaneum so as to avoid injury to calcaneal vessels and to maintain the viability of the flap.
    • In Wagner's method deep fascia of heel is sutured to drill holes made on the anterior edge of tibia and fibula. Above-knee cast is essential.
    • Advantages are—it is an end-bearing stump having good proprioception. Patient can walk without prosthesis. Low energy consumption ambulation is possible.
    • Disadvantages—posterior displacement of heel pad; poor cosmesis.
    • Boyd's amputation—anterior part of the calcaneum is excised (osteotomy) just distal to the peroneal tuberosity and calcaneotibial arthrodesis is created. It is done to prevent posterior migration of heel pad.
zoom view
Fig. 1.580: Different levels of amputation in lower limb.
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Fig. 1.581: Ray amputation for toes—racquet incision.
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Fig. 1.582: Ray's amputation done for gangrene of great toe. It is usually not sutured.
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Fig. 1.583: Forefoot amputation.
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Fig. 1.584: Syme's incision and level of amputation.
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Fig. 1.585: Incision for Syme's amputation.
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Fig. 1.586: Elephant boot used after Syme's amputation.
  • Modified Syme‘s amputation
    Here heel flap is elliptical. Tibia and fibula are divided slightly higher. But variation here is the elliptical flap.
    zoom view
    Fig. 1.587: Modified Syme's incision is elliptical one.
  • 316Pirogoff‘s amputation
    It is like Syme's amputation except posterior part of the calcaneum is retained along with heel flap. It provides longer stump than Syme's amputation.
    zoom view
    Fig. 1.588: Pirogoff's amputation.
  • Below-knee amputation
    Here we use a long-posterior flap with scar placed over anterior aspect is used. Prosthesis placement is better here with greater range of movements without limp and without support. It is also called as Burgess amputation. Fibula should be divided first, higher than the proposed site of cut of tibia otherwise its sharp end will press on the skin flap. Tibial stump should be beveled anteriorly. Posterior muscles are sutured across the bone end, to the periosteum in front. In more proximal type of below-knee amputation, fibula often is removed to allow the proper use of flap. Length of the flap should be 11/2 times the circumference of the site (around 12 cm). Stump length is 14–17 cm from knee joint. Minimum length required for prosthesis is 8 cm. If need to extend more proximally, it is better to do above-knee amputation. Modern artificial limbs like suction socket prosthesis are used now.
    zoom view
    Fig. 1.589: Below-knee amputation technique—incision, flap and levels of cutting bones.
    zoom view
    Fig. 1.590: Below-knee amputation—long posterior flap. Note the placing of the drain.
    zoom view
    Fig. 1.591: Below-knee amputation flap necrosis has occurred which eventually granulated with repeated dressings. Area is ready for skin grafting.
    zoom view
    Fig. 1.592: Bilateral below-knee amputations done for vascular causes with diabetes.
  • 317‘Peg-leg’ amputation
    • It is amputation 5 cm below the knee level – proximal most below-knee amputation. It is not practiced nowadays. Here anterior flap is rotated posteriorly like a hood and patient kneels and bears weight which is well-accustomed to pressure. It is done whenever prosthesis cannot be used probably due to economic causes (in developing countries).
    zoom view
    Fig. 1.593: ‘Peg-leg’ amputation is below-knee amputation done close to the knee joint (5 cm stump) with folding flap and metallic support down. It is not used now.
  • Transcondylar-Gritti-Stokes amputation with long posterior flap.
    • Femur is divided just above the articular surface and patella is anchored to the divided femur. There is risk of nonunion between patella and femur. This procedure is no longer performed.
  • Above-knee amputation
    • Usually equal anterior and posterior flaps are used. Lower third and middle third level amputations are done. Ideally the required length of the femur as stump is 25 cm from the tip of the trochanter. Femur length lesser than 10 cm is not possible and here one needs to do hip disarticulation. In children as growing epiphysis of femur is in lower end, it is essential to preserve as much length of femur as possible. It is done in ischaemia, trauma, sepsis, gangrene which is spreading above. often patient might earlier have undergone below-knee amputation but now as indicated need above-knee amputation. It is usually contraindicated in children (done only in undue definitive indication) or if stump is less than 7.5 cm.
    • Advantages are technically easy, healing chances are better and faster. Disadvantages are cosmetically poor, rehabilitation is difficult, and fitting of prosthesis is not proper, patient needs a third support for walk with often a limp.
    zoom view
    Fig. 1.594: Above-knee amputation, incision and approach.
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    Fig. 1.595: Above-knee amputation wound which is infected in a diabetic patient.
  • Hip disarticulation
    It is done whenever it is not possible to save the minimum 10 cm length of the femur. Incision used is either single posterior flap—Solcum's approach (better) or anterior racquet incision—Boyd's approach.
  • Hind quarter amputation
    Inter-innominate abdominal amputation (Sir Gordon Taylor's amputation): Removal of one side pelvis with innominate bone, pubis, muscles and vessels. Original ligation of common iliac artery is modified to individual ligations of external and internal iliac vessels. Internal iliac artery is ligated beyond the origin of the superior gluteal artery to keep the large posterior flap viable. Now hind quarter name is replaced by hemipelvectomy. It may be standard hemipelvectomy with classic gluteal flap; extended hemipelvectomy with removal of posterior part of the sacrum; conservative hemipelvectomy with retaining part of the pubis, ilium bones on that side. Internal hemipelvectomy is new method wherein hemipelvectomy is done with preserving the limb.
    318
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    Fig. 1.596: Hindquarter amputation done for run over of vehicle over pelvis, right thigh. Patient also underwent colostomy. Patient survived with severe morbidity.
  • Krukenberg's amputation
    Done in upper limb following any trauma. Here forearm amputation is done in such a way that it creates a gap between radius and ulna like a claw to have a hold or grip.
  • Interscapulothoracic amputation (Forequarter amputation) (Littlewood's posterior approach or Berger's anterior approach):
    zoom view
    Figs 1.597A and B: (A) Forequarter amputation done for electric burn which caused extensive damage to upper limb, (B) Forequarter amputation done for sarcoma proximal to shoulder joint.
    It is removal of entire upper limb with scapula and lateral 2/3rd of the clavicle and muscles attached to it. It is done in malignancies involving scapula, upper part of humerus and near shoulder joint.
  • In emergency conditions like severe sepsis, gas gangrene and machinery entrapment, Guillotine amputation is done without suturing. Suturing is done at later period. All tissues are divided at same level.
    zoom view
    Fig. 1.598: Upper limb Guillotine amputation—above elbow done for trauma induced gas gangrene.
 
Postoperative Period
  • Physiotherapy is advised.
  • Regular dressings are done.
  • Crutch is used initially, after 3 months prosthesis is placed.
  • Rehabilitation is important.
    zoom view
    Fig. 1.599: Patient with axillary crutches.
 
COMPLICATIONS OF AMPUTATIONS
 
Early
Haemorrhage, haematoma, infection.
319
 
Late
Pain, ulceration of stump, ring sequestrum formation, flap necrosis, painful scar, Phantom limb—feeling of amputated part in toto or partially with pain over it.
 
Haematoma
It is identified by pain, swelling over the stump underneath the flap. It is aspirated using a wide bore needle. Haematoma may delay healing; may precipitate infection or flap necrosis due to pressure. After aspiration, pressure dressing is needed. If haematoma reforms after 2–3 aspirations, it should be drained by opening the wound on one corner and inserting haemostat into the wound.
 
Infection of the Stump
It may cause abscess formation, delay in wound healing, flap necrosis, giving way of the wound. Removing few or all sutures to relieve pressure and draining the pus underneath is needed. Infection may also lead into poor scar, adherent scar which causes difficulty in placing the prosthesis.
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Fig. 1.600: Above-knee amputation stump having small sinus.
 
Flap necrosis
It is a common complication. Main causes for flap necrosis are poor blood supply, infection, haematoma underneath, inadequate length of the flap causing stretching of flap. Small area of necrosis can be excised. Wider area needs laying opening of the wound or revision of the stump or higher level amputation. Anaemia, poor nutrition, nutritional deficiencies, diabetes mellitus, immunosuppression, smoking, old age are other factors causing flap necrosis.
 
Stump neuroma
It can occur due to proliferation of the nerve fibrils beyond the point of nerve division and is usually due to failure of cutting of the nerve more proximal to the level of division of the bone. It causes pain and tenderness over the stump. It is usually relieved by analgesics, re-assurance and prosthesis. Occasionally, it may require re-exploration of the wound, excision of end neuroma and also cutting nerve more proximally.
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Figs 1.601A and B: (A) Below-knee amputation stump infected. (B) tibia is exposed.
 
Stump Pain after Amputation
It is a common problem. Causes are—infection, poor blood supply, causalgia, stump neuroma, phantom pain/limb, deep vein thrombosis, adherent scar, formation of spurs and osteophytes at amputated bone end. Scar adhesion to bone is prevented by keeping adequate length of deep fascia underneath intact. Spurs and osteophytes are confirmed by X-ray and needs removal using bone nibbler after appropriate skin incision.
 
Phantom Limb
It is typical awareness of sensation that as if amputated part is still present partly or in toto; often such part may be painful or disturbing or hyperaesthetic. Exact cause is not known; but it is probably due to presence of severe pain at the amputated part just prior to amputation making brain area for that part in alert situation causing phantom limb. Reassurance, prosthesis, analgesics help to control the condition. It is said that it can be prevented by proper pain control for 24 hours prior to amputation; but it is often difficult. It is common in upper limb.
 
Ulceration over the Stump
320It is not uncommon. It is due to necrosis, infection, lengthy bone stump pressing on the summit of the flap, prosthesis, nutritional deficiencies, diabetes mellitus, ischaemia. Ulcer may be small/large; superficial/deep. Callous chronic ulcer at the end of the stump is called as Douglas ulcer. Small ulcer is later treated by regular dressings and suturing. Large ulcer needs flap to cover the defect. Osteomyelitis of the stump should be ruled out in chronic stump ulcer. Ring sequestrum may be typical in such situation. Revision amputation is needed for the stump.
 
Contracture of the Joint
Contracture of the joint proximal to the amputated stump is common. It is mainly due improper positioning after amputation due to pain, poor exercise and occasionally due to inflammation of surrounding soft tissues. Contracture interferes with proper fitting and functioning of the prosthesis and delays rehabilitation. Proper positioning, passive stretching and exercises, strengthening exercises with help to correct it. Rarely needs surgical release of the contracture.
 
Other Complications
  • Scar hypertrophy, skin thickening, hyperkeratosis, papilloma, eczema, lymphoedema, boils, bursae over bony point can occur which are treated accordingly.
  • Spur, osteophyte formation, causalgia, jactitation of the stump, stump aneurysm, stump fracture— are other complications.
 
PROSTHESIS
It is the substitution to a part of the body to achieve its optimum function.
(Orthroses are supplement for limb function.)
 
In Lower Limb
  • Syme's amputation: Elephant boot, Canadian Syme's prosthesis.
  • Below-knee amputation: Patellar-tendon bearing (PTB) prosthesis and solid ankle cushion heel (SACH).
  • Above-knee amputation: Suction type prosthesis. It is placed above the stump. It is better and well-tolerated.
  • Nonsuction type prosthesis: It is placed at the ends. It requires additional support.
  • Hind-quarter amputation: Tilting table prosthesis (TTP) or Canadian prosthesis is used here.
  • Patellar tendon-bearing prosthesis (PTB prosthesis): Here all the weight bearing is done below knee; movement is controlled by his own knee joint. Patellar tendon is the main key weight-bearing area within the socket; stump posteriorly up to the popliteal fossa is also important to provide counter pressure so that patellar tendon is kept in place. Medial and lateral paratibial areas and medial condylar flare also bear significant weight. Head of the fibula, tibial tubercle, cut ends of tibia and fibula are pressure intolerant areas. Socket should have proper relief areas to these intolerant parts.
  • Computer-assisted designing and computer-assisted manufacturing (CAD – CAM) socket is an automated processing method which fulfills all above criteria accurately with modifications. It is more comfortable and is made up of thermoplastic or laminated plastic with closed cell polyethylene foam.
  • Suspension for below knee amputation prosthesis is leather cuff strap above femoral condyles. Exo- or endoskeleton is used. For athletics endoskeleton is preferable.
  • SACH (Solid Ankle Cushion Heel) foot is used. It is multiaxial, optimizes gait, and facilitates walking on rough ground. It needs minimal maintenance. It is preferred in old people. Energy storing foot is often used wherein ankle joint is replaced by a plastic spring.
 
In Upper Limb
  1. Above-elbow prosthesis is a high technology prosthesis. It is sophisticated device with harness, socket, elbow joint unit, control cable, forearm and wrist device.
  2. Below-elbow prosthesis.
    Krukenberg's amputation does not require any prosthesis.
 
Advantages of Prosthesis
  • Cosmetic.
  • Function of the part relatively can be got.
  • Ambulation in lower limb prosthesis.
 
Disadvantages
  • Infection.
  • Pressure ulcers.
  • Joint disability.
 
Prosthesis Types
  • Exoskeletal prosthesis.
  • Endoskeletal prosthesis with modular system.
    Internal prostheses are one used inside. They are placed by open surgery. They are nonreactive, long-durable materials, e.g. hip prosthesis in total hip replacement.
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Figs 1.602A to C: Below-knee amputee with prosthesis. It gives good range of movements, normal walk and comfort.
321U. Reconstruction
CHAPTER OUTLINE
  • ❖ Graft
  • ❖ Skin Grafts
  • ❖ Flaps
  • ❖ Tendon
  • ❖ Tendon Repair
  • ❖ Tendon Transfer
  • ❖ Tendon Graft
 
GRAFT
Graft: It is transfer of tissue from one area to other without its blood supply or nerve supply.
Autograft: It is tissue transferred from one location to another on the same patient.
Isograft: It is tissue transfer between two genetically identical individuals, i.e. between two identical twins.
Allograft: It is tissue transfer between two genetically different members, e.g. kidney transplantation (Human to human) (Homograft).
Xenograft: It is tissue transfer from a donor of one species to a recipient of another species (Heterograft).
 
SKIN GRAFTS
Skin Grafting: It is transfer of skin from one area (donor area) to the required defective area (recipient area). It is an autograft.
 
Types
  1. PARTIAL THICKNESS GRAFT
    (Split-thickness skin graft—SSG)
    Also called as Thiersch graft, is removal of full epidermis + part of the dermis from the donor area.
    It may be:
    • Thin SSG.
    • Intermediate SSG, all depends on the amount of thickness of dermis taken.
    • Thick SSG.
 
Contraindications
SSG can not be done over bone, tendon, cartilage, joint.
 
Technique
  • Donor area: Commonly thigh, occasionally arm, leg, forearm.
  • Knife used is Humby's knife.
  • Blade is Eschmann blade, Down's blade.
  • Using Humby's knife graft is taken, punctate bleeding is observed which says that proper graft has been obtained.
  • Donor area is dressed and dressing is opened after 10 days, not earlier.
  • Recipient area is scraped well and the graft is placed after making window cuts in the graft to prevent the development of seroma. Graft is fixed and tie-over dressing is placed. If graft is placed near the joint, then the part is immobilised to prevent friction which may separate the graft. On 5th day, dressing is opened and observed for graft take up. Mercuro chrome is applied over the recipient margin to promote epithelialisation.
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Figs 1.603A and B: Split skin grafting knife and set; and harvesting.
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Fig. 1.604: Commonest donor area for spilt skin grafting is thigh.
 
Stages of Graft Intake
  1. Stage of plasmatic imbibition: Thin, uniform, layer of plasma forms between recipient bed and graft.
  2. Stage of inosculation: Linking of host and graft which is temporary.
  3. Stage of neovascularisation: New capillaries proliferate into graft from the recipient bed which attains circulation later.
Note:
Graft is stored at low temperature of 4°C for not more than 21 days.
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Figs 1.605A to D:
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Figs 1.605A to E: Technique of split skin grafting.
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Fig. 1.606: Skin stapler can be used to fix the SSG to the margin of the recipient bed.
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Fig. 1.607: Humby's knife with Eschmann blade.
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Fig. 1.608: Harvesting a skin graft.
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Figs 1.609A and B: Donor area of split skin graft in the thigh and graft placed over raw area in the leg.
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Figs 1.610A to C: Mesher used in split skin grafting to increase its surface area to cover wider area like burns wound. A large defect can be covered by this. It can cause expansion of skin up to six times.
324
 
Disadvantages of SSG
  • Contracture of graft. Two types:
    1. Primary contracture means SSG contracts significantly once graft is taken from donor area (20–30%). Thicker the graft more the primary contracture.
    2. Secondary contracture occurs after graft has taken up to recipient bed during healing period, due to fibrosis. Thinner the graft more the secondary contracture.
  • Seroma and haematoma formation will prevent graft take up.
  • Infection.
  • Loss of hair growth, blunting of sensation.
  • Dry, scaling of skin due to nonfunctioning of sebaceous glands. So after healing, oil (coconut oil) should be applied over the area.
  • Graft failure.
 
Advantages
  • Technically easier.
  • Wide area of recipient can be covered. To cover large area like burns wound, graft size is increased by passing the graft through a Mesher which gives multiple openings to the graft, which can be stretched on the wider area like a net. It can cause expansion up to 6 times.
    zoom view
    Figs 1.611A to C: Mesh graft placed over donor area and photo of it, once it takes up.
  • Graft take up is better.
  • Donor area heals on its own.
Note:
Mercurochrome/merbromin once used as a local applicant to the edge of the grafted area (SSG) and small raw areas to promote epithelialisation. It is applied once a day. But it is no longer used now.
  1. FULL THICKNESS GRAFT (Wolfe graft)
    • It includes both epidermis + full dermis.
    • It is used over the face, eyelid, hands, fingers and over the joints.
    • It is removed using scalpel blade. Underlying fat should be cleared off properly. Deeper raw donor area is closed by primary suturing. If large area of graft is taken, then that donor area has to be covered with SSG which is a disadvantage in full thickness graft.
 
Advantages
  • Colour match is good. Especially for face.
  • No contracture (unlike in SSG).
  • Sensation, functions of sebaceous glands, hair follicles are retained better compared to SSG.
  • Functional and cosmetic results are better.
 
Disadvantages
  • It can be used only for small areas.
  • Wider donor area has to be covered with SSG to close the defect.
 
FLAPS
It is transfer of donor tissue with its blood supply to the recipient area.
 
Parts of Flaps
Base, pedicle, tip of flap. Vasculature is usually through the pedicle in the centre of the flap. Tip is the place where often flap goes for necrosis.
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Figs 1.612A and B: (A) Traumatic exposure of the bone. Flap is needed to cover this defect. It could be cross leg flap or rotation flap. Skin grafting is not possible in this situation, (B) Flap which has taken up well-placed over the defect on the bone with osteomyelitis.
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Figs 1.613A and B: (A) Hand-held Doppler to hear audible signal of perforator to do rotation flap in the leg, (B) Different methods of immobilisation is needed for flap and SSG. Fixation is often used in limbs.
 
Types
  1. Random pattern flaps: Here vascular basis is subdermal plexus of blood vessels. No known blood vessel is supplying it. Rectangular flap with length to width ratios 1 : 1 or less than 1.5 : 1.
  2. Axial pattern flaps: Here superficial vascular pedicles pass along their long axes, e.g. forehead flap, deltopectoral flap, groin flap. Anatomically a known blood vessel is supplying it. It is long lengthy flap.
    zoom view
    Fig. 1.614: Anatomy and blood supply of a skin flap.
Anatomical types depending on the types of tissue in the flap:
  1. Cutaneous flap: Forehead flap, deltopectoral flap.
  2. Fasciocutaneous flap: Radial forearm flap, scapular flap, lateral arm flap, groin flap.
    zoom view
    Fig. 1.615: Groin flap is based on superficial circumflex iliac artery. It can be used in defects in hand and forearm. It is a cutaneous flap.
  3. Muscle flap: Gluteus maximus muscle flap, gracilis flap, tensor fascia lata muscle flap.
  4. Myocutaneous flap: Pectoralis major myocutaneous flap, latissimus dorsi flap—composite flap.
  5. Osteomyocutaneous flaps: Radius with brachioradialis and skin, rib with intercostal muscles and skin—composite flap.
  6. Local rotation flaps, transposition flaps: When the flap moves laterally it is called as transposition flap. When the flap rotates laterally towards defect it is called as rotation flap. Transposition flap is squarely designed which moves laterally to close the defect creating a larger area on its original place which has to be covered with split skin graft.
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Fig. 1.616: Rotation flap. It is commonly used in gluteal region in managing bedsores.
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Fig. 1.617: Pectoralis major myocutaneous flap.
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Figs 1.618A and B: Transposition flap.
  1. Z’ plasty: It is a procedure which involves transposition of two interdigitating triangular flaps. There is change in direction as well as gain in length of the common limb of Z. Angle size and length of the limb are the most important factors. It is used in managing contracted scars, facial scars, Dupuytren's contracture and to cover the excised defects like pilonidal sinus (example). There should be transverse skin slack available equal to the length between the axes of Z. It can be single or multiple Z plasty. Complications are flap necrosis near the angle tip, infection, failure.
  2. Free flaps: Vascular pedicle of the flap, both artery and vein are anastomosed to recipient vessels using operating binocular microscopes.
  3. Omental flaps.
  4. Island flap: Localised flap is swung around a stalk from the donor area to the recipient area often with the pedicle buried underneath the skin bridge in between. Pedicled flap is also an island flap.
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Fig. 1.619: Technique of ‘Z’ plasty. It is used in contracture release. Dupuytren's contracture and pilonidal sinus.
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Fig. 1.620: Rhomboid flap
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Fig. 1.621: Technique of V-Y plasty and Y-V plasty.
Note:
  • Flaps mobilised from donor area with its pedicle is placed and sutured to recipient area. Once flap takes up usually in 3–6 weeks, base of the flap is cut and sutured to recipient area.
  • 327Saltatory flap is mobilising the flaps in stages from distant donor area towards recipient area. It requires many staged surgeries and long-term hospitalisation.
  • Waltzing is a technique wherein flap is moved from donor area and attached adjacent to the recipient defect area. Later in 2nd stage, it is moved towards the defect formally. It reduces the tension on the flap and increases the success rate.
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Fig. 1.622: Bilobed flap is used in lesions of the nose commonly.
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Fig. 1.623: Advancement flaps, used in distal defects.
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Fig. 1.624: On table marking of glabellar flap to place after excising a lesion in the root of the nose.
  • Positioning of the patient for long time is important to have a good flap take up which is a real discomfort to the patient.
  • Delaying of the flap after mobilisation is done to reorient its blood supply so as to decrease flap necrosis and increase flap survival. Delaying period is 10–14 days. Flap is raised properly as required and resutured to same place so as to allow the formation of reorientation of vasculature near the tip of the flap. This delayed flap is raised again in 10-14 days to place in required area.
 
Different Flaps Used are:
Forehead flap
  • It is fasciocutaneous flap from forehead based on anterior branch of superficial temporal artery. Superficial temporal artery is terminal smaller branch of external carotid artery. It begins under the parotid behind the neck of mandible, runs vertically upwards, crossing the root of zygoma at preauricular point; 5 cm above the zygoma it divides into anterior and posterior branches. Anterior branch anastomoses with supraorbital and supratrochlear branches of ophthalmic artery. Artery supplies scalp of temple region and side, parotid, ear, facial muscles. Superficial temporal artery gives transverse facial artery which runs from anterior margin of parotid, and middle temporal artery which runs deep to temporalis muscle.
  • It is used for defects in cheek (carcinoma, cancrum oris) and nasal reconstruction.
  • Standard forehead flap is taken from forehead above the level of eyebrow starting from the opposite side of the midline with base just above the zygoma. Width of the flap is usually about 3–4 cm. Flap is dissected from the distal end of the marked area going deep up to epicranium, raising the flaps using scissor dissection. Flap is held up using skin hooks. Flap is rotated towards the defect area in the cheek. Inner area of the flap is covered with split skin graft. Donor flap area is covered with another split skin graft. After 3 weeks, base of the flap is disconnected; remaining proximal part of the flap can be replaced into forehead donor area. SSG over donor flap area takes up well. This flap often can be rotated under (deep to) the zygoma also.
  • 328A lined forehead flap can be used. After flap elevation, under surface of the flap is lined by split skin graft prior to rotation. This grafted lined flap is resutured into the donor area for 2 weeks until undersurface of graft takes up well; after 2 weeks flap is rotated towards the defect area (cheek).
    zoom view
    Fig. 1.625: Saltatory flap. Flap raised from the abdomen is reached to the cheek in stages—from abdomen to wrist; from wrist to cheek.
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    Fig. 1.626: Waltzing of flap.
  • Delaying of the flap is often done in forehead flap. Flap after elevation, is replaced into the original position to have optimum vascular reorientation; after 2 weeks it is again rotated towards defect. Delayed flap reduces the flap necrosis chances.
  • Often bipedicled forehead flap (Narayanan's flap) is used taking both from anterior and posterior branches of the superficial temporal artery. This flap is moved to defect in cheek with anterior branch part staying outside and posterior part will line the mucosal area.
  • A different type—middle forehead flap is used for nasal reconstruction.
    zoom view
    Figs 1.627A and B: Forehead flap based on superficial temporal artery. It is fasciocutaneous flap.
  • 329Problems—Poor color match, contraction of flap and donor area is cosmetically nonacceptable.
Deltopectoral cutaneous flap (Bakamjian flap)
  • It is based on first three perforating branches of the internal mammary artery (mainly 2nd perforator). Flap runs horizontally across the chest wall anteriorly towards shoulder tip from its base over the sternal border. Its upper border is along the line of the clavicle; its lower border is along the line of anterior axillary fold line. Raw area often requires a spilt skin grafting. It is usually rotated upwards often with waltzing. It is tubed and attached above. Tube is drained to prevent any collection to occur.
    zoom view
    Fig. 1.628: Deltopectoral cutaneous flap.
  • Rotation angle is important to prevent any kinking in the pedicle. It is usually used to cover the defects in cheek, chin, mastoid and parotid region. Often flap is delayed to get adequate length.
Groin flap
  • It is based on superficial circumflex iliac artery which is 2–3 cm below and parallel to the inguinal ligament. Artery originates from femoral artery over medial border of the sartorius and ends at anterior superior iliac spine. 1:1 rectangular flap with deep fascia is used. Secondary defect can usually be closed with sutures. It is used mainly for defects in wrist/forearm where positioning is easier.
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Fig. 1.629A and B: Groin flap used for burns defect in the hand.
Latissimus dorsi muscle/myocutaneous flap
It is based on thoracodorsal artery, a branch of subscapular artery. Skin over the upper and anterior border of latissimus dorsi is used for transfer. It is commonly used to cover the defect after mastectomy. But it does not give the bulk. It is technically easier. It can be used as muscle flap also. It helps as skin cover. Prosthesis is needed to place underneath to provide bulk in post-mastectomy defect.
Pectoralis major myocutaneous flap (PMMF)
It is based on the pectoral branches of thoracoacromial artery. Usually skin below and medial to nipple over the muscle is used. Muscle pedicle is made as broad as skin. It is used to cover the defect over the cheek/neck/pharynx/intraoral lesions after wide excision with removal of skin over the tumour. Vessel marking is 2 cm medial to coracoid process, obliquely below the clavicle at the junction between middle third and outer third. Skin with muscle is dissected from the deeper structures like ribs, intercostal muscles and pectoralis minor. Flap is raised upwards up to the coracoid. Lateral pectoral vessels if possible are retained, otherwise can be sacrificed. Defect below is usually closed primarily with sutures. Often it needs spilt skin grafting. Pectoralis major flap can be used along with deltopectoral flap with proper planning.
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Figs 1.630A and B: Pectoralis major myocutaneous flap used for carcinoma cheek.
Gastrocnemius muscle flap
It is either medial or lateral and is commonly used to cover the upper part of the tibia and knee joint. It is technically easier and functional deficit occurring at donor area is insignificant. It is rarely used as myocutaneous flap.
Transverse rectus abdominis muscle flap (TRAM flap)
330It is either superior pedicle based on the superior epigastric vessels or inferior pedicle based on the inferior epigastric vessels. Superior pedicle based flap is used to cover postmastectomy area or chest wall defect. To cover post mastectomy area opposite side superior pedicle is used to reduce the arc through which flap has to rotate (but rotating from opposite side is technically difficult). Inferior pedicle flap is used to cover the defects in groin and thigh. Proper marking of the flap is essential. Skin incision is made like an ellipse. Anterior rectus sheath is cut in the line of incision and is raised upwards carefully of the rectus muscle up to the xiphisternum. Muscle is gently separated of the posterior rectus sheath with care not to injure the epigastric vessels. Once dissection is complete lower part of the muscle is cut in superior pedicle to rotate upwards carefully. In the upper part again anterior rectus sheath is opened to pass the flap towards the defect in subcutaneous plane. TRAM flap gives bulk and contour to the defect. But it is technically difficult. Usually opposite side of the defect is taken as flap as it is easier to rotate from opposite side. Defect in the abdomen usually needs mesh to support and close. It is not possible to do this flap in obese individuals and if patient has undergone laparotomy earlier (with a lengthy scar). Inferior cut end of the inferior epigastric artery in superior pedicle flap can be anastomosed to a vessel in recipient bed to improve the perfusion (supercharging). Inferior epigastric artery in inferior pedicle can be additionally perfused using opposite inferior epigastric artery (recharging).
Radial forearm flap
It is perfused from the radial vessels and raised on the flexor aspect of the forearm. Perforating branches of these vessels supply deep fascia and skin over it. Flap can be fasciocutaneous or osteofasciocutaneous/osteomyofasciocutaneous if radial bone is also used as part of the flap. Radial forearm free flap is commonly used for mandible defects. It is technically easier and safer. Flap is raised along with skin, segment of the radius along its intermuscular septum through which vessels pass and brachioradialis as components. Care is taken in dissecting vessels of the bed and not to injure the radial nerve. In free flap artery is sutured to the recipient artery like facial artery using microscope. Other similar flaps are—ulnar forearm flap, scapular flaps, and vascularised fibular transfer.
Limberg flap
It is a type of rhomboid flap used in pilonidal sinus with base at gluteal skin.
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Figs 1.631A to C: Rhomboid flap used to cover the defect after excising a lesion in the arm.
Cross leg flap
It is commonly used to cover the defect in the foot/leg from opposite leg.
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Figs 1.632A and B: Cross leg flap.
 
TENDON
  • Tendon is the continuity of the muscle to have its action at the site especially in hand, foot and digits.
  • It is covered by synovial sheath with a thin layer of fluid in between which allows smooth gliding of the tendon.
Tendon after injury heals by:
  1. Intrinsic healing method occurs through synovial fluid when tendon is not under stress.
  2. Extrinsic healing method occurs through proliferation of fibroblasts across epitenon. It occurs when tendon is under stress. It forms a mass of fibrous tissue at the site called as “tenoma”. It may interfere with the proper gliding of the tendon.
  • Tendon injuries may be cut wound, lacerations, injury associated with nerve or vessel injury.
331
 
TENDON REPAIR
  1. Primary repair is done within 24 hours.
  2. Delayed repair within a week after 24 hours.
  3. Secondary repair anytime after one week.
 
Types of Suturing the Tendon
  1. Kessler method. Here knot comes in the cut part of the tendon.
  2. Goldner method. Here knot comes away from the cut ends of the tendon.
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Fig. 1.633: Types of tendon suturing.
Complications of tendon suturing are infection, adhesion, stiffness and failure.
 
TENDON TRANSFER
  • It is the transfer of one tendon from its existing site to another site where its function is required to have a function required at the newer site.
  • Function of the transferred tendon should be maintained by other tendons.
  • Tendon should be able to acquire the function at the newer site properly.
  • For example, in ulnar claw hand, the tendon of flexor digitorum superficialis (FDS) (of index finger) is transferred to lumbrical canal of the digits to have flexion at MCP joint and extension of proximal IP joint.
 
TENDON GRAFT
  • When tendon suturing or transfer is not possible because of inadequate length, tendon of a muscle which is not of much help functionally, is taken as a graft to obtain required length.
Problems in tendon graft: Infection, adhesions, graft failure, stiffness of the part.
332V. Transplantation
CHAPTER OUTLINE
  • ❖ Preoperative Evaluation
  • ❖ Organ Procurement
  • ❖ Graft Rejection
  • ❖ Renal Transplantation
  • ❖ Immunosuppressive Agents
  • ❖ Liver Transplantation
  • ❖ Bone Marrow Transplantation
  • ❖ Pancreatic Transplantation
  • ❖ Small Bowel Transplantation
  • ❖ Dialysis
  • ❖ Cimino Fistula
 
PREOPERATIVE EVALUATION
  • General evaluation: Pulmonary, cardiac, GIT, renal status and cancer screening.
  • Immunologic evaluation: Serology for hepatitis, HIV, cytomegalovirus.
  • Placing the organ in the same position is called as orthotopic transplantation, e.g. liver.
  • Placing the organ in new position is called as heterotopic transplantation.
 
Donor Criteria
  1. Cadaver donor
    • Individuals with severe brain injury resulting in brain death.
      Brain death is defined as “complete irreversible cessation of all brain functions”.
Other criteria for cadaver donor:
  • Normothermic patient.
  • No respiratory effort by the patient.
  • Brain—dead donor.
  • The heart is still beating.
  • No depressant drugs intake should be there while evaluating the patient.
  • Individual should not have any sepsis, cancer (except brain tumour).
  • Not a HIV or hepatitis individual.
  1. Living donor
    • Living unrelated donor.
    • Living related donor.
    • Individual should have normal health.
 
Requirements
  • ABO typing.
  • Serology tests.
  • Angiogram.
  • Intravenous urography.
  • HLA typing.
 
Human Leucocyte Antigens (HLA)
They are cell surface molecules which are highly antigenic. They play main role in graft rejection and hence called as major histocompatibility complex/antigens MHC) (Dausset, 1958). Class I are located in nucleated cells. Class II are located in dendritic cells/macrophages/B cells, etc.
 
ORGAN PROCUREMENT
 
Principles of Organ Procurement
  • 333Once brain death has been confirmed in cadaver donor, after giving inotropic support drugs (T3 and argipressin) various organs are surgically removed carefully with preservation of their vessels. After removal, organs are flushed with chilled preservative solution (in specific organ procurement like of kidney, in situ perfusion of organs (kidneys) is done by placing double balloon catheter into the abdominal aorta and a balloon catheter into the femoral vein) and placed in sterile bags containing saline and organ preservative solutions which are then immersed in 0–4°C box containing ice. Donor specimens are transported to the site of the recipient centre. Wisconsin and Euro-Collins solutions are commonly used.
  • Non-heart beating donors (NHBD)—here organs are procured from individuals who are just dead on arrival to the hospital or who have died in the hospital in spite of resuscitation. Category I—Dead on arrival; Category II—Unsuccessful resuscitation; Category III—‘Awaiting cardiac arrest’ after support withdrawal; Category IV—Cardiac arrest with brain death.
  • University of Wisconsin solution contains—potassium lactobionate; sodium phosphate; magnesium sulphate; adenosine; allopurinol; glutathione; raffi-nose; hydroxyethyl starch; insulin; dexamethasone; potassium; sodium; with 320 mosmol/l osmolality and pH of 7.4.
  • Living donor's organs are used commonly in kidney transplantation from genetically related individuals. It can be used from genetically unrelated donors after proper MHC match. Donor nephrectomy is done through loin incision (commonly from left side). Laparoscopic donor nephrectomy has become popular and safe.
 
Technique of Organ Procurement
  • Positioning the donor on the operating table: Supine position, with arms abducted on boards and legs laid flat and uncrossed. The neck is extended by placing a sandbag under the shoulders (as during thyroidectomy).
  • Midline sternotomy incision is used extending up to the pubic symphysis with a supraumbilical horizontal part. Abdomen and thorax are exposed properly. Retroperitoneal right sided mobilisation is done (Cattel-Braasch manoeuvre). Cannulation of inferior mesenteric vein is done. Aortic cannulation is done. Perfusion of preservative solution is done.
  • Sequence of the thoracic organ procurement: First the heart (care must be taken to leave enough supradiaphragmatic IVC for both organs such as the liver and the heart); then the lungs separately or together are procured. Cooling of the abdominal organ has to be continued until the last thoracic organ is procured.
  • Sequence of abdominal organ procurement: The small bowel is the most sensitive organ for ischaemia; therefore, it is retrieved first. The second organ to be procured is the pancreas followed by the liver. Liver and the pancreas could also be retrieved en block and split on the back table. Finally, the kidneys are the last organs to be procured.
  • The most popular tool kit comprises the iliac vessels, which consists of common, external and internal artery and the vein.
 
Organ Packing in Steps (Eurotransplant or National Transplant Organisation)
The first bag is filled with a cold preservative solution. The procured organ must be completely covered by the preservative solution, and the bag must be closed (well tied) without any air. The second bag or a wax-impregnated fibre container is filled with cooled saline or Ringer lactate solution. The first tied bag must be completely covered in one of the solutions and closed (well tied) without air. Third bag dry, without air, well tied and sometimes covered with a sterile drape is also used. Finally the organ is placed in an icebox and well covered with nonsterile melting ice, the box is firmly closed to make the organ ready for transportation.
zoom view
Fig. 1.634: Incision for organ procurement.
 
GRAFT REJECTION (TRANSPLANT REJECTION)
Host immune system rejects the transplanted organ, recognizing it as foreign body. Immunosuppressive drugs are used to suppress immune response to promote graft take up. In humans, the MHC is called the human leucocyte antigen (HLA) system and is located on the short arm of chromosome 6. The immune response to a transplanted organ consists of both cellular (lymphocyte mediated) and humoral (antibody mediated) mechanisms. The T cells (CD4, CD8 T cells) are central in the rejection of grafts. The rejection reaction consists of the sensitization stage and the effector stage. Initial nonimmuonologic ischaemic injury which increases T cell antigen which through MHC initiates macrophage mediated delayed hypersensitivity and also helps B cells to produce antibodies. Cytokines, natural killer cells, apoptosis also play in graft rejection.
 
Types of Rejections
  1. Hyperacute rejection: The transplanted tissue is rejected within minutes to hours because vascularization is rapidly destroyed. Hyperacute rejection is humorally mediated as the recipient has preexisting antibodies against the graft, which can be induced by prior blood transfusions, multiple pregnancies, prior transplantation. The antigen-antibody complexes activate the complement system, causing massive thrombosis in the capillaries, which prevents the vascularization of the graft. The kidney is most susceptible to hyperacute rejection; the liver is relatively resistant.
  2. 334Acute rejection: It occurs within 6 months of transplantation.
    • Acute cellular rejection is mediated by recipient lymphocytes against donor antigen.
    • Humoral rejection occurs due to presence of low level donor specific antibodies or preformed antibodies.
  3. Chronic rejection: Chronic rejection develops months to years after acute rejection episodes have subsided. Chronic rejections are both antibody- and cell-mediated. The use of immunosuppressive drugs and tissue-typing has increased the survival in the first year, but chronic rejection is not prevented in most cases. Chronic rejection appears as fibrosis and scarring in all transplanted organs. In liver transplants, chronic rejection is characterized by the vanishing bile duct syndrome. In kidney recipients, chronic rejection (chronic allograft nephropathy) manifests as fibrosis and glomerulopathy. It is due to previous acute rejection, hypertension, improper immunosuppression, reperfusion injury, long cold ischaemic time, post-transplant infection.
 
Treatment
  • Assessment and monitoring: It is done by clinical examination; organ-specific assessment (urine output, urine analysis, creatinine estimation, US abdomen, graft kidney biopsy in kidney; liver function tests, liver biopsy); blood parameter estimation.
  • Immunosuppression: Cyclosporine, tacrolimus, sirolimus, azathioprine, mycophenolate mofetil, antilymphocytic globulin, basiliximab, daclizumab, steroids, monoclonal antibodies are used at different regimes, combinations and doses. Complications are—infection; development of carcinoma, lymphoma; hirsuitism, alopecia, hypertension, nephrotoxicity, neurotoxicity.
 
IMMUNOSUPPRESSIVE AGENTS
 
Induction Therapy
  • It is used immediately after transplantation (up to 3 weeks).
  • Antilymphocytic globulin (ALG)—human lymphocytes are injected into rabbit/horse to develop antisera—ALG. It acts against T cells. It inhibits cell mediated immunity, allograft rejection, graft versus host reaction. It is used in transplantation of kidney, pancreas, heart, small bowel. Anaphylaxis, anaemia, thrombocytopenia, allergy (serum sickness) are the reactions. Rabbit serum is better than horse serum in terms of preventing the graft rejection (acute). Rabbit serum has antibodies against CD2,3,48,11a,18,25; HLADR, HLA class I.
  • Monoclonal antibody—OKT3 (1975 by Kohler, Milstein – got Nobel prize) is developed by hybridoma technique, is a monoclonal antibody which acts/blocks at TCR complex (T cell receptor complex CD3) affecting the function of native T cell and cell-mediated immunity. Within 60 minutes of IV injection of OKT3 it blocks T cell function removing the circulating T cells. Problem with OKT3 is its immune reactions. So often it is combined with steroid or indomethacin. It can cause acute cytokine release syndrome.
  • Interleukin 2 receptor (IL2 R) inhibitors—α chain of IL 2 R is related to activated T cells. Basiliximab (chimeric) and daclizumab (human) are two anti-CD25 monoclonal antibodies which bind with α chain of IL 2R. These drugs are well tolerated through a peripheral IV line; stops acute rejection; with less risk of infection and malignancy. It does not cause serum sickness or cytokine release syndrome. But all alone its effects are inadequate and so it should be used only in concomitant with other immunosuppressants.
  • Rituximab is an anti-CD20 monoclonal antibody as a depleting agent on B cell. It is used to control humoral mediated rejections. It is used in heart transplantation.
  • Alemtuzumab—an anti-CD52 human monoclonal antibody which is expressed in B cell, T cell, monocyte, macrophage. It causes prolonged lymphocyte depletion for 6 months. It is used along with tacrolimus in kidney transplantation. Steroid can be spared while using his. This drug is also used in lymphoma, multiple sclerosis and rheumatoid arthritis.
  • IVIG (intravenous immunoglobulin) derived from pooled plasma neutralises the circulating autoantibodies, blocks the T cell cytokines, lymphocyte proliferation and apoptosis.
 
Maintenance Therapy
All transplant patients require maintenance therapy for prolonged period. Different drugs are used. Steroid and azathioprine are old drugs commonly used.
  • Prednisolone:
    • It inhibits cytokines, binding of IL 2 to receptors, blocks macrophage migration, and inhibits delayed hypersensitivity reaction. But it causes Cushing's syndrome, hypertension, peptic ulcer, cataract, diabetes, osteoporosis, muscle wasting. Often methyprednisolone may be used.
  • Antiproliferating agents:
    • they inhibit differentiation and division of lymphocytes by blocking the purine, pyrimidine and folic acid metabolism as a structural analogue.
    • Azathioprine is a purine analogue containing 6 mercaptopurine with a labile sulfhydryl chain. Conversion of inosine nucleotide to adenosine and guanosine is blocked. Drug inhibits both humoral and cell-mediated immunity. Toxic effects are—bone marrow suppression, hepatotoxicity.
    • Mycophenolate mofetil (MMF): It inhibits inosine monophosphate dehydrogenase of purine metabolism blocking lymphocyte proliferation. Dose is 2 g/day. It is now more commonly used than azathioprine. Diarrhoea and bone marrow suppression are the side effects.
    • Leflunomide: It blocks pyrimidine synthesis in lymphocytes by inhibiting dihydroorotate enzyme. This drug is used in rheumatoid arthritis. FK 778 is its analogue which is under trial in renal transplant.
  • T cell directed immunosuppressants:
    • Cyclosporine (Borel, 1972) is extracted from fungus tolypocladium inflatum. It is selective inhibitor of TCR mediated activation suppressing T cells. It inhibits formation of mature CD4 and CD8 T cells in thymus. It contains 11 amino acids with molecular weight 1202. It is a very good immunosuppressant. But it does not cause myelosuppression. It is metabolised in the liver by cytochrome P-450. Side/toxic effects are—nephrotoxicity, hypertension, hirsuitism, gingival hyperplasia, hyperkalaemia, neurotoxicity, tremor, hepatotoxicity, risk if infection (CMV, Candida, pneumocystis carinii, secondary infections) and malignancy (lymphoma, skin and CNS). IV dose given initially is 4 mg/kg in 500 ml of saline; later changed to oral therapy as 12 mg/kg daily; after few weeks dose is tapered to 5 mg/kg/day. Regular serum cyclosporine estimation twice weekly with estimation of haematocrit, blood urea and serum creatinine is needed.
    • 335Tacrolimus (FK 506, 1984, Japan) is derived from fungus streptomyces tsukubaensis. It is macrocyclic lactone (MW 822) causes similar effect like cyclosporine. Drug binds with intracellular binding protein immunophilin forming complexes which block the phosphatase activity of calcineurium so that inhibits IL 2 production. It is used in liver transplant, in acute rejection of kidney. Side effects are similar as cyclosporine but will not cause hirsuitism and gingival hypertrophy. It causes alopecia and diabetes.
    • Sirolimus (rapamycin) is a macrolide antibiotic which inhibits signal transduction from IL2 R to nucleus. It inhibits allograft rejection. It is used along with other immunosuppressants like cyclosporine. It causes anaemia, thrombocytopenia and proteinuria. Nephrotoxicity is less with sirolimus.
  • Costimulation blockage agent like belatacept which is a fusion protein of extracellular part of CTLA4. It s a good immunosuppressant used monthly or bimonthly.
 
Risks Related to Immunosuppression
They are mainly infection and malignancy. Individual drug- related toxicity also can occur.
 
Infection
  • Opportunistic infections are common with immunosuppression. Cytomegalovirus (CMV) infection is common causing pneumonia, hepatitis, pancreatitis, GI problems. Pneumocystis carinii infection is also common.
  • Trimethoprim, sulfamethoxazole, acyclocvir, ganciclovir, valganciclovir, clotrimazole, pneumococcal vaccine, hepatitis B vaccine, pentamidine nebulizer are different drugs used to prevent sepsis.
  • BK virus associated nephropathy is controlled by cidofovir, IV immunoglobulin.
 
Malignancy
  • Malignancy potentiality increases by 10 times.
  • Skin cancers and carcinoma cervix are common.
  • Virus-mediated tumours like carcinoma cervix (HPV); hepatoma (Hepatitis B and C); Kaposi's sarcoma (herpes virus 8); lymphoma (EBV) are common. EBV related lymphoma is post-transplant lymphoproliferative disorder (PTLDs). Rituximab, anti-CD20 monoclonal antibody reduces B cells is effective in these patients. Hyper CMS IG is used as prophylaxis in high-risk groups.
 
RENAL TRANSPLANTATION
 
The Criteria for an Ideal Deceased Kidney Donor
  • Normal renal function.
  • Without hypertension requiring treatment; without diabetes mellitus.
  • No malignancy other than a primary brain tumour or treated superficial skin cancer.
  • No generalised viral or bacterial infection.
  • Acceptable urinalysis; age between 6 and 50 years.
  • Negative assays for syphilis, hepatitis, HIV, and human T-lymphoproliferative virus.
Three types of donors:
  1. Living related donors.
  2. Living nonrelated donors.
  3. Cadaver donors.
    Highest chances of success in any transplant (renal) is seen when the donor is the identical twin.
    Compatibility should be checked by tissue typing, i.e. ABO blood group system and major histocompatibility complex.
Evaluation of living donor:
  • Tissue typing, ABO, MHC typing.
  • Renal function—blood urea, serum creatinine.
    zoom view
    Fig. 1.635: Renal transplantation.
    zoom view
    Fig. 1.636: Another method of getting arterial perfusion of the transplanted kidney by suturing (Carrel stitch) external iliac artery to renal artery side-to-end.
    If there were no obstacles, there would have been no achievements.
  • 336IVP.
  • Selective renal angiogram. Single vessel is better.
  • HIV/hepatitis evaluation.
Usually left kidney is taken for transplantation because of long left renal vein. It is placed in right iliac fossa with ureter connected to the urinary bladder; renal artery to internal iliac artery (end-to-end); renal vein to external iliac vein (end-to-side). Renal artery (end) to external iliac artery (side) through Carrel stitch is also used for arterial continuity.
 
Technique
Before the removal of kidney, the donor receives IV mannitol to prevent kidney ischaemia, diuretics and IV heparin. After removal of donor kidney, protamine sulphate is given to the donor. Removed donor kidney is perfused with cold perfusion fluid at 4°C and cold intravascular electrolytes. Solutions used to preserve the donor kidney are Euro-Collins solution or University of Wisconsin (UW) (both contains inert sugar which prevents swelling of cells). First renal vein, then renal artery and at the end ureter is anastomosed.
Azathioprine, cyclosporine and prednisolone should be started 3 days prior to surgery. Diuretics and mannitol should be continued as required.
Bilateral nephrectomy in recipient is required only in:
  • Polycystic kidney disease.
  • Haematuria.
  • Severe hypertension.
Kidney will stand cold ischaemia for 72 hours.
Note:
Overall survival is 90% in one year and 80% in five years.
 
Postoperative Management
  • Immunosuppression: By cyclosporine, azathioprine, prednisolone, antithymocytic globulin and antilymphocytic serum.
  • Proper fluid balance has to be taken care of.
 
Complications
  • Acute tubular necrosis.
  • Rejection (Rejection is identified by radioisotope study and percutaneous kidney biopsy). Chronic rejection is the common cause of graft failure.
  • Obstruction of the collecting system.
  • Infection.
  • Urine leakage—5%.
  • Secondary haemorrhage.
  • Renal infarction.
  • Hazards of immunosuppression:
    • Infection by unusual organisms like cytomegalovirus, herpes, pneumocystis carinii, varicella and other bacterial infections, candidial infection.
    • Changes in the cellular component of blood.
    • Uncommon malignancies of CNS, skin.
    • Nephrotoxicity, GIT bleeding and perforation.
    • Hirsutism, delayed wound healing, cataract formation.
    • Renal artery stenosis—10%.
    • Renal vein thrombosis—5%.
    • Lymphocele.
 
LIVER TRANSPLANTATION
Children respond better for liver transplantation. Tissue typing and cross-matching are not that necessary and do not influence the results.
If the transplantation is done at the same site after doing hepatectomy, it is called as orthotopic liver transplantation. If it is placed in a different site it is called as ectopic or heterotopic liver transplantation. Success rate in liver transplantation is better.
  • Liver transplantation is the choice for end stage liver disease. Liver transplant is an accepted and effective treatment. Many tumours can be treated by transplantation. Cirrhosis, hepatitis, sclerosing cholangitis, biliary atresia, tumours are indications.
  • CTP (Child Turcote Pugh) scoring system (ascites, encephalopathy, bilirubin, albumin, PT-INR); Model for end stage liver disease (MELD score) consists of total bilirubin, INR, creatinine; Paediatric end stage liver disease scoring (PELD); are different scorings used to assess the patients.
  • MELD Score = 0.957 x Loge(creatinine mg/dL) + 0. 378 x Loge(bilirubin mg/dL) + 1.120 x Loge (INR) + 0.643
 
Indications
  • Primary biliary atresia, metabolic liver disease.
  • Cirrhosis.
  • Malignant disease of the liver.
 
Contraindications for Liver Transplantation
  • Active sepsis, SBP and HIV.
  • Extrahepatic malignancies.
  • Large hepatocellular carcinoma and cholangiocarcinoma.
  • Unfit for surgery—severely advanced cardiopulmonary disease.
  • Active alcohol or substance abuse.
  • Inability to comply with immunosuppression protocols because of psychosocial situations.
 
Donor Criteria
They are related to donor liver function, hepatitis screening, history of consumption of alcohol and toxic substances. Marginal donor and expanded donor criteria are in use in places due to very high demand for donor for transplantation. ABO compatibility is important. HLA matching is not necessary unlike in renal transplantation.
 
Donor Operation
It is by a midline incision from suprasternal notch to pubic symphysis. Initially dissection is done with a beating heart; but later with a cold preservation into aorta and portal vein and local ice application. UW solution extends cold ischaemic time for 24 hours but usually within 10 hours transplantation is done. IVC segment is removed with hepatic veins. Portal vein is transected. Celiac artery with branches along with hepatic artery is dissected and transected at celiac artery origin. Bile duct is transected.
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DDLT (deceased donor liver transplantation) donor
LDLT (living donor liver transplantation) donor
  • 50 years or younger
  • Young, non-obese, tall
  • No hepatobiliary disease
  • No infection, malignancy, no fatty liver
  • Hemodynamic and respiratory stability (systolic blood pressure >100 mmHg, and central venous pressure >5 cm/H2O); an acceptable PaO2 and haemoglobin level
  • Enough liver to donate
  • No severe abdominal trauma, systemic infection, or cancer
  • Enough residual liver
  • Normal kidneys—diuresis greater than 50 ml/h and normal creatinine;and finally, a dopamine requirement less than 10 μg/kg/min
  • Suitable anatomy of liver
  • Simple technically
  • Technically complex procedure
  • Recipient complication is low (of bile duct)
  • Recipient complication is higher
  • Graft quality is average
  • Graft quality is good
  • Donor's complication—nil
  • Donor's complication—25% morbidity; 0.4% mortality
Note:
  • Remnant liver—> 30% of the original liver volume with complete venous drainage is safe for donor survival.
 
Recipient Operation
Bowel preparation, prophylactic antibiotics, administrative immunosuppressive agents are needed before surgery. Bilateral subcostal incision is used with midline upward extension. Falciform ligament, left lateral ligaments, hepatogastric and hepatoduodenal ligaments are divided. Right and left branches of hepatic arteries are ligated. CBD and cystic ducts are divided with ligatures. Portal vein is dissected. Infra and suprahepatic vena cava are exposed. Portal vein and suprahepatic vena cava are clamped. Venovenous bypass between portal and femoral veins and internal jugular vein is created with a flow of blood through it more than 2.5 ml/minute. Warming circuits and ultrafiltration is needed. Suprahepatic vena caval cuff is created at the opening of the right, middle and left hepatic veins. Donor IVC is sutured to recipient IVC first above and then below as end-to-end. Recipient IVC can be preserved entirely and donor IVC is sutured to recipient IVC as end-to-side. Preservative solution is passed. Portal vein is sutured. Reperfusion injury can occur at this stage with hyperkalaemia and acidosis. Arterial reconstruction is done between donor celiac artery to recipient gastroduodenal artery. Bile ducts are sutured as end-to-end with or without T tube. Often choledochojejunostomy is also done.
Graft should be:
  • 40% of the estimated standard liver volume.
  • 0.8 to 1% of the body weight of the recipient is necessary for the recipient recovery.
 
Segmental/Lobar/Split/Living Donor Liver Transplantation
It is newer beginning but becoming preferred one. It is based on segmental anatomy and liver regeneration capacity. Minimum liver mass required is more than 1% of graft to body weight ratio. Right lobe is better. It is basically used in children; but useful in adults also. MELD score in donor should be less than 20 for living donor transplantation. Regeneration occurs very significantly in recipients in first 2 weeks reaching standard in 1 month. Regeneration is slow in living donor liver in 1 year. Graft to standard liver ratio should be more than 40%. Function of liver in living donor should be optimum. Proper imaging of the donor for entire anatomy including vasculature is important. Individual branches of portal vein, hepatic artery and bile duct are dissected and isolated. Liver is carefully separated from IVC; small branches of hepatic vein are ligated. Main hepatic vein is isolated; liver parenchyma is dissected with finger/Kelly fracture technique. After completion of parenchymal division, vessels are transected; dissected liver is perfused with cold preservative solution. Diseased liver of the recipient is removed completely. Graft is anastomosed in usual manner hepatic vein, portal vein, hepatic artery, bile duct. Living donor transplantation has got higher chances of morbidity, complications compared to cadaveric transplantation.
 
Postoperative Management
  • Antirejection drugs to be given.
  • Liver shows low immunogenicity and high regeneration capacity causing long-term outcome. Initially cyclosporine or tacrolimus with MMF or azathioprine with prednisolone is given. ICU care is needed.
  • Electrolyte and fluid management, sepsis management, prevention of encephalopathy, observation for complications are important.
 
Complications and Problems of Liver Transplantation
  • Bleeding on table and postoperatively can occur especially when recipient liver is cirrhotic. FFP, platelet and blood are needed. Re-exploration is needed if bleeding persists postoperatively.
  • Hepatic artery thrombosis is the common vascular complication leading into graft failure, CBD necrosis and anastomotic dehiscence.
  • Immediate graft failure as primary nonfunctional graft can occur (5% of liver grafts).
  • Bile leak due to CBD ischaemia which can be identified by HIDA scan, ERCP, revision anastomosis is needed.
  • Infection is common especially enterococci, staphylococci, gram-negative organisms, Candida, Aspergillus, etc. Antibiotic and antifungal therapy is needed.
338
  • Acute rejection (30%) of T cell mediated is seen within 10 days commonly but can occur up to 6 months. Liver biopsy confirms the rejection. Higher steroid therapy, polyclonal anti-T cell antibodies are used.
  • Chronic rejection is seen after 6 months; appears gradually with liver cell dysfunction and hyperbilirubinaemia. Liver biopsy shows very few numbered biliary radicles—vanishing bile duct syndrome. It is due to humoral immunity. It is difficult to control; eventually needs retransplantation.
  • Recurrence of the earlier disease to the transplanted liver like hepatitis, biliary sclerosis, sclerosing cholangitis. Hepatitis can be controlled by lamivudine (antiviral DNA polymerase for HBV), interferon α, ribavirin for HCV.
  • Complications of immunosuppressive drugs like hypertension, hyperglycaemia, hyperlipidaemia, osteoporosis, malignancy, infection, bone marrow suppression are often difficult to manage.
 
Survival
  • 5-year survival is 70% in adults and 80% in children.
  • It depends on age, general condition, earlier disease, associated problems, MELD scoring.
  • The risk of rejection is highest (40%) during the first 3–6 months after transplantation and decreases significantly thereafter.
 
BONE MARROW TRANSPLANTATION
 
Indications
  • Leucaemias.
  • Aplastic anaemias.
  • Immune deficiencies, etc.
Recipients are initially treated with total body irradiation. As bone marrow is an active immune system, proper tissue typing is essential. Infant bone marrow is better marrow as a donor. Marrow aspirated from donor's bone is transplanted by intravenous injection to the recipient.
Immunosuppression with cyclosporin-A is always needed. It will take few weeks to show the response.
 
Problems
  1. Graft rejection.
  2. Graft-versus-host disease (GVH) is more dangerous.
 
PANCREATIC TRANSPLANTATION
  • It is used in diabetic patients, taken from cadaver donor to replace insulin.
  • It can be combined with kidney transplantation to patients who have diabetes with end stage kidney disease.
  • Donor criteria are individuals without pancreatitis.
  • Entire pancreas with duodenum (Lillehei) or part of the pancreas (body and tail of the pancreas) can be transplanted.
  • It is placed in the right iliac fossa with anastomosis done between portal vein and iliac vein, duodenum fixed to bladder.
  • Graft take up is 60–70%.
 
Complications
Graft pancreatitis, pancreatic leak, bleeding, urinary infections like cystitis, failure.
zoom view
Fig. 1.637: Pancreatic transplantation with duodenum and small bowel to achieve adequate exocrine function. Exocrine function is achieved immediately; endocrine (insulin) function is achieved after few days.
zoom view
Fig. 1.638: Pancreatic transplantation.
 
Isolated Pancreatic Islet Transplantation
Islets of Langerhans are obtained by mechanical disruption of pancreas by injecting collagenase into the pancreatic duct. Tissue disrupted is collected and purified by density gradient centrifugation. These islet cells are injected into the liver through portal vein. Islet cell rejection is prevented by covering them with semipermeable membrane which prevents antibodies reaching islet cells but allowing insulin to get secreted. By this method animal pancreatic islet cells transplantation is also under trial.
 
SMALL BOWEL TRANSPLANTATION
  • Indication is short bowel syndrome following massive resection, atresia, necrotising enteritis, Crohn's disease.
  • Bowel anastomosis with a stoma (ileostomy) is usual method.
  • As small bowel is rich in lymphoid tissue, graft versus host reaction is a major problem. So graft take up is poor.
  • It is an immunological challenge even though technically easier.
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DIALYSIS
It is technique for the removal of waste product of metabolism, normalisation of plasma electrolytes and removal of plasma water.
 
Types
  • Peritoneal dialysis.
  • Haemodialysis.
 
Peritoneal Dialysis
Indications
  • Acute renal failure until renal function recovers.
  • Chronic renal failure until long-term dialysis is instituted.
Contraindications
  • Abdominal surgery.
  • Hypercatabolic states.
  • Infection.
  • Pre-existing malignancy.
Insertion of Catheter
A rigid plastic catheter is inserted through the abdominal wall into the peritoneal cavity using a trocar through a small cut made in the skin under L/A. Catheter is bound to abdomen.
Dialysis is done using sterile dialysate solution instilled into and drained out of abdomen.
Continuous ambulatory peritoneal dialysis (CAPD) is the preferred method of dialysis in some centre.
 
Haemodialysis
Indications
  • Acute renal failure.
  • Chronic renal failure.
  • Acidosis.
  • Electrolyte disturbance.
  • Intoxication.
  • Uraemia (pericarditis and polyneuropathy due to uraemia are absolute indications).
zoom view
Fig. 1.639: Patient with CRF undergoing haemodialysis using a dialysis unit.
zoom view
Figs 1.640A and B: Arteriovenous fistula between radial artery and cephalic vein at wrist is done to attain increased venous engorgement and arterialisation so as to achieve rapid blood flow which is necessary for haemodialysis. Patient with chronic renal failure who requires regular haemodialysis needs this.
Haemodialysis requires access to circulation which is achieved by creating a fistula between the radial artery and the cephalic vein at the wrist (Cimino fistula). Here dialysis occurs in a dialysing machine across a semipermeable membrane (usually cellulose membrane).
Complications
  • Access site—arterial and venous stenosis, thrombosis, infection.
  • Hypotension.
  • Dyspnoea.
  • Bleeding (due to dysfunctional platelets due to uraemia and due to heparin use).
  • Disequilibrium syndrome.
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Even though repeated dialysis (in CRF, at least twice a week is needed) helps, patient needs repeated blood transfusions, which will lead into haemochromatosis/iron overload. Patient should be given erythropoietin injection 3,000 units twice weekly to prevent repeated blood transfusions. But it is expensive. Transplantation is the best answer eventually, in all these individuals.
 
CIMINO FISTULA (CIMINO-BRESCIA)
It is an arteriovenous fistula created for haemodialysis. Usually at wrist, radial artery is anastomosed to cephalic vein side-to-side and a created good fistula shows continuous thrill and bruit, with increased venous engorgement along with hyperdynamic circulation. At the ankle, often fistula is created between posterior tibial artery and saphenous vein; in the thigh between femoral artery and long saphenous vein. Distal gangrene is not common.
 
Complications
Infection, bleeding, hyperdynamic circulation.
341W. Stings and Bites
CHAPTER OUTLINE
  • ❖ Snake Bite
  • ❖ Spider Bite
  • ❖ Bee Bite
  • ❖ Mammalian Bite
 
SNAKE BITE
Snakes belong to Crotalidae, Elapidae and Viperidae family.
Common poisonous snakes are cobra, krait and viper.
Common snakes are cobra, Russell's viper, saw scaled viper, pit viper, krait.
It causes renal failure, pulmonary oedema, cardiac complications and neurological problems.
 
Clinical Features
 
Local
  • Burning pain, oedema and erythema.
  • Swelling, echymoses and haemorrhagic bullae.
  • Tissue necrosis, ulceration and gangrene.
 
Systemic
  • Weakness, perioral paraesthesia, muscle twitching.
  • Shock.
  • Pulmonary oedema.
  • Renal failure.
  • Neurological manifestations.
  • Bleeding tendency.
Vipers affect multiple organs and soft tissues. Cobra and coral snakes are neurotoxic.
 
Investigations
  • Blood count.
  • Coagulation studies like bleeding time, clotting time and prothrombin time.
  • Blood urea and serum creatinine.
  • Serum electrolytes.
  • Creatine phosphokinase (CPK).
  • Urine analyis for RBCs, albumin, myoglobin.
  • PO2 and PCO2 assessment.
 
Management
 
First Aid
  • Reassurance.
  • Immobilisation.
  • The site has to be incised and cleaned.
  • Tourniquet to occlude lymphatics only but not venous or arterial circulation.
  • The snake has to be identified.
  • The patient must be transferred to proper medical centre as early as possible.
  • The bite wound is identified and assessed.
  • It is thoroughly cleaned with debridement.
  • Polyvalent antisnake venom (against cobra, krait, vipers) should be given. It should be given earliest within 4–24 hours.
    Dose is 20–150 ml depending on the type, severity and age of the individual. It is dissolved in normal saline and given as IV infusion in 500 ml saline with 20 drops/minute as flow rate. If the snake has been identified monovalent serum is better and more potent.
  • Tetanus toxoid.
  • IV fluids, blood transfusion and plasma.
  • Antibiotics.
  • Urine output measurement.
  • Monitoring by regular checking of blood urea, serum creatinine and bleeding and clotting time.
  • In cobra bite, there is neuromuscular blockade and paralysis occurs. So neostigmine should be given 0.5 mg IV every half hourly and later repeated as required. It is given along with 0.6 mg of atropine.
  • In viper bite DIC is common. So heparin is given as 10,000 to 15,000 units loading dose and later 5,000 units as maintenance dose 8th hourly.
  • Human fibrinogen, whenever required.
 
Complications of Snake Bite
  • Cellulitis and gangrene of the part.
  • Deep venous thrombosis (DVT).
  • Pancytopenia.
  • DIC and haemorrhage.
  • Neurological complications.
  • Septicaemia.
  • Renal failure.
  • Marjolin's ulcer.
 
SPIDER BITE
 
Types
  1. Black Widow Spider Bite
    • It causes neurotoxicity.
    • It causes muscle spasms, pain and abdominal cramp and rigidity.
    • Hypertension, tachycardia and diaphoresis are the other features.
    • Its effects last for 2–3 days.
    • Cleaning the wound, antibiotics, antihistamines, specific antivenins are the line of treatment.342
  2. Brown Spider Bite
    • It releases sphingomyelinase-D which causes necrosis of the skin and haemolysis.
    • Local effects include skin rash, blister formation, necrosis of the skin and extensive ulceration.
    • Systemic effects are anaphylaxis, arthralgia, thrombocytopenia, haemolysis and renal failure.
    • Often it can be life-threatening especially in children and elderly.
    • The effects last for 2–3 weeks.
    • Wound debridement, antibiotics, antihistamines, steroid therapy, antivenins and management of systemic complication.
zoom view
 
BEE BITE
Honey bee has got barbed stinger with two lancets. These lancets get attached to human skin to release the venom. Bee dies after bite.
Wasps: Yellow jacket wasps are more aggressive.
Bee venom contains dopamine, histamine, neurotoxin and toxic peptides.
 
Clinical Features and Management
  • Allergic reactions.
  • Anaphylaxis.
  • Pain in the local region, oedema, pruritus, flushing.
  • Hypotension, laryngeal oedema, bronchospasm.
  • Muscle spasm, convulsions.
  • Renal failure in severe cases.
  • Soda bicarbonate is used to neutralise the bee venom.
  • Antibiotics and antihistamines.
 
MAMMALIAN BITE
  • It includes human bites also.
  • Infection rate is more in mammalian bites.
  • Proper wound toileting is very important.
  • Within 12 hours, incised wound is closed primarily.
  • All lacerated wounds and wound which is seen after 12 hours is left open. Wound is closed secondarily.
  • Antibiotics are must in all mammalian bites.
  • Human bite is very dangerous bite.
343X. Pain
CHAPTER OUTLINE
  • ❖ Gate Control Theory
 
Pain is a subjective one and is difficult to assess and quantify. Pain perception varies from person-to-person and from time-to-time.
 
Pain Pathway
Pain receptors in the skin
Neurotransmitters of pain like substance P or peptides are activated
Sensory nerves
Posterior horn of spinal cord
Spinothalamic tract
Thalamus
Cerebrum
Pain perception
 
GATE CONTROL THEORY
Gate control system is located at the junction of first and second neuron. Large diameter ‘A’ fibre is stimulated by temperature and touch. Fine ‘C’ fibre is stimulated by pain. If ‘A’ fibre once gets stimulated, blocks the gate mechanism, then pain from ‘C’ fibre cannot pass through the gate to reach the brain for perception.
Pain modulators like endorphins and opioid peptides in brain and spinal cord inhibit the release of substance ‘P’.
 
Causes of Pain
  • Inflammatory causes due to any infection or infestations.
  • Hypoxia due to poor blood supply like in myocardial infarction, peripheral vascular disease.
  • Trauma.
  • Obstruction like intestinal obstruction.
  • Colicky pain like ureteric, biliary, intestinal.
  • Compression over nerve roots like in inter vertebral disc prolapse.
  • Advanced malignancies cause severe distressing pain, which requires proper pain control.
  • Ulcers, perforation, peritonitis, abscess formation are all other causes.
 
Clinical Assessment of Pain
  • Its severity, nature, cause should be assessed.
  • Cause should be thoroughly analysed by doing all investigations like haematocrit, sinology, CT scan, culture of the fluid like pus, blood.
Pain is a most common symptom which patient complains to a clinician. Latin word ‘poena’ means penalty/punishment. Pain is the one patient feels; tenderness (sign) is one surgeon/clinician elicits.
 
Specific Points in History in Relation to Pain to be Asked are:
  • Original site of pain is very important. In acute appendicitis original site of pain is in umbilicus; but later it is referred to right iliac fossa. Shift of pain towards other site.
  • Time and mode of onset of pain—it is sudden onset and rapidly progressive in acute appendicitis; it is of insidious onset and of long duration with episodic nature in chronic peptic ulcer.
  • Type/nature of pain—superficial/deep; dull ache or sharp severe/pricking/bursting/vague aching (continuous mild pain), throbbing, scalding (burning sensation particularly felt during urination in cystitis, pyelonephritis, urethritis), pins and needles pricking sensation in peripheral nerve injury or irritation, shooting pain (seen in intervertebral disc prolapse and sciatica—pain shoots along the course of nerve), stabbing (sudden, severe, sharp, episodic—seen in perforated duodenal ulcer), distension pain (a feeling of restricted or distended like in paralytic ileus or intestinal obstruction), colicky pain is due to muscular contraction in a hollow tube in an attempt to obviate the obstruction by forcing the content out—gripping, episodic pain with vomiting and sweating (seen in intestinal colic, ureteric colic of stone, biliary colic of stone), twisting pain of bowel volvulus/twisted ovarian cyst/torsion testis, constricting pain around the chest by angina, etc.
  • Severity of the pain: In acute conditions like peritonitis and abscess pain will be severe compared to chronic one.
  • Progression of pain: It may be persistent and progressive; or initially mild gradually increases, later gradually subsides; fluctuation in intensity whether increases and decreases in intensity at regular intervals; quickly reaches maximum and remains like that.
  • Duration of pain
  • Periodicity of pain: Pain appears, persists for few weeks and then disappears for few weeks; again reappear. Such periodicity is often observed in chronic peptic ulcer; trigeminal neuralgia.
  • Precipitating/aggravating factors: Abdominal pain may get worsened by taking food like in gastric ulcer. Pain due to appendicitis, ureteric stone aggravates by change of position, walking, jolting. Pain of urinary bladder stone aggravates in standing position. In reflux oesophagitis pain increases while scooping. Pain in pancreatitis increases while lying down. Pain in intervertebral disc prolapse aggravates by lifting the weight.
  • Relieving factors of pain: Pain reduce by certain methods and patient uses that method to relieve the pain. Hunger pain of early morning in duodenal ulcer is relieved by taking food. Pain of pancreatitis is relieved in sitting and bending forward. Propped up position relieves pain of reflux oesophagitis. In acute peritonitis, pain reduces temporarily by lying still.
  • Associated symptoms: Acute pain may be associated with pallor, sweating and vomiting. Migraine pain with vomiting and visual disturbances; intestinal/ureteric colic with sweating, vomiting and cold periphery; acute pyelonephritis and urinary infections with chills/rigors and fever; ureteric colic with haematuria; biliary colic with jaundice and pale stool are other examples of such association.
  • Time of occurrence of pain is often important in diagnosing the condition. In duodenal ulcer, hunger pain occurring in early morning or later evening is typical. Migraine occurs in early morning; frontal sinusitis induced headache occurs a few hours after getting up.
  • Pain may move from one place to other: Radiation of pain It is extension of pain from original site to another site with persisting of pain at original site. This radiating pain is of same character of original site. Penetration of duodenal ulcer posteriorly causes pain both in epigastrium and back—is an example. Pain of pancreatitis radiates to back. Referred pain: Pain is not felt at the site of the disease but felt at distant site. Diaphragmatic irritation causes referred pain at the tip of shoulder through same segmental supply of diaphragm (phrenic nerve C4, C5) and shoulder (cutaneous supply C4, C5). Hip joint pathology may cause referred pain in knee joint—through articular branches of femoral, obturator and sciatic nerves. Other examples—referred ear pain from carcinoma tongue through lingual and auriculotemporal nerve; referred pain in the epigastrium from the heart; referred pain in the abdomen from pleura; referred pain over the testis from the ureter. Shifting/migration of pain: Origin of pain is one site; later pain shifts to another site and pain at original site disappears. Pain when begins in viscera, it is felt at the same somatic segmental area in the body; but once parietal layer is involved by inflammation/pathology pain is felt at the anatomical site. Example is pain of acute appendicitis where original visceral pain is at the umbilicus (T9 and T10 segments supply both umbilicus and appendix) shifts later to right iliac fossa when once the parietal peritoneum of that area is inflamed.
Types of pain:
  • Superficial pain: It is sharp usually localised pain, due to irritation of peripheral nerve endings in superficial tissue by chemical/mechanical/thermal/electrical injury. Segmental pain: It occurs due to irritation of particular nerve trunk/root; located in particular dermatome of the body supplied by the sensory nerve trunk or root.
  • Deep pain: It is due to irritation of deeper structures like muscles/tendons/bones/joints/viscera. It is vague and diffuse when compared to superficial pain. It is often referred to common segmental areas of representation. Often spasm of skeletal muscle of same spinal cord segment can occur.
  • Psychogenic pain: It may be functional/emotional/hysterical.
  • Other pain: like due to thalamic/spinothalamic diseases/causalgia (intense burning pain along the distribution of the partially.
Grading of pain: It is done using pain scale. It is compared to a 10 cm line numbered 0 to 10. This is called as visual analogue scale (VAS). Minimum is 0 means no pain. 10 is the worst excruciating pain. 2 is mild; 4 is discomforting; 6 is distressing; 8 is intense.
 
Management of Pain
  • Correct the cause like removal of renal stone, cholecystectomy for gallstones.
  • Analgesics.
  • Surgical removal of tumour.
  • Injection of phenol or alcohol.
  • Electric stimulation, massaging, infrared therapy, wax bath.
  • Proper physiotherapy.
  • Hormone therapy.
  • Injection to ganglion like in trigeminal neuralgia.
  • Chemotherapy for malignancies.
  • Radiotherapy.
  • Sympathectomy for vascular diseases, causalgia.
  • Cordotomy for severe pain in case of advanced tumours.
  • Mental relaxation.
  • Attending pain clinic.
  • Continuous epidural anaesthesia/analgesia using opioids.
  • Patient controlled analgesia (PCA) is injecting opioids through epidural route or intravenous route by patient himself after training him.
  • Intravenous infusions of the analgesia.
 
Drugs for Pain
345Drugs can be given orally, intramuscularly, few intravenously, intrathecally, per rectally as suppositories, sublingually.
Acute pain
Drugs/opioids/epidural anaesthesia/drug infusion
Chronic pain due to malignancy
First level simple analgesics (aspirin, paracetamol, NSAIDs, tricyclic antidepressants)
Second level intermediate opioids codeine, tramadol, dextropropoxyphene
Third level strong opioids like oral morphine, intravenous morphine, subcutaneous diamorphine, epidural diamorphine. Analgesic infusion is also useful. Neurolytics are used whenever there is limited life-expectancy. Other methods are Subcostal phenol injection for rib secondaries/celiac plexus block using alcohol/intrathecal hyperbaric phenol/percutaneous anterolateral cordotomy/pituitary ablation/hormone ablation/palliative radiotherapy/steroids/ flecainide therapy
Chronic pain in benign disease
Local anaesthetics/steroid injections/nerve stimulation like acupuncture/nerve decompression/pain due to sympathetic overactivity is corrected by IV pentolamine (alpha adrenergic block), stellate ganglion block, block using guanethidine, percutaneous chemical lumbar sympathectomy using phenol. Other methods for chronic pain are paracetamol/NSAIDs/antidepressants/opioids/carbamazepine/ neuroablative surgeries
 
Narcotic Analgesics
  • Morphine 10–15 mg. Very useful in intractable pain. It can cause nausea, constipation, and respiratory depression. Its action is neutralised by naloxone.
  • Pethidine 50–100 mg IM.
  • Diamorphine 5–10 mg. It is used only in intractable pain.
  • Pentazocine 30–60 mg.
  • Dihydrocodeine.
  • Codeine phosphate is commonly used after intracranial surgery. It should not be given intravenously as it may precipitate severe hypotension. Codeine also causes constipation.
  • Bupremorphine.
 
Non-narcotic Drugs
  • Aspirin.
  • Ibuprofen.
  • Naproxen.
  • All these NSAIDs cause gastric irritation and may risk the gastric bleeding. NSAIDs are nonspecific cyclo-oxygenase inhibitors. So gastric protection and platelet function are lost. Rectal diclofenac as suppository is good analgesic.
  • Paracetamol is effective analgesic and antipyretic agent. It is relatively less common to cause gastric bleeding.
Note:
Specific COX2 inhibitors are contraindicated in ischaemic heart disease.
 
Other Drugs
  • Anticonvulsants.
  • Antidepressants, anxiolytics.
  • Carbamazepine for neuralgia.