Introduction to Clinical Approach and ExaminationCHAPTER 1
Clinical examination is an art. It is an important basic essential part in surgical learning. Surgery is categorized as clinical surgery; surgical principles and operative surgery. So surgery is not just cutting. It involves proper clinical analysis; and application of principles while treating patients surgically.
Clinical observation has been a part of medicine since Egyptian, Babylonian, Chinese and Indian physicians began examining the body thousands of years ago. Clinical reasoning and bedside diagnosis first played a role in ancient Greece when Hippocrates began measuring body temperature, evaluating the patient's pulse and palpating the abdomen.
A clinician should be good in theoretical knowledge as well as a master in practical knowledge, as both go hand in hand. Without theoretical knowledge of a disease it is like sailing in an unchartered sea; having book knowledge without patients to treat is like not seeing the sea at all—William Osler.
Note:
- The ‘patient’ word is derived from Latin—Pati means ‘to suffer’.
- All patients in a surgical ward need not undergo or need surgery. Conditions like cellulitis, amebic colitis or acute pancreatitis commonly do not require surgery but treated by surgeons.
- A surgeon should be a good clinician and physician all together to impart proper treatment to his patients. Even though there are many subspecialties in surgery now, basic clinical surgery remains the same. It is the pillar of surgical basics.
- Clinical examination has mystical power. History and examination skills still remain at the very core of clinical practice.
- “Clinical examination skills will gradually atrophy and become redundant if not rejuvenated and stressed upon. Technology should become an extension of what we are doing rather than a replacement”. Investigations are just one more piece of evidence that has to be interpreted by a doctor—Asghar Rastegar MD.
CLINICAL METHODS
(Word ‘clinical methods’—was used in September 1897, by Sir Robert Hutchison from London who was founder and author of the famous Hutchison's clinical methods book) (Figs. 1-1 to 1-3).
Clinical methods are schematically divided as
History taking: It is very important part. Careful detail history taking many times gives clue about the exact disease. 70–80% of diagnosis can be made by proper history taking.
Physical examination: It includes general examination; inspection of the part (diseased or suspected) which is proper observation prior to palpation for specific findings; palpation is done only once inspection is completed in detail; percussion done in specific areas like abdomen and chest; auscultation for altered or specific sounds in particular region.
Fig. 1-1: Sir Henry Wade—Surgeon, Scientist, Soldier. He said “The wards are the greatest of all laboratories”.
Fig. 1-3: Sir Henry Hamilton Bailey; he was a British surgeon and excellent clinician; he wrote Clinical book “Demonstration of Physical Signs in Clinical Surgery” in 1927 and textbook “A Short Practice of Surgery” in 1932. Finest illustrations which he provided in his books were with the help of his photographer wife Vera Gillender. He lost his left index finger due to infection while doing surgery; it is observed in the photos in his book of clinical examination. He died of obstructed carcinoma colon.
Investigations: Investigations are done to arrive into final diagnosis by various methods like X-ray, CT scan, ultrasound, blood tests and so on. Types of investigations are decided based on the clinical suspicion of the disease.
Final diagnosis: It is to plan the therapy, predict the outcome.
Treatment: Treatment plan or protocol which often differs for individual patient. Postoperative/post-therapy management. Progress of the patient.
Follow-up: Management after discharge and further treatment which is often needed after treatment.
SYMPTOMS AND SIGNS
- Two important parts in clinical methods are symptoms and signs.
- Symptom is the one patient complains of. It is the subjective sensation of the patient.
- Sign is the one which clinician elicits. It is an indication of existence of an objective evidence of a disease.
- Even though both symptoms and signs are complimentary to each other, sign by and large often becomes more relevant.
Sign
- Sign is an indication of existence of an objective evidence of a disease, i.e. such evidence is perceptible to the examining physician, as opposed to the subjective sensation (symptoms) of the patient.
- Usually many signs are observed, confirmed by clinical methods like mobility, fixity, fluctuation, transillumination and clinical conclusion is arrived at.
- Sometimes by one sign diagnosis is clinched, and so called as diagnostic sign. Blumberg sign (release sign—while releasing the pressed fingers over the abdomen rebound tenderness is elicited) is diagnostic of peritonitis.
- Pathognomonic sign (patho = disease, gnoma = signature, pathognomonic = signature of the disease): Specially distinctive or characteristic sign of a disease or pathological condition on which a diagnosis can be made. Hernial sac which is resonant on percussion and reduces with gurgling is pathognomonic of enterocele.
- Accessory sign (Assident sign): Any nonpathognomonic sign of disease, which adds on to the surety of the diagnosis when present.
- Antecedent sign: Any precursory indication of an attack of disease. These signs are to be identified at the earliest.
HISTORY TAKING
Clinician should spend adequate time for detailed history taking from the patient. Clinician should show no hurry during conversation; hear sympathetically; behave patiently with the patient; keeping a pleasant face with a smile; should show good bedside (examination table) manners to gain confidence from patients; clinician should avoid harsh words while conversing with patients and relatives. Patient should be made comfortable while taking history. Successful history taking should make patient to completely open out towards the matter needed.
If the patient is a child or patient is dumb, then history is given by the mother or close relative who takes care of the individual. Name and relation of the person who is giving history should be noted down.
History taking should be done in an order and every history should be documented properly. In critical patients it is better to have video documentation of the history taking and explaining the relatives towards the risk involved and therapeutic aspects.
History taking is the first step as—gathering information; it is a sensitive, respectful, nonjudgmental, confidential thorough interview between patient and the clinician.
General History
Name
Correct name of the patient should be asked and noted down. It is better to remember each patient by name while doing rounds, at least up to the discharge from the hospital. This helps to build a zone of comfort with the doctor for the patient. It may be helpful to keep a pocket note book to write down in short about the details of the patient. Asking patients name gives the identity; creates cordial relationship; achieve patient's cooperation.
Age
- Noting the age of the patient is important.
- Certain diseases are specific to certain age group. Cleft lip and palate; phimosis, meningocele, cystic hygroma, exists since birth. Congenital anomalies occur in young age group.
- Branchial cyst even though of congenital origin occurs in later age group in 2nd or 3rd decade.
- Certain tumors like Wilm's tumor (kidney) and neuroblastoma occur in early childhood.
- Sarcomas develop in adolescents. Usually carcinomas occur after middle age. But malignancies can occur at any age group.
- Benign prostatic hyperplasia occurs in old age often causing retention of urine.
- Polio, acute osteomyelitis and arthritis and tuberculosis occur in children.
Sex
Certain diseases occur only in one particular sex other than gender specific diseases. Hemophilia occurs only in males but females can be carriers. Thyroid diseases are more common in females. Carcinoma lung, stomach, kidney are more common in males but can occur in females. Gallstones, hysteria, mobile kidney, carcinoma breast are common in females.
Religion
Carcinoma penis is not seen in Muslims and Jews due to their religious practice of early circumcision in childhood. Duodenal ulcer perforation is common in Muslims during fasting month of Ramzan. Carcinoma breast is common in Parsees.4
Residence
Complete postal address and method of communication must be taken down. Many diseases have got geographical distribution. Hydatid disease is common in Australia, Iran, Greece, etc; schistosomiasis is common in Egypt; trypanosomiasis is common in Africa; amebiasis is common in tropical countries; leprosy in West Bengal; gallstones in Bihar and north east India; peptic ulcer in South India; endemic goiter in mountain region [Republic of Guatemala country at the ranges of Andes Mountain and Republic of Panama used to have high prevalence (38%) of endemic goiter due to iodine deficiency until iodized salt usage has standardized]; madura foot in Madurai; kangri cancer in Kashmir (Figs. 1-4A to C); filariasis in Surat, Orissa; guinea worm infestation in Tamil Nadu, north Gujarat, Rajasthan.
Occupation
- Some diseases are common in people with certain occupations. Varicose veins are common in people who stand for long hours like bus conductors, garden workers, watchmen, traffic policemen, barbers, surgeons, and nurses, etc.
- Sportsmen are more prone to injuries to ankle, knee and elbow.
- Certain malignancies can occur as occupational disease. High-risk of leukemia is present in people exposed to ionizing radiation and working in nuclear reactors. Aromatic amines, benzenes, asbestos, nickel, arsenic, coal tar, petroleum are carcinogens (can cause cancers). Carcinoma urinary bladder is more common in workers in aniline dye factories.
- Exposure to ultraviolet radiation can cause skin cancers.
- Vibrating tools can cause Raynaud's phenomenon and osteoporosis of wrist bones.
- Certain adventitious bursae can develop due to friction—like housemaid's knee (prepatellar bursitis); clergyman's knee (infrapatellar bursitis); student's elbow (olecranon bursitis).
- Inguinal hernia can occur in heavy weight lifters, hookworm infestation is common in farmers; plumbers may develop lead poisoning; carbon monoxide poisoning can occur in automobile workers; pneumoconiosis in silica workers; jaundice in trinitrotoluene workers.
Social Status
Tuberculosis is common in low socioeconomic group; peptic ulcer disease is common in high socioeconomic group.
Figs. 1-4A to C: Kangri is a special device used in Kashmir to warm the body to tolerate extreme cold; pot with hot charcoal is placed in a bamboo basket which is kept close to the abdomen under the clothes so as to keep the body warm. Kangri cancer is common in Kashmir; it is squamous cell carcinoma in lower abdomen.
Social status is classified as:
- Class I—professionals;
- Class II—executive and higher management;
- Class III—lower management and clerical;
- Class IV—skilled laborers;
- Class V—unskilled laborers.
CHIEF COMPLAINTS
Main complaints of the patient are mentioned in the chronological order of occurrence. Complaints of same duration should be narrated in the order of severity. For example:
- Lump in the breast—6 months.
- Ulcer in the swelling of breast—2 months.
- Pain in the breast—1 month.
- Fever—1 month.
Proper leading questions should be avoided but sometimes are necessary to elicit clear relevant history. But this should be used only after proper initial detailed history. History should be elicited in language which the patient is comfortable. One should not elicit diagnosis from the patient. Negative reply of the patient is also very relevant and so it should not be ignored.
Main complaint gives the idea as which system in the body is grossly affected. For example—constipation and diarrhea in gastrointestinal disease; pain in right iliac fossa in appendicitis; hematuria (blood passage in urine) in urinary stones or tumors.5
HISTORY OF PRESENT ILLNESS
It is detailed history in relation to onset of the present disease until date. It should be in order of occurrence. Each symptom should be questioned/enquired in detail before going to next part of the history.
Mode of Onset of Symptom
It may be gradual, or sudden or initially slow but later progress rapidly. History suggestive of whether it is related to any trauma or any earlier disease should be asked.
Progress of the Disease
Whether the symptoms are decreasing or increasing; in severity gradual or rapid; or waxing and waning should be asked (increase-decrease-increase). For example—pain due to ureteric stone is colic and often intermittent; pain of acute appendicitis is progressive and persisting. Pain of intussusception (telescoping one segment of the bowel to adjacent segment) appears and disappears. Pain of salivary calculus is waxing and waning.
Related Symptoms Suggestive of Complications of the Disease
Though patient may not be able to reveal these should be specifically asked for by leading questions. For example—history suggestive of melena or steatorrhea in jaundice; history of hematemesis in acid peptic disease; difficulty in swallowing in thyroid disease.
Associated Symptoms
Patient may or may not reveal any changes in weight; if not revealed direct enquiry into the weight gain or loss to be made as it is very important aspect to be noted in gastrointestinal, visceral and advanced malignancies.
Often history like back pain, headache, visual problems, disability may require to be elicited carefully which in fact patient may presume them as not relevant.
Note: Detailed enquiry of specific symptoms like pain, fever, loss of weight, vomiting, jaundice and constipation should be made (discussed under “specific symptoms” later in this chapter).
PAST HISTORY
Old (earlier) diseases should be detailed in order. Often patient may not know the name of the disease which he had earlier. History suggestive of specific disease should be elicited like tuberculosis, syphilis, leprosy, bronchial asthma, diabetes mellitus, and tropical diseases. When such disease has occurred; detailed history of treatment taken; response to treatment should be asked for. Often patient might have got hospitalized for the treatment which should be asked in detail like place where he is hospitalized; duration; type of treatment (type of drugs, injections, etc.). Earlier treatment summary/prescriptions if present should be taken and studied for reference.
History of earlier surgery/trauma; its detail like duration of hospital stay, recovery period, any postoperative complications, drain placed or not, response of surgery, whether patient is relieved of symptoms completely or partially should be asked for any operative notes available for reference.
History of taking chemotherapy earlier (for malignancies or tuberculosis or leprosy), their side effects if any should be asked for. Detailed chemotherapy regime in malignancy and going through earlier documentation are also important.
Previous history of radiotherapy, its detail, number of days, type, dose, complications, and response to radiotherapy should be asked for.
Long-term drug intake should be asked if any in all patients. Examples—steroids (for asthma, joint diseases, ulcerative colitis, etc; dose, type—tablet or inhalation); hormone intake like thyroxine, oral contraceptives; antithyroid drugs like carbimazole or propylthiouracil; psychiatric drugs; analgesics like diclofenac or ibuprofen; oral antidiabetics or insulin; antihypertensives; anticoagulants like warfarin. Side effects, duration of intake and relevant documents should be collected and analyzed.
History of allergy to any drugs like penicillins, septran, analgesics and other antibiotics should be asked. Type of allergy—rashes, anaphylaxis, edema, utricaria or acute problems should be asked for. Allergy to food or other allergens should be noted. Allergy to egg and certain diets are not uncommon.
PERSONAL HISTORY
History of personal habits like smoking beedi or cigarettes with duration/frequency/number of beedi or cigarettes per day; history of drinking alcohol with duration, quantity, whether addicted, whether associated with alcohol-induced problems should be noted.
Diet
Vegetarian or nonvegetarian; spicy or bland; more carbohydrate (rice) or protein or fatty diet—should be asked for. Type of diet is also relevant in many diseases like atherosclerosis, diabetes. History of tapioca intake should be taken especially in people from Kerala which is commonly associated with chronic pancreatitis.
Drinking Habits
Alcohol Intake
A problem drinker is one whose physical, social and mental well-being is harmed by drinking. One unit of alcohol equals to 8 grams of alcohol in 290 mL of 4% beer. Teetotaler is one who has not taken alcohol in last one year.6
Occasional drinker is one not taken alcohol in last one month. Light drinker is one who drinks alcohol <25 units per week in males; <15 units in females. Moderate drinker is the one who drinks alcohol 25–35 units/week in males; 15–25 units in females. Heavy drinker is the one who drinks alcohol 36–50 units/week in males; 26–35 units in females. Very heavy drinker is the one who drinks alcohol >50 units/week in males; >35 units/week in females.
Alcohol abuse leads into medical, psychiatric and social problems. Consumption of more than 21 units of alcohol per week for women; more than 28 units per week for a man is harmful. Alcohol addiction is a syndrome with withdrawal symptoms (tremor, sweating, anxiousness); symptoms are relieved by drinking; drinking in the morning; increase in quantity of the alcohol intake gradually with tolerance for more quantity; stereotyped pattern of drinking; craving for alcohol; impossible to achieve abstinence; avoiding other activities.
Alcohol causes medical problems like peptic ulcer with bleeding, cirrhosis of liver with its consequences, gynecomastia, testicular atrophy, neuropathy, pancreatitis, diabetes, osteoporosis, nutritional deficiencies, accidents; psychiatric problems like anxiousness, delirium, panic attacks, blackouts, confusion, dementia; social problems like accidents, crime, debt, violence, loss of job, family problems.
Other Drinking Habits
Drinking tea, coffee, soft drinks (cococola, pepsi, sprite, etc.); quantity, frequency should be asked for. Drinking in more quantity of any of these beverages is harmful to health especially gastrointestinal tract. Drinking more hot tea may cause carcinoma esophagus.
Smoking
Light smoker—one packet of cigarette/day for 2–10 years. Moderate smoker—1–10 packets of cigarettes/day. Chronic heavy smoker is 10–20 packets of cigarettes/day for 2–10 years. Use of beedies for smoking is equally bad and dangerous to health (Fig. 1-5).
Other Habits
Eating betel nut and leaves—pan, supari, slaked lime and tobacco; snuff inhalation; hookah, chilam smoking; history of contact with sexual workers (can cause sexually transmitted diseases like HIV, syphilis, gonorrhea) should be asked for. Use of protective sex in such situation is important. History of taking narcotics is also important. Tablets, powders, injections are used for narcotic drug intake. Multiple injection pricks may be evident in these patients. Smoking, alcohol and narcotic intake, pan chewing are addictions.
Appetite and Weight
Weight gain or loss; increased appetite or loss of appetite are important. Increased appetite is seen in bulemia or some hormone disorders. Appetite is decreased in anorexia nervosa and in tuberculosis, sepsis, malignancies. Feeling fullness and satisfied after intake of small quantity of food is called as early satiety. It is suggestive of gastric carcinoma or other gastrointestinal malignancies or infections.
Bowel and Micturition Habits
Frequency in bowel habits, passing blood or mucus, tenesmus and constipation should be asked for. Frequency in urination (number/day and number/night), hematuria, burning and pain during urination should be enquired.
Sleep Habits
Whether patient gets proper sleep, duration of sleep hours or sleeplessness (insomnia) or lethargic; feeling sleepy during day and working time should be asked for. Often patient interprets sleepy nature for tiredness. It should be clearly clarified as tiredness may be due to anemia, renal failure, specific diseases like malignancy, tuberculosis, jaundice. Patient may be taking sleeping tablets for insomnia. Name and dose of the drug should be noted down. Alcohol withdrawal also often causes sleeplessness, irritability, etc.
In Females
A detailed menstrual history should be noted. Time of attaining menarche/menopause/regularity of the cycle/presence of pain/dysmenorrhea/white discharge/date of last menstrual period are noted in detail. Pregnancy history with number of pregnancies/abortions/normal delivery or cesarean section (LSCS)/last child birth should be noted. Any complications during pregnancy and need of any blood transfusions should be asked for.
FAMILY HISTORY AND GENETIC HISTORY
Many diseases run in family. Examples are—piles; breast cancer; diabetes mellitus; tuberculosis; bleeding disorders; hypertension, etc. If any of the family member is suffering from any disease; its detail, type, therapy for the same, whether he has undergone any surgery for the same should be mentioned in detail. Number of siblings and their health details should also be taken.7
Tuberculosis as infectious disease, carcinoma breast as familial, hemorrhoids, hypertension and diabetes mellitus as hereditary can occur in family members.
Marital status, number of children their ages and work/education; number brothers/sisters to patient (whether they are suffering from any diseases); parents and their details in relation to health should be asked for. Details about patient's maternal or paternal relatives (uncles) and whether they are suffering from any illnesses should be asked for.
OTHER RELEVANT HISTORY
In younger age group history of immunization for different diseases like poliomyelitis, tetanus, diphtheria, hepatitis is taken. History suggestive of allergy/reactions during earlier drug intake; history of long-term drug therapy like insulin, steroids, antidiabetics, antihypertensives, diuretics, hormones, etc. should be noted. History suggestive of bleeding disorders (hemophilia in males, other coagulopathies, acquired bleeding disorders due to chronic liver disease) should be asked for.
ASSESSMENT OF SPECIFIC SYMPTOMS AND SIGNS
Pain
Pain is a commonest symptom which patient complains to a clinician. Latin word ‘poena’ means penalty/punishment. Pain is the one patient feels (symptom and is subjective); tenderness (sign) is the one surgeon/clinician elicits during examination.
Pain is the nature's warning to say that something is not well within the body; though we look upon it as a curse but actually it is a boon.
Tenderness sometimes (occasionally) can be a symptom as the patient feels the pain while he himself palpates the painful area; but it is usually recorded as ‘pain present while palpating or feeling by the patient himself’.
‘Rebound tenderness’ is the term used when the patient experiences more pain on release of pressure from the diseased area (usually used in abdomen).
Types of Pain
Superficial pain: It is usually sharp localized pain, due to irritation of peripheral nerve endings in superficial tissue by chemical/mechanical/thermal/electrical injury. It is due to irritation of nerve roots or trunks or endings by pressure or infiltration or inflammation. It is usually well localized, sharp and short duration (acute onset) unlike deep pain. It can cause increased systolic blood pressure and heart rate and pupillary dilatation. When superficial pain is very severe; there will be generalized vasoconstriction of skin, skeletal muscles, brain and gastrointestinal tract due to autonomic reaction.
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.
Deep pain has either autonomic (organ pain) or somatic (deeper tissue pain) pathways to reach brain. It is dull aching or colicky or crushing or discomfort. Its localization is vague as representation in spinal column is common for skin and deeper structures. Deep pain is often associated with nausea, tiredness, sweating, pallor, decrease in blood pressure and heart rate (bradycardia). Skeletal muscles supplied by the same spinal cord segment may develop involuntary spasm due to deep pain.
Psychogenic pain: It may be functional/emotional/hysterical.
Other types of pain: Due to thalamic/spinothalamic diseases/causalgia [intense burning pain along the distribution of the partially injured (and healed) nerve] pain develops along the distribution.
Central pain: Central pain is the one which originates from the brain. It can be functional due to emotional or anxiety status or hysteria. It can be thalamic or spinothalamic lesions or originating from gray matter or hyperexcitability status of the brain even after etiology of pain is no more existing. Due to irritation of the central nervous system, there develops irritability, weakness, sleeplessness, loss of appetite, tachycardia.
Expression of the pain is related to the pain threshold. When, in certain area severe pain is present; pain in less severe area is masked. If pain threshold is less, pain intensity will be severe; if pain threshold is more, then pain may be less severe. Often to small extent body develops adaptation to pain. In acute pain, where patient is in shock (like in trauma/road traffic accidents) pain will not be felt for certain (shorter) period immediately after the event. It is due to sudden activation of sympathetic system as defence.
Features of Pain
Exact site, type and character, origin, time of onset, mode of onset, progression and end, duration, severity, movements of pain, aggravating or relieving factors and associated symptoms should be asked for.
Common features of pain | Specific features of pain |
|---|---|
| |
|
|
Specific Points in History in Relation to Pain
Original Site of Pain
Original site of the pain gives fair idea of the anatomical location of the origin of pain. It is very important in identifying probable site of pathology/cause. Pain in the epigastrium means pain is probably originating from stomach/duodenum/pancreas/left lobe of liver; pain in right hypochondrium means pain could be originating from gallbladder/liver; pain in groin means it could be due to hernia/lymph nodes/cord structures. One should also confirm whether pain is superficial (abdominal wall or surface in the skin or subcutaneous) or deep (intra-abdominal/intrathoracic/deep in the muscle or bone). Patient should point the site of the pain with one finger (index finger). Often pain may be in one site or multiple sites; if it is in multiple sites one should confirm where exactly pain started first and severity in each sites. In acute appendicitis original site of pain is in umbilicus; but later it shifts to right iliac fossa.
Time and Mode of Onset of Pain
It may be sudden onset, rapidly progressive in acute appendicitis; it is of insidious onset and of long duration with episodic nature in chronic peptic ulcer; pain after trauma means very important and may be an emergency like internal organ injuries (liver, spleen, and kidney) or due to fracture bone.
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 few hours after getting up. Cyclical mastalgia occurs premenstrually and gets relieved in oestrogenic phase. Mittelschmerz occurs between 12–14 days of menstruation is actually ovulatory pain in females. Dysmenorrhea presents as spasmodic pain in both iliac fossa often with low back pain; it occurs few days prior to menstruation and is relieved by menstruation.
Mode of onset may be dramatic wherein pain begins in few seconds reaches peak in minutes with severe intensity. It is seen in perforated duodenal ulcer, ruptured abdominal aortic aneurysm, torsion of ovarian cyst or of testis or mobile spleen. It may be acute onset if pain reaches its peak in hours usually due to acute inflammation like cellulitis, abscess, paronychia etc. In chronic onset pain begins insidiously reaches to its peak only few weeks to months from the onset—like pain of osteoarthritis (joint pain), pain due to spondylosis.
Type/Nature of Pain
It may be superficial/deep; localized or diffuse; 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 pain (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 (due to muscular contraction in a hollow tube in an attempt to obviate the obstruction by forcing the content out, which is gripping, and episodic associated 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.
Often patient perceives pain in different way; in such situation detailed history is needed to find right type of pain.
Colicky pain is sudden in onset, gripping nature (gripping nature is most important in colicky pain) which begins suddenly, and disappears suddenly. It has got two features; it comes and goes in a sinusoidal pattern; it is migrating constrictive and gripping in nature; it is due to spasmodic contraction of the hollow tube as forcible attempt to push the contents across the constriction or obstruction. Patient develops tachycardia, vomiting and sweating. It is either intestinal or ureteric or biliary or salivary (salivary calculus) or Fallopian tube or uterine in origin.
Distension pain is encircling and restricting the wall like of bowel/bladder, capsulated neoplasm or fascial compartment (leg/forearm/thigh/arm). It may cause tightness/bursting sensation.
Constricting pain occurs in chest, abdomen, limbs or head; it is like a iron band tightening in the part. Example is constricting pain of angina pectoris.
Stabbing pain is sudden, severe, sharp and for a short period.
Severity of the Pain
Pain may be mild/moderate/severe (agonizing, terrible). Severe pain wakes the patient suddenly from his sleep; stops him working further; makes him to roll around the bed; makes him restless and anxious; prevents him from getting proper sleep.9
Severe pain is common in acute appendicitis, acute pancreatitis, ureteric colic, perforation of bowel, acute peritonitis, intestinal obstruction, acute abscess.
Type and severity of the pain depends on the etiology for the pain and extent of the disease. It may be due to inflammation, abscess formation, nerve irritation, distension of organ, stretching of fascia or capsule, obstruction or infiltration by neoplasm.
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 or quickly reaches maximum and remains like that.
Pain progresses to maximum and may remain like that or it reaches maximum and suddenly or slowly disappear completely or severity may progress with waxing and waning (fluctuating pain) variably or pain progresses to peak, disappears fully and may reappear with original severity. In duodenal ulcer perforation initially severe pain appears for certain period later pain reduces but eventually becomes more severe. Initially leak of acid chemical into the peritoneal cavity causes pain which gets diluted by peritoneal fluid leads into reduction in pain but once bacterial peritonitis develops there is reappearance of severe pain.
Duration of Pain
Duration of pain should be mentioned in minutes/hours/days/weeks/months/years. It can be acute/subacute/chronic. Exacerbations of pain with period of remissions are common which should be mentioned. It is often seen in peptic ulcer, osteoarthritis. Colicky pain lasts usually for a minute in each episode; anginal pain lasts for 3–5 minutes; but an acute pain of pancreatitis persists.
Periodicity of Pain
Pain appears, persists for few weeks and then disappears for few weeks and again reappears. Such periodicity is often observed in chronic peptic ulcer; trigeminal neuralgia. Peptic ulcer pain may be seasonal. Migraine headache occurs once in few weeks or during menstruation in females.
Precipitating/Aggravating Factors
Abdominal pain may get worsened by taking food like in gastric ulcer. Pain due to appendicitis, ureteric stone aggravates in change of position, walking, jolting. Pain of urinary bladder stone aggravates in standing position. In reflux esophagitis pain increases while bending. Pain in pancreatitis increases on lying down. Pain in intervertebral disc prolapse aggravates by lifting the weight. Pain in sigmoid diverticulitis may increase by exercise or movement. Pain in gastritis aggravates by taking nonsteroidal anti-inflammatory drugs (NSAIDs). Peritonitis pain increases by coughing, deep breathing and moving abdomen. Ischemic claudication pain aggravates by walking. Cardiac angina aggravates by exertion.
Relieving Factors of Pain
Pain reduces by certain methods and so patient uses those methods 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 position. Propped up position relieves pain of reflux esophagitis. 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 hematuria; biliary colic with jaundice and pale stool are other examples of such association. Ruptured ectopic pregnancy, aortic aneurysm have severe pain with severe pallor.
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 back. In ureteric colic pain radiates from loin to groin; frequently to testis in male. In myocardial infarction, pain develops in the left side chest which eventually radiates towards left side neck and left upper limb.
Referred pain: Pain is not felt at the site of the disease but felt at distant site. It is due to common area of representation in brain for visceral and somatic components and inability of brain to differentiate between two sites. Diaphragmatic irritation causes referred pain at the tip of shoulder as the segmental supply of diaphragm (phrenic nerve C4, C5) and shoulder (cutaneous supply—C4, C5 through supraclavicular nerves) is same. Hip joint pathology may cause referred pain in knee joint—through articular branches of femoral, obturator and sciatic nerves. Other examples—referred pain in ear 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. Foregut pain refers to upper abdomen in the midline; midgut in the middle of the umbilical region; hindgut to lower abdomen in the midline. It is through the corresponding somatic area of the skin in relation to corresponding visceral nerve distribution.
Shifting of pain: Origin of pain is at 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) which shifts later to right iliac fossa when once the parietal peritoneum of that area is inflamed.
Migration of pain: It is a feature of spreading inflammation from one site to adjacent/distant site. In perforated duodenal ulcer duodenal content later spills over the right paracolic gutter and so pain from epigastrium shifts downwards with spread of peritonitis; in perforated/burst appendicitis initial right iliac fossa pain migrates towards left iliac fossa indicating spreading of peritonitis (peritonitis initially localized becomes generalized).10
Hiccup (Singultus)
It is spasmodic contraction of diaphragm. It is commonly idiopathic which subsides on its own.
Types
- Postoperative hiccup is common. It is due to increased abdominal pressure, pushing the under surface of the diaphragm upwards. It may be due to paralytic ileus, gastric dilatation, and intestinal obstruction.
- Peritonitis involving diaphragmatic surface can cause hiccup.
- Renal failure (usually advanced one) causes hiccup. Typical facial look, brown dry tongue with typical pallor; edema face and feet may be obvious. Blood urea, serum creatinine and electrolytes should be done.
Vomiting
Vomiting is a common symptom heard in clinical practice.
It may be due to—pregnancy, traveling sickness, labyrinthitis, gastritis, peptic ulcer, migraine, meningitis, intracranial tumor, ureteric colic, pyloric stenosis, carcinoma stomach (pylorus), intestinal obstruction, intracranial space occupying diseases, acute peritonitis, cholecystitis, pancreatitis, metabolic causes like diabetic ketosis, and drug induced.
- Color, quantity, smell of the vomitus should be asked. Coffee ground colored vomitus is seen in upper GI bleed. When bled blood comes in contact with gastric juice, hemoglobin forms acid hematin coloring content blackish or dark brown. Vomitus may contain frank blood/clots.
- Presence of undigested material should be asked for.
- Esophageal obstruction by achalasia cardia or stricture causes regurgitation.
- Nonbilious vomiting means obstruction proximal to sphincter of Oddi.
- Bilious vomiting occurs in small bowel obstruction; which may be either yellow or green colored.
- Fecal content in the vomitus suggests ileal/large bowel obstruction. Feculent vomiting is also seen in gastrocolic fistula. Content is brown in color with fecal odor.
Nausea
It is sense (feel) of vomiting. It may or may not end up with vomiting. It can be none (0); nausea present but able to eat (1); oral intake is reduced (2); No oral intake, on IV fluids (3).
Itching (Pruritus)
It is due to local or general causes. Multiple scratch marks are often obvious.
It may be due to:
- Skin diseases: Utricaria, eczema, scabies (Psoriasis will not cause itching).
- Local causes: Clothing, washing soap, washing powder, fungal, parasites like fleas, scabies; vaginal and rectal discharge.
- Systemic causes: Obstructive jaundice due to bile acid irritation, Hodgkin's disease, leukemia, uremia, allergy/hypersensitivity, drug reactions, diabetes mellitus, etc.
- Allergic reactions: Drugs can cause itching.
Fatigue
It is subjective sensation of weakness (asthenia/lethargy). It is graded as none (0); fatigue over baseline (1); moderate fatigue (2); severe (3); bedridden (4).
Anorexia
It is loss of appetite: it is seen in anorexia nervosa, gastrointestinal (GI) cancers, tuberculosis, debilitating illness like sepsis. Anorexia is graded as none (0); loss of appetite (1); significant reduction in oral intake (2); unable to take orally requiring IV fluids (3).
Satiety is sense of fullness after completion of meals. It is normal. Early satiety is a feature of GI malignancy; patient feels full and satisfied with small quantity of food.
Flatulence and Regurgitation
- Flatulence is frequent belching more than normal.
- Regurgitation is effortless return of food into the mouth. It is associated with powerful involuntary contractions of abdominal muscles. It is seen esophageal/OG junction obstructions like carcinoma and achalasia cardia.
- Heartburn is burning sensation behind the sternum due to acid reflux into the esophagus.
Defecation
Frequency, physical characters of the stool, pain during defecation should be asked for. Stool may be brown/black/pale/white/silvery in color. It may be hard/soft/watery in consistency. It may be bulky/pellets/string or tape like. It may contain blood; blood may be mixed with stool or on the surface of the stool or may appear after passing stool. Stool may be mixed with mucus or pus. Pain may be before or after defecation or throughout the defecation.
Constipation
It is defined as having bowel movement fewer than three times per week; with hard, dry, small sized stool; difficult to evacuate. It is graded as none (0); needs diet modification (1); needs laxatives (2); needs manual evacuation or enema (3); due to obstruction (4).
- Constipation can be relative wherein patient can pass flatus but not feces; or absolute wherein patient neither can pass feces nor flatus.
- Constipation can occur due to many causes—habitual, congenital cause like congenital megacolon (Hirschsprung's disease), anorectal malformations and acquired causes like colonic carcinoma, stricture.
Diarrhea
Diarrhea is defined as more than 3 stools per day, containing 300 mL or more of fluid per day. It is usually soft, often foul smelling. Often it may be associated with incontinence. It is graded as frequency of 3–4 times/day (1); frequency 4–6/day (2); frequency >7/day or with incontinence or need parenteral nutrition (3); needs intensive care with hemodynamic collapse (4).
- Surgical causes of diarrhea: Intestinal tuberculosis, carcinoma colon, amoebic infection, intestinal resection, ulcerative colitis, irritable bowel syndrome.
- Diarrhea may be acute onset or chronic; it may be watery/bloody/mucus/bloody mucus/dysentery/painful diarrhea/painless/early morning diarrhea.
- Steatorrhea is copious, frothy, pale stool.
PHYSICAL EXAMINATION
It should be done in privacy. Female patients should be examined in presence of a female/nurse. Examination should be done with limited clothing to elicit proper findings. Broad day light is ideal for examination. Usage of other lights may mislead or mimic some clinical findings like jaundice (Figs. 1-6 to 1-9).
General Examination
This part of the examination is essential preliminary step in all patients. Patient's intelligence level should be assessed while taking history. Uneducated people can still be intelligent.
General examination is done for proper diagnosis and differential diagnosis; for selecting the patient for anesthesia; to decide type of surgery to be done (mesh hernioplasty is done in inguinal hernia if patient is having chronic respiratory disease or if there is poor abdominal muscle tone); to predict the prognosis (patients with gastrointestinal cancer showing palpable supraclavicular lymph node means poor prognosis). It usually includes—looking for pallor, pulse, respiration, edema feet, clubbing, cyanosis, jaundice, blood pressure. Each will be discussed in detail.12
Figs. 1-6A and B: Both sides should be examined and compared like—in limbs (hands, feet, forearms, arms, joints), eye, ears, face in bilateral anatomical areas.
Fig. 1-7: Systemic examination is a must. Note the chest wall swelling in this patient. Clothings should be removed properly while examining the patient. This swelling may be due to secondary in the rib or primary tumor.
Mental Status
Mental status and level of consciousness should be assessed in general but in particular in specific clinical situations like head injury, hepatic encephalopathy, septic shock, etc.
Grading of the mental status | |
Grade I | Properly oriented in time, space and person |
Grade II | Conscious but without orientation of time, space and person |
Grade III | Drowsy and semiconscious |
Grade IV | Unconscious but responding to painful stimuli |
Grade V | |
Built and Nutritional Status
Built and nutritional status of the patient is important to assess.
Built is structural organization of underlying skeleton. It is related to age and sex of the patient. Gigantism is height to that age is in excess than normal (in adult more than 6.5 feet). It may be due to racial; familial; endocrinal (hyperpituitarism, hypogonadism); genetic (Klinefelter's syndrome); metabolic (Marfan's syndrome, homocystinuria); overeating; cerebral causes. Dwarfism is height to that age and sex is far less than normal (below 4.5 feet). It can be due to hereditary, chromosomal (Turner's syndrome, Down's syndrome); delayed growth; nutritional (Rickets); endocrinal (hypopituitarism, hypothyroidism, excess androgens, congenital adrenal hyperplasia, insulin insufficiency); skeletal (achondroplasia, spinal deformities); systemic diseases (uremia, cyanotic heart diseases, cirrhosis).
In normal adult, height of the person is equal to length of arm span. Upper segment from vertex to pubic symphysis is equal to lower segment from pubic symphysis to heel.
In infants upper segment is more than lower segment and height is more than arm span. This infantile body frame persists in achondroplasia, cretinism, and juvenile myxedema.
Greater arm span than height and greater lower segment is observed in Marfan's syndrome, homocystinuria, Klinefelter's syndrome, Frohlich's syndrome.
Nutrition is the proportion of soft tissue structures (muscles, soft tissues, fat) in relation to the bony structure. In gastrointestinal malignancy or in other malignancy with metastases patient will be cachexic. Protein deficiency causes rough skin, brittle hair, and edema feet. Fat deficiency causes cachexia, hollow cheeks, and loss of fat in hips, abdomen and subcutaneous tissues of elbow. Deficiency of minerals and vitamins has got specific features.
Severe malnutrition causes wasting of muscles, ill skeletonized look. Reduced weight, loss of subcutaneous fat, edema (generalized), alopecia, decreased hand grip and respiratory muscle power are features.
Assessment of nutrition body mass index (BMI) which is weight in kilogram divided by height in meters square. BMI less than 18.5 suggests malnutrition. Triceps skin fold thickness, mid arm muscle circumference are other tools used to assess malnutrition. Biochemical estimation of serum albumin, prealbumin, transferrin and retinol binding proteins are useful (Figs. 1-10A and B).
Example: If body weight is 80 kg and height is 1.8 meter; then BMI is 80/1.82 = 80/3.24 = 24.69.
Obesity may be due to idiopathic cause (more intake), mental retardation, alcohol intake, genetic, hypothalamic causes, endocrine (thyroid/parathyroid/adrenal disorders), testicular atrophy, drugs like insulin, oral antidiabetics, steroids, estrogens.
Body Weight
Body weight is controlled by rate of energy expenditure; it is regulated by energy-related hormones. Neuropeptide Y present in the nervous system promotes anabolism by stimulating the secretion of the insulin. Corticotropin-releasing hormone has got catabolic activity. Hypothalamus controls the energy reserve in body.
Nutritional status | BMI (kg/m2) |
Underweight Normal Overweight (Preobesity) Obesity
Superobesity Super superobesity | <18.5 18.5–24.9 25.0–29.9 >30
>50 >60 |
Weight Gain
It is increase in weight. It is graded as <5% (0); 5–10% (1); 10–20% (2); >20% (3). It is seen in obesity, pregnancy, myxedema, water retention, Cushing's syndrome. Weight gain also occurs in liver/kidney/cardiac failures, hypoproteinemia, lymphedema, increased muscle mass by anabolic steroids, hormone-related causes; ovarian cyst, etc.
Weight Loss
- Weight loss is graded as <5% (0); 5–10% (1); 10–20% (2); > 20% (3). But time duration of weight loss is also important.
- Definition of significant weight loss (2009): Weight loss more than 5% (up to 7.5%) in 30 days; weight loss more than 7.5% (up to 10%) in 60 days; weight loss more than 10% in 180 days.
- Weight loss can occur with adequate food intake or with diminished food intake.
- Weight loss is assessed by loosening of clothes; clothes mainly trousers at waist will be too commodious.
- It can be due to increased utilization—like thyrotoxicosis, anxiousness, drug induced; decreased absorption—like chronic pancreatitis, carcinoid disease, hypermotility of bowel, short bowel syndrome; abnormal calorie loss—like gastrointestinal fistula, worm infestations, diabetes.
Causes are—anorexia nervosa, depression, psychosis, gastric ulcer, colitis, worm infestations, liver/biliary/pancreatic diseases, gastrointestinal malignancies, surface malignancies with visceral spread, leukemia, lymphoma, sarcoma with spread, chronic bacterial infections, tuberculosis (pulmonary or erxtrapulmonary like abdominal, urinary), autoimmune diseases like rheumatoid arthritis, systemic lupus erythematosus, alcohol intake, smoking, Addison's disease, chronic lung and cardiac diseases, acquired immune deficiency syndrome (AIDS), chronic renal failure [CRF/CKD (chronic kidney disease)].
Wasting
It is obvious on the upper half of the body as there is often edema due to hypoproteinemia in lower half of body. It is observed in starvation, severe gastroenteritis, tuberculosis, anorexia nervosa, diabetes mellitus, advanced carcinomas, gastrointestinal malignancies, and old age.
Severity of wasting can be assessed by looking at shoulder girdle, loose skin of arms, trunk and buttocks (Fig. 1-11).
Nutritional deficiency is assessed by skin texture, arm circumference, muscle mass, body weight, BMI (Figs. 1-12A and B).
Malignant Cachexia
Here the patient looks emaciated, languid, sallow, with pale face, loose wrinkled skin, loss of fat, dry skin, with lost appetite/weight/energy and with oral infection—candida and stomatitis. Profound loss of weight is typical. Usually they do not experience any pain (Figs. 1-13A and B).
Attitude of the Patient
It is typical changed position of the body or part of the body like limbs. In posterior dislocation of hip, limb is shortened and internally rotated. Comatose patient/paraplegic or quadriplegic patient is silent and immobile. Patient in shock or with peritonitis may not move due to pain. Patient with ureteric stone may be restless and rolling in the bed due to severe colicky pain. Different attitudes in different fractures of the limbs are typical and useful in diagnosing the site of fractures.
Figs. 1-13A and B: Typical malignant cachexia—emaciated, languish, sallow and pale look with dry wrinkled skin.
Decubitus of the Patient
Position of the patient in the bed is called as decubitus. Decubitus is derived from the Latin word decumbere means ‘to lie down’. First part of the body on which patient is rested is followed by the word decubitus; hence right lateral decubitus means the patient is lying on his right side (left side up) and left lateral decubitus means patient is lying on his left side (right side up) (Figs. 1-14 and 1-15).
- It is often typical in certain diseases like cerebral irritation, cerebral palsy, etc. In hemiplegia patient lies with one side immobile, with affected arm flexed and legs externally rotated and extended. In tetanus patient develops stiff neck. In ureteric colic, patient is restless with rolling and tossing over the bed. In acute peritonitis patient lies in the bed still and motionless. In cardiac diseases, patient is comfortable in sitting up position. In pneumonia, patient lies on the affected side to make that side immobile and restricted so as to reduce the pain.
- Rigid dorsal decubitus is seen as patient lying on back immobile with flexion of both hips.
- Decubitus in tetanus are opisthotonus (spine arching backwards with body resting on head and feet—common); orthotonus (straight); pleurosthotonus (lateral bending); emprosthotonus (forward bending). Opisthotonus is also seen in meningitis, strychnine poisoning, uremia, rabies.
- In cardiac diseases patient attains left lateral position to allow expansion of the liver capsule.
- Lateral decubitus with curled up body is called as ‘coiled up decubitus’. It is observed in colicky abdomen of any cause and cerebral irritations.
- Decubitus in thromboangiitis obliterans (TAO)—is sitting on the bed with flexion of hip, knee and holding foot in both palms.
- Kneeling prayer's decubitus in orthopnea is typical as patient kneels forward in the bed holding a pillow. It kinks the iliac veins to reduce the venous return to the heart. Squatting decubitus is seen in cyanotic heart disease (Fallot's tetralogy).
Stature of the Patient
It is the total height from vertex to sole. Stature may be short or tall.
- Turner's syndrome is seen in females with only one X chromosome (it is XO instead XX) having short stature, narrow pelvis and wide shoulder with webbing; widened neck with prominently running skin fold from neck to shoulder.
- Achondroplasia is often called as circus dwarf with large head, flat nasal bridge, stunted trunk, hand and fingers with waddling gait.
- Rickets shows bow legs, scoliosis, rickety rosary, Harrison's transverse sulcus across rib cage.
- Tall stature is seen in Klinefelter's syndrome [(extra X chromosome as XXY instead XY) in males with low testosterone levels, presents with female distribution of fat in pelvis and breasts but normal hairs in face and pubis with small testes and azoospermia (low sperm count)]; Marfan's syndrome (mucopolysaccharides abnormality); hypogonadism; thyrotoxicosis; adrenal disorders; hypothalamus diseases; familial and nutritional.
Posture of the Patient
It is positional relationships of different parts of the body. Posture of the body is observed in standing, sitting as well as in recumbent position. Normal posture is—moderate lordosis of cervical and lumbar spine; kyphosis of thoracic and sacrococcygeal region; forward pelvic inclination 30°; normal rotation of femur; line from the mastoid down passes through the middle of the shoulder and hip, anterior to knee and lateral malleolus.
Gait of the Patient
Gait is the typical way which the patient walks. He is made to walk in a straight line for at least 8–9 meters. While walking, positions of the body, upper and lower limb movements, regularity and smoothness of movements, distance between the feet are all observed.16
- Abnormal gait may be due to mechanical or structural abnormality [congenital dislocation of hip (CDH) or poliomyelitis]; pain (osteoarthritis); altered muscle tone (hemiplegia, foot drop with high stepping gait); psychological.
- Waddling gait is seen in bilateral congenital dislocation of the hip and bilateral coxa vara; Trendelenburg gait is seen in Legg Calve Perthes’ disease, arthritis of hip, poliomyelitis, unilateral coxa vara; high stepping gait in foot drop; circumduction in hemiplegia; festinating gait in Parkinson's disease. Other gaits are—spastic gait, ataxic gait, stuttering gait, antalgic gait in avoiding pain.
- Limp is dragging of the limb during walking.
Face Look/Facies
Face reveals the inner emotions of the mind and body going through. It is the mirror of mind. Typical face is diagnostic of some diseases. Deformity of face as congenital is often obvious (Fig. 1-16).
Different facies (Face/gum look) |
Hippocratic facies: It is seen in patients with acute severe peritonitis with terminal illness. Features are sunken bright eyes, pinched nose, dry, shrivelled tongue, crusted lips, cold clammy forehead, distended abdomen with features of peritonitis. Adenoid facies: High vaulted palate, narrow dental arch, protruding incisor teeth, earlier was considered as feature of enlarged adenoid is now not accepted. In fact, these features are familial anomaly; nasal obstruction, oral breathing leading into wide opened mouth in a child. Risus sardonicus: Face of tetanus with trismus—painful smiling. It is due to contraction of zygomaticus major muscle in face leading to sardonic smiling face (Sardinia plant when eaten is supposed to produce convulsive laughter ending in death; sardonic means mockery). Facies of cretinism: Cretin is a neonate with deficient thyroid hormone (cured by thyroid hormone supplement); pale, puffy, wrinkled face; dry cold skin; protruded tongue; open anterior fontanelle; palpable (in endemic type) or impalpable (in sporadic type gland is atrophic) thyroid gland; diagnosed at birth; with broad flat face and nose, wide apart eyes with thick eyelids, protruded tongue with widely open mouth, with dull facial expression. Face of myasthenia gravis: Unilateral or bilateral intermittent ptosis; drooping jaw; sneering smile face due to reduced action of risorius and zygomatic muscles; here weakness of all muscles is found; in particular of eyelids showing drooping of eyelids with weakness of the face muscles and jaw; lagging of eye lids due to fatigue and ‘myasthenia smile’ due to weakness of risorius and zygomatic muscles—are typical. Facies of congenital syphilis: Bossing of frontal bones; interstitial keratitis; Hutchinson's teeth; saddle nose. Facies of hepatic cirrhosis: Sunken eyes; jaundiced sclera; watery conjunctiva; dull diffusely pigmented sallow face. Moon face of Cushing's syndrome: Rubicund (red) round face like of full moon; pursed lips; with hirsuitism. Virile facies: In a woman suffering from adrenocortical hyperplasia or tumor is typical (face looks like that of men). Carcinoid facies: Typical facial flushing seen in metastatic carcinoid tumor. Face with typical pale look with half bloated and partially closed eyes is seen in chronic renal failure. Mask face is seen in Parkinsonism; it is due to muscular rigidity of skeletal muscles including of face; but ocular muscles are not involved and so eye movements are normal but with stare. Acromegaly (due to increased growth hormone in pituitary acidophilic adenoma) shows large face due to overgrowth of soft tissues in face, nose, tongue, air sinuses; large hands (due to enlargement of bones of distal phalanges)—facies of ‘Punch and Judy’ or an ‘Ape man’. Skin is greasy; mental acumen is normal (in myxedema, skin is dry with decreased mental acumen). Lower teeth project in front of the upper; the tongue is enlarged and so mouth is kept open. Down's syndrome/Mongolism is a congenital abnormality with extrachromosome 21 and total chromosomes 47 (instead of 46); males and females and all races are equally affected. Features are—mental retardation, floppiness, short stature, upward slanting of outer ends of the palpebral fissures slant upwards with prominent epicanthic folds, flat face, protruded tongue and squint. Face of myxedema shows dull face, rose purple flush over the cheek, eyelid puffiness, with loss of hairs over the lateral 1/3rd of the eyebrow (lateral madarosis), swollen lips and enlarged tongue. In scleroderma, progressively thickened, pale, waxy skin with reduced facial expressions, microstomia, telangiectases on cheeks, mouth and nose, with fine white horizontal scars in the neck in transverse skin creases (with esophageal stenosis and vasculitis) are seen. Tabetic facies—drooping of upper eyelid; wrinkling of the forehead; sad expression. Face in Wilson's disease (hepatolenticular degeneration)—face of fixed emotion. Face in lupus erythematosus—butterfly erythema over bridge of nose and cheek. Face in Addison's disease—generalized darkening of the skin of face along with the pigmentation of the mucous membrane of mouth. Face in Addisonian pernicious anemia—‘Lemon yellow’ face. Face in primary polycythemia—red discoloration of the nose, lips, ears and palpebral conjunctiva. Facial look are typical in chronic alcoholic, drug addict, depressed or anxious individuals. Scars, discoloration, discrepancies, swellings in the face should be observed and examined. Discoloration may be due to underlying hemangiomas (Fig. 1-17). Gums and teeth should be examined for redness, carious teeth, gum hypertrophy, loosened tooth, etc. (Fig. 1-18).17 |
EXAMINATION OF SKIN AND MUCOUS MEMBRANE
It is the largest organ of the human body with surface area of 2 m2 and weight of 4 kg. Many of underlying diseases reflect on the skin with different features. It is assessed by changes in color, texture and surface. Common color changes are pallor, cyanosis and jaundice. Color of the skin (brown/black) is determined by pigment—melanin. Generalized pigmentation is seen in Addison's disease. Localized pigmentation can occur in varicose vein disease, hematological diseases, naevus and malignant melanoma.
Figs. 1-19A and B: Lower eyelid is retracted to see the conjunctiva for pallor. Note the normal conjunctiva and conjunctiva with pallor.
Pallor
- Causes for pallor are—anemia, massive bleeding, shock and anxiety status.
- Pallor is common in tuberculosis, malignancy, renal failure, myxedema, sepsis, malaria, malnutrition.
- It is checked in lower palpebral conjunctiva, mucous membrane of lips and cheeks, nail beds and palmar creases (Figs. 1-19A and B).
Pigmentation of Skin
It is usually an increase in natural brown pigmentation of the skin. It is determined by the pigment melanin the amount of which is under the influence of hereditary or environmental factors. Often pigmentation by other colors like blue/red also can occur.
Pigmentation can be generalized or localized.
- Localized: It occurs in pregnancy (around areola, midline abdomen); venous diseases of lower limb (medial third of leg and ankle); erythema eb agne (in the exposed part of leg); ultraviolet and high voltage irradiation; café au lait spots of neurofibromatosis; naevi; melanomas; pellagra (nicotinic acid deficiency); hyperthyroidism (bronzing of eyelids); rheumatoid arthritis.
- Depigmented patches are seen in leprosy. There may be loss of sensation, deformities also (Fig. 1-20).
Cyanosis
It is due to increased reduced hemoglobin in the blood causing blue/purple discoloration of the skin and mucous membrane. A minimum of 5 g/dL of reduced hemoglobin should be present in the circulation to cause cyanosis. So in severe anemia (Hb% below 5 g%), cyanosis is not seen.
Two types of cyanosis are observed—peripheral and central.
- Peripheral cyanosis is due to poor perfusion of peripheral vessels causing reduction in oxyhemoglobin in the capillaries. It is seen in peripheral vasoconstriction due to any cause like exposure to cold temperature, reduced cardiac output, profound shock where blood is diverted from periphery to vital organs like brain, liver, and kidney. Peripheral cyanosis is checked in nail bed, palm and toes, tip of the nose. Here limb is cold and inhaling pure oxygen may not reduce it. Tongue is not involved in peripheral cyanosis.
- Central cyanosis occurs due to reduced oxygen saturation of arterial blood as a result of poor oxygenation in the lungs. It may be due to congenital heart disease with left to right shunt (cyanotic heart disease), congestive cardiac failure, lung diseases, and low oxygen partial pressure in high altitude. Limb temperature is normal in this type. Clubbing and polycythemia is common here and pure oxygen inhalation reduces the central cyanosis. It is confirmed by checking the tongue, nail bed, palms and toes. Central cyanosis is due to arterial hypoxemia (chronic obstructive pulmonary disease/COPD), pulmonary fibrosis, pulmonary embolism, pulmonary edema or pneumonia); or due to arterial hypoventilation due to mechanical chest wall causes, hypoventilation, laryngeal obstruction, malignancy. Congenital cyanotic heart diseases, left sided cardiac failure are cardiac causes of central cyanosis.
- Methemoglobinemia or sulphemoglobinemia (abnormal pigments) also causes cyanosis but with normal arterial tension.
- In carbon monoxide poisoning, carboxyhemoglobin prevents reduction of oxyhemoglobin and so there will not be any features of cyanosis but cherry-red discoloration is seen. Here mixed (both central and peripheral) cyanosis develops. Hemoglobin here contains iron in ferric +3 rather +2 ferrous form. It is a pigmentary cyanosis. Mixed cyanosis often is also seen in cor pulmonale. Lung fibrosis and emphysema causes central cyanosis; right-sided failure or congestive cardiac failure causes peripheral cyanosis.
- Local cyanosis develops in peripheral vascular diseases like Raynaud's phenomenon, thromboangiitis obliterans (TAO), venous diseases.
- Differential cyanosis: Patent ductus arteriosus (PDA) with reversal of shunt causes only lower limb cyanosis. PDA with reversal of shunt with transposition of great vessels causes only upper limb cyanosis. PDA with reversal of shunt with preductal coarctation of aorta causes cyanosis of left upper limb and both lower limbs (Fig. 1-21).
Note: Cyanosis is clinically evident when reduced hemoglobin is 5 g% or more or methemoglobin is 1.5 g% or sulphemoglobin is 0.5 g%.
Polycythemia
It is excess of circulating red blood cells giving the patient a purple-red florid appearance; it heightens the color of all the skin, cheeks, neck, backs of hands and feet whereas cyanosis is limited to tips of hands, feet and nose.
Jaundice/icterus
(Icterus is a purely a clinical term; jaundice is biochemical finding of raised serum bilirubin).
It is yellowish discoloration of skin and mucous membrane. Serum bilirubin level more than 2 mg/dL causes yellowish discoloration. Tissues and body fluids are also discolored yellow. Bilirubin has more affinity to elastic tissue, blood vessels and nervous tissue. So it is better seen in sclera and skin. During recovery, bilirubin takes longer time to get cleared from elastic tissue and so clinical jaundice persists for little longer time than biochemical disappearance of jaundice.
Initially it is pale lemon yellow color, later gets darkened, becomes yellow-orange, olive greenish yellow as seen in obstructive jaundice. Jaundice is due to deposition of bile pigments with excess of it in plasma. Greenish color is due to deposition of biliverdin.
It is checked in upper sclera (better seen against white background; by asking the patient to look at his feet and clinician pulls the upper eyelid upwards). It also can be checked in nail bed, ear lobule, nasal tip, and under surface of the tongue. It is checked using normal daylight instead of torch light (Figs. 1-22A to E).
Scratch marks observed on the dorsum of the body (forearm, neck, back) is due to deposition of bile acids which release excess histamine causing itching.
Jaundice may be due to prehepatic cause (excess hemolysis); hepatic (liver dysfunction—hepatitis, sepsis, drugs, cirrhosis); posthepatic (CBD stones, carcinoma pancreas, drugs—obstructive); congenital hyperbilirubinemia (Gilbert's syndrome causing altered bilirubin transport and so increase in unconjugated bilirubin; Criggler-Najjar syndrome causing disturbance in bilirubin conjugation and so increase in unconjugated bilirubin; Dubin Johnson syndrome and Rotor's syndrome causing disturbance in excretion of bilirubin and so increase in conjugated bilirubin).
Figs. 1-22A to E: Jaundice/icterus is checked in sclera by asking the patient to look on the feet and examiner pulls up the upper eyelids. It is also checked on palate, under surface of the tongue, finger tips, in nasal tip and ear lobule.
Aged red cells get lysed in the reticuloendothelial cells and breakdown into haem and globin. Haem is divided into globin and bilirubin. Bilirubin is combined with albumin and transported to liver. In the liver bilirubin get separated from albumin and conjugated to bilirubin glucuronide by glucuronyl transferase. This conjugated bilirubin glucuronide is water soluble and can be excreted in kidney (So in obstructive and hepatic jaundice bile pigment—bilirubin is seen in the urine). This conjugated bilirubin is excreted through biliary canaliculi reaching intestine. In the intestine, it is converted into stercobilinogen and urobilinogen by intestinal bacteria. 70% of this is absorbed in the colon and brought back to liver via enterohepatic circulation. Unabsorbed stercobilinogen colors feces brown. Circulating urobilinogen is taken up by kidneys for excretion. If direct bilirubin in the serum is more than 0.4 mg%, then bilirubin is seen in urine. Normal urinary urobilinogen is 100–200 mg/day. It is absent in obstructive jaundice. Normal fecal stercobilinogen is 300 mg/day. It is also absent in obstructive jaundice (Fig. 1-23).
Hypercarotinemia
It mimics jaundice and is due to increased yellow pigment carotene. It is seen equally on face, palm, sole and skin but not seen in sclera. It is common in vegetarians who eat more raw carrot. Mepacrine therapy also causes yellow discoloration.
EXAMINATION OF NAILS
Nail is a skin appendage made up of keratin containing nail plate, matrix with bed underneath. Nail plate is the main body which is made of layers of flat dead cells, containing keratin; its shape is due to the curvature of distal phalanx underneath. Proximal growing alive part is called as nail matrix which produces cells to form eventual nail plate. Whitish crescent shaped base of the nail is called as lunule. Nail bed contains epidermis and dermis with capillaries, nerves and lymphatics. Between epidermis and dermis of the nail bed tiny grooves are present which are called as matrix crests. Epithelium beneath the tip of the nail plate is called as hyponychium; both are attached by a band called as onychodermal band. Proximal most part is embedded in the nail sinus and is called as nail root. A band of epithelium called as eponychium overhangs the nail root in front with cuticle as its distal margin (Figs. 1-24A and B).
Skin fold overlapping the lateral margins of the nail is called as nail wall. Tissue around the margins of the nail is called as paronychium which is the site of paronychia infection. Rate of growth of nail is 3 mm/month. Nails of fingers regrow completely after removal in 6 months; nails of toes take 12–18 months to regrow completely. Fingernails grow 4 times faster than toenails. Nail of index finger grows faster.
Deformities of the Nail
- Pallor can be seen in nail bed. In iron efficiency anemia (Plummer Vinson syndrome) nails may be brittle/flat (platynychia)/spoon shaped (kolionychia) (Figs. 1-25 and 1-26).
- Splinter hemorrhages are seen in nail bed in bacterial endocarditis, bleeding disorders.
- Discolored, deformed, pitted nails are seen in psoariasis.
- Hypoalbuminemia causes whitening of the nail bed—Terry's sign.
- Specific discolorations are seen in Raynaud's disease, silver and mercury poisoning.
- Ribbing, brittleness, falling of nails are seen in syringomyelia, leprosy and tabes dorsalis.
- Nail bed infarcts are seen in vasculitis due to SLE or polyarteritis.
- Onychogryphosis (in toe) is heaping up of nail and curling over the end of the toe due to failure of normal sliding mechanism of the nail and is due to trauma or old age (Figs. 1-27A and B).
- Ingrowing toenail is common in margins of the nail of great toe where irregular edge of the nail grow beneath the lateral nail fold due to improper trimming of the nail causing repeated pain and infection.
- Dry, brittle, fragile dark nails are seen in vitamin A, B (B12), D and calcium deficiency. Deficiency of protein, folic acid, and vitamin C causes hangnails. Linoleic acid deficiency causes splitting and flaking of the nails.
Figs. 1-25A and B: Nails should be examined both in hands and feet (fingers and toes) for change in color, splinter hemorrhage, clubbing, pallor, koilonychia and other features.
Figs. 1-26A and B: Changes in the toenail also should be observed. Note the pallor and koilonychia in the toenails.
- In uremia, nails become dull white proximally with distal brown portion with a well-demarcated transverse line of separation—Lindsay line.
- White nail is seen in hypoalbuminemia (leuconychia of cirrhosis); red nail (red half moons) in congestive cardiac failure; blue nail is in Wilson's disease; black nail in Peutz-Jeghers/Cushing's syndrome or Addison's disease. Leukonychia striata is white patches in nail and leukonychia punctata is white dots in nail—are of no pathological significance. Yellow nail syndrome has got slowly growing curved yellowish or yellowish green nails in association with lymphedema, bronchiectasis or pleural effusion.
- Nails are absent or hypoplastic since birth in ectodermal dysplasia, a familial condition. Scarring and loss of nails occurs due to repeated blistering of fingertips in epidermolysis bullosa, a genetic disorder.
- Scarring and destruction of the nailbed is called as pterygium of nail which is seen in lichen planus (Fig. 1-28).
- Onycholysis is whitening of the distal nail, seen in psoriasis, thyrotoxicosis due to separation of the distal nail plate.
- Onychorrhexis is softening or brittleness of nailbeds, commonly seen in females due to constant wetting of nails.
- Onychauxis is hypertrophy of nails.
- Onychia is deformity of the nail—seen in fungal infection or tuberculosis. It is due to inflammation of nails.
Clubbing (Hippocratic Fingers)
It is bulbous enlargement of soft parts of the terminal phalanges with both transverse and longitudinal curving of the nails. It is due to interstitial edema and dilatation of the arterioles and capillaries. There is loss of normal angle between surface of the nail and the skin covering the nail bed.
When a normal nail is viewed from side, plane of the nail and the plane of the skin covering the base of the nail bed form an angle of 130–170° (Lovibond angle). In clubbing tissue hypertrophy beneath the nail bed makes the base of the nail bulge upwards distorting the nail growth causing nail to be curved in both directions. So in clubbing plane of the nail and plane of the skin covering the nail bed form an angle which is greater than 180°.
Causes of Clubbing
- Causes: It can be pulmonary (Carcinoma bronchus, lung abscess, bronchiectasis, tuberculosis with secondary infection); cardiac (cyanotic congenital heart disease, infective endocarditis); gastrointestinal (ulcerative colitis, Crohn's disease, cirrhosis); endocrinal (myxedema, acromegaly, exophthalmic ophthalmoplegia—thyroid acropachy); other causes (hereditary, idiopathic), unilateral in Pancoast tumor, subclavian/innominate artery aneurysm: unidigital in trauma or tophi deposition in Gout, only in upper limbs in heroin addicts due to chronic obstructive phlebitis.
Causes of Clubbing | |||||
Respiratory | Cardiac | Abdominal | Mediastinal | Extrathoracic | Others |
|
|
|
|
|
|
Figs. 1-29A and B: Schamroth's sign. When distal phalanges of the two index fingers (or opposing fingers) are held in apposition, a closed triangular space (diamond-shaped gap) will form in normal individual, but will be absent in clubbing; it is due to widened distal phalangeal depth (DPD) than distal interphalangeal depth (DID).
- Disappearance of diamond-shaped gap between nails when fingers are apposed is called as Schamroth's sign (Figs. 1-29A and B).
- Pathogenesis: Hypoxia leads to opening up of deep arteriovenous fistulas which increase the perfusion of the fingers and toes causing its hypertrophy. It may be due to reduced venous blood ferritin which escapes oxygenation in the lungs, which after entering the systemic circulation stimulates dilatation of arteriovenous anastomosis leading to hypertrophy and clubbing of terminal phalanx (Figs. 1-30A to E).
- Hypertrophic pulmonary osteoarthropathy is severe clubbing with subperiosteal bone thickening and thickening of the synovium which is often associated with lung cancer.
- Pseudoclubbing is seen in hyperparathyroidism and is due to undue bone resorption resulting in disappearance of terminal phalanges causing telescoping of soft tissues into the terminal phalanges which appears like clubbing. Nail is not having curvatures here.
SKIN CHANGES AND ERUPTIONS
Nonpalpable Eruptions
- Macule: It is not raised above the skin; there is alteration in color of skin; it is seen but not felt (nonpalpable); capillary naevi or erythema blanch on pressure, purpuric macules do not blanch on pressure. Macule is <1 cm nonpalpable lesion. Macules can be generalized as seen in typhoid, syphilis, purpura or localized type which is called as roseolar.
- Patch: Circumscribed flat nonpalpable colored area in the skin with diameter >1 cm. Patches are seen in vitiligo, bruises. Macule and patch are nonpalpable lesions.
Palpable Eruptions
- Papule: It is raised tiny nodule; usually of few mm in size; it may be epidermal or dermal; seen in measles, chickenpox, smallpox, drugs like sulfonamides, occasionally in tuberculosis, sarcoidosis. It is < 5 mm sized palpable lesion.
Figs. 1-30A to E: Typical clubbing. In normal individual angle from skin to nail fold is 130 to 170 degree (Lovibond angle). In clubbing it is more than 180°. In clubbing both longitudinal and transverse curvatures are increased.
- Granule and nodule: Large papule >5 mm diameter up to 2 cm is called as granule; size more than 2 cm size is called as nodule. It may be cutaneous/subcutaneous origin; hard (rheumatoid arthritis)/soft (lipoma).
- Plaque: Confluence of papule/nodule; flat topped, raised/sunken seen in psoriasis. Papule, nodule and plaque develops due to proliferation of dermal cells which may be inflammatory or neoplastic in origin (Figs. 1-31 and 1-32).
Note:
Different eruptions occur in different conditions. Drug reactions commonly observed in the skin can involve systemically causing renal failure, respiratory distress or cardiac problems. Viral, bacterial, parasitic infections, radiation and chemotherapeutic agents can cause different skin eruptions, like vesicles, pigmentation, dermatitis, alopecia, thrombophlebitis, etc. (Figs. 1-33 to 1-42).
Fig. 1-31: Psoriasis; it can involve nails also. It is red, scaly, patches or papules or plaques. Plaque psoriasis is commonest type. Pitting of nails is common. Immune system mistakes a normal skin cell for a pathogen causing overproduction of new skin cells; it is probably genetically related but stress and environmental factors also responsible.
Fig. 1-37: Acute drug reaction in a child causing burn like injury of the entire skin of the body. It could be TEN (toxic epidermal necrolysis).
Fig. 1-41: Toxic epidermal necrolysis TEN, Lyell's syndrome (Alan Lyell, 1956). It is severe drug reaction often life-threatening; mimics Steven Johnson syndrome.
Fluid Collections in the Skin
- Vesicles: They are small blisters (<5 mm in size); elevations from epidermis containing clear or milk like fluid within; seen in chickenpox, smallpox, herpes. There is cleavage in the layers of the epidermis causing intraepidermal vesicles or cleavage can occur at epidermo-dermal interface causing subepidermal vesicles.
- Bulla: Large blister (>5 mm diameter); unilocular/multilocular; may contain serous/seropurulent/hemorrhagic fluid within (Fig. 1-43).
- Pustules: They are circumscribed epidermal elevations containing purulent exudate (white/yellow/greenish yellow); due to bacterial (like streptococcal) infection. It may develop in hair follicle or independently.
- Wheal: It is elevated patches on the skin with pallor at the center than the periphery; it is edematous elevation with itching; it is seen in allergic conditions (urticaria). Fluid accumulation occurs in diffuse pattern in wheal. Urticaria is elevated round lesion with white center and pale red periphery.
Others
- Scales: It is formed by desquamating layer of skin; occurring due to imperfect keratinization; small (dandruff), large (psoriasis).
- Crusts: It is dried exudation of serum, blood or pus over the skin, may be thin/thick; adherent/friable; colored yellow (serum)/dark red (blood)/green (pus).
- Café au lait spots: They are coffee brown colored patches in the skin; if more than 5 in number and with each more than 1.5 cm in size is significant; seen in von Recklinghausen's disease of neurofibromatosis with regular outline and deep indentations; occasionally also seen in Albright's syndrome where the outline is irregular.
- Petechiae: Tiny hemorrhagic spots less than 1 mm in size.
- Purpura: Hemorrhagic spots of 2–5 mm in size (Fig. 1-44).
- Ecchymosis: Hemorrhagic spots more than 5 mm in size.
- Hematoma: Hemorrhage causing elevation of skin (Fig. 1-45).
- Scar over the skin may be present; it may be due to old trauma, earlier surgery, healed infected area or childhood branding as a tradition (Fig. 1-46).
Fig. 1-43: Pemphigus is bullous lesions in the skin due to development of antibodies against desmoglein of skin. It can be erythematous lesions also.
Fig. 1-44: Henoch-Schönlein purpura. It is purplish rash involving legs and buttocks due to inflammation and bleeding of small vessels in the skin, bowel, kidney and joints. Purpuric rashes are reddish purple spots; joint swellings mainly in knee and elbow due to hemarthrosis; abdominal pain, bloody stools, intussusception as gastrointestinal features; hematuria and proteinuria due to involvement of kidneys. It is common in children (boys) after an attack of upper respiratory tract (viral) infections; common in seasons other than summer; may also be due to insect bite, exposure to cold, and drugs.
TEXTURE OF THE SKIN
Texture of the skin gives idea about different conditions and often severity. It should be seen as well as felt.
- Dry skin: Seen in dehydration and myxedema.
- Moist skin: Seen in myocardial infarction, shock of sudden onset (hemorrhage), toxic thyroid.
- Thick skin: Seen in myxedema, acromegaly, and scleroderma.
- Thin skin: Seen in old people, and wasting diseases.
Fig. 1-46: Branding using heated iron rod at various parts of the body during childhood to prevent evil effect is an old belief which was practiced in many parts of the world. One of the common sites is around the umbilicus. It forms a circumferential burn scar.
PIGMENTED LESIONS IN THE SKIN
It may be due to Naevus of different types, malignant melanoma, pigmented carcinoma (basal cell or squamous cell type), seborrheic keratosis, café au lait spots, cutaneous hemangiomas, spider naevus (an acquired condition with single dilated feeding skin arteriole with many small radial branches, which is compressible as it fades on pressure and is common on the upper trunk, face and arms), Campbell de Morgan spot (bright uniform deep red, painless noncompressible spot of 1–3 mm in size with collection of dilated capillaries fed by one or cluster of arterioles, seen in upper parts of the trunk of individual after the age of 45), Vin rose patch (congenital dilatation of the subpapillary dermal vascular plexus with pale pink skin), systemic diseases like liver cell dysfunction, adrenal diseases, drug induced, solar keratosis, etc. (Figs. 1-47 and 1-48).
HAIR
Hair is skin appendage with flat stratified multilayered keratinized squamous epithelium. Hair growth cycle shows three phases—anagen; catagen; telogen. Hair grows at a rate of 1.25 cm per month. Anagen is the initial growth phase of the hair; next catagen phase shows shrinkage of the hair follicle with diminished blood supply and nutrition to the hair follicle and this phase lasts for 2 weeks; eventual telogen phase lasts for 2–4 months where static hair lasts with resting phase. Once again new anagen phase begins at its hair follicle with shedding out the earlier hair.
Fetal entire skin is covered by fine, silky, Lanugo hairs which are shed by 8th month of intrauterine life. Fine, nonpigmented childhood hair (both male and female) is called as vellus. Long, pigmented, soft silky hair called intermediate hair is common in shoulder region (often is also seen along with vellus hair in Cushing's syndrome). Terminal hair is coarse, pigmented; nonsexual terminal hair present in scalp, eyebrows, arms and legs. Ambosexual hair is present in axillae, lower pubic triangle and limbs; sexual hair is present in upper pubic triangle, face, nose, ears, trunk and limbs in males (in females if present it is abnormal—hirsutism).
Fig. 1-48: Seborrheic keratosis (basal cell papilloma, senile wart, verruca senilis). Note the sulci and gyri appearance; it is often better evident using a dermoscopy. It is brown/black/tan colored waxy, scaly slightly elevated single or multiple lesions. They are not precancerous; but mimic carcinoma. It is benign cutaneous basal layer overgrowth with oily look. It is common in old age; may run in families. It can be removed by scraping, cryosurgery, cautery or laser. Excision is done if diagnosis is not certain.
Hair can overgrow or curl on its own. Plica polonica is a condition where long hairs of the scalp gets thickened, rough and curl on its own causing difficulty in combing and poor cosmesis. It is matted, filthy condition of hair which is sticky and moist; hairs cannot be disentangled; often mimics bird's nest. It may be due to poor hygiene. A condition called plica polanica which is first observed in Poland wherein long hairs in young females suddenly curl and twist on its own to create tough rough hairs. It is difficult to treat (Fig. 1-49).
Falling of Hair
Normally 50–100 hairs fall daily. Excessive hair fall is seen in infectious fevers like typhoid, chemotherapy for malignancies, drugs (heparin, allopurinol, bismuth, vitamin A, amphetamine) and hereditary. As hair follicle cells divide very quickly, chemotherapeutic agents inhibit hair growth and cause hair fall; after chemotherapy hair growth resumes in 3–10 months. Other causes of hair fall—SLE (systemic lupus erythematosus), myxedema, hyperthyroidism (Fig. 1-50).28
Patchy hair loss is seen in fungal infections, alopecia areata, syphilis.
Loss of hair in outer third of eyebrow is seen in leprosy, myxedema. Absence of axillary, pubic and facial hairs is seen in hypopituitarism, hypogonadism.
Alopecia
Alopecia is often an autoimmune disease. Alopecia can occur with normal or abnormal scalp skin. Abnormal scalp skin in alopecia is observed due to scarring as in SLE, lichen planus, radiotherapy, scleroderma, dermatitis, tinea capitis, folliculitis. Normal scalp skin in alopecia is observed in alopecia areata, secondary syphilis, traction alopecia, alopecia totalis, endocrine causes, telogen effluvium (here hair bulbs of anagen phase shrinks entering into telogen phase and hair falls later; 300–400 hairs fall daily in this condition). Alopecia can be—localized; generalized; male pattern.
Alopecia areata: It may be due to noninflammatory, autoimmune condition, may be associated with SLE, thyroid disorders, where there is single or multiple patches of hair loss. It can be familial (30%); it is patchy hair loss with normal scalp skin.
Alopecia totalis—when whole scalp is involved.
Alopecia universalis—when whole body is involved.
Androgenic alopecia: Male pattern of baldness with frontal recession of hairline.
Excessive Hair Growth
It is seen in women in Cushing's syndrome, adrenocortical syndrome, myxedema, ovarian tumors, drugs (androgen, minoxidil, diazoxide, anabolic steroids, phenytoin).
Hirsutism is exaggeration of hair growth (excessive) in females in androgen sensitive area where normal hair growth is absent. It may present as alone (due to polycystic ovarian disease) or may be accompanied with virilization (enlargement of clitoris, amenorrhea, temporal balding, reduction in size of breasts, loss female body contour) (Fig. 1-51).
Hirsutism is either due to excessive secretion of androgens from ovary (raise in levels of serum testosterone) or from adrenal glands [secretes proandrogen-dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulphate (DHEAS); causes raise in serum DHEAS]. Hirsutism can be seen as idiopathic, familial; seen in anorexia nervosa; epilepsy, pulmonary tuberculosis; spina bifida, poliomyelitis. Hirsutism can be physiological as in pregnancy.
EDEMA
It is the collection of fluid in the interstitial spaces or soft tissues. Edema will be clinically evident only when fluid accumulates more than 5 liters. Pitting on pressure occurs only when circumference of the limb is increased by 10% (Figs. 1-52A and B).29
Figs. 1-52A and B: Pitting edema leg. Pitting is elicited over the ankle (malleolus) or lower leg on medial aspect on a bony point using pulp of the thumb (ideally) or other fingers; deep continuous pressure for 30 seconds is applied and released to observe the pitting.
Mechanism
Normal hydrostatic pressure at the arteriolar end of the capillary bed is 35 mm Hg; at the venular end it is 12–15 mm Hg. Oncotic pressure of plasma is chiefly maintained by plasma proteins and is 20–25 mm Hg. Fluid volume in different compartment of the body is maintained by hydrostatic pressure at the arteriolar end that tend to push the fluid into the interstitium; oncotic pressure at the venous end which tend to push the fluid from the interstitium to intravascular space. The normal lymphatic flow helps to recirculate the albumin extruded from intravascular compartment into the interstitium.
Fluid accumulates in the interstitial space following—increased capillary permeability like in acute inflammation (cellulitis); increased capillary pressure (cardiac failure); decreased osmotic pressure (hypoproteinemia); lymphatic block (filariasis).
Pitting on pressure is the cardinal sign of edema. Firm pressure is applied using pulp of the finger/thumb for few seconds on the skin over a bone surface like lower part of medial aspect of leg just above the malleoli. Indentation or pitting is seen on releasing the finger. Slow reaccumulation of fluid in few minutes is observed.
Nonpitting edema is observed in late stage of lymphedema.
Edema is commonly observed in most dependent part—lower limbs. In bedridden patient, it may be seen on sacral region. Often limb edema may also be associated with ascites or pleural effusion. Upper limb edema can also occur. Edema can be unilateral or bilateral (Fig. 1-53).
Edema can be generalized or localized.
Generalized edema is called as anasarca. It is due to cardiac, renal, hepatic or nutritional (Figs. 1-54 and 1-55).
Localized edema is due to cellulitis, lymphatic causes (filariasis, radiotherapy, lymph node block dissection, Milroy's disease), venous diseases (DVT, thrombophlebitis, varicose veins), pretibial myxedema of thyrotoxicosis. Allergic edema can occur on face or other parts of the body also (Fig. 1-56).
Fig. 1-53: Upper limb edema can occur as unilateral or bilateral. It can be due to axillary vein thrombosis, as a part of generalized edema, lymphedema (filarial), or due infection (cellulitis)
Causes may be classified as bilateral (cardiac, renal, hepatic, IVC obstruction, allergic, nutritional, toxic) or unilateral (lymphatic, traumatic, infection, metabolic like gout, DVT/varicose veins, hereditary) (Figs. 1-57A and B).
In CCF (congestive cardiac failure) edema is in most dependent position—in lower limbs and is more in evening.
In LVF (left ventricular failure) pulmonary edema develops early and so dyspnea, basal crepitations, and cough are typical. In pericardial effusion, lower limb edema, ascites, hepatomegaly (soft smooth liver), raised JVP without pulmonary edema is observed.
Edema due to renal cause develops first in eyelids and face, and then it becomes generalized into legs and ascites.
In edema due to hepatic cause like portal hypertension, ascites develops first due to increased portal pressure and hypoproteinemia, and then lower limb edema develops.30
Figs. 1-54A and B: Severe ascites with everted umbilicus (smiling umbilicus); ascites with edema limbs and face as generalized is called as anasarca.
Fig. 1-55: Bilateral edema is due to cardiac/renal/liver diseases. It could be due to myxedema, pretibial myxedema (in primary thyrotoxicosis) or other metabolic causes. Anemia and hypoproteinemia also cause bilateral edema.
Figs. 1-58A to D: Superior vena caval obstruction causing dilated veins in the chest wall. Note the direction of flow from above downwards towards lower abdomen and to inferior vena cava.
In myxedema, edema is nonpitting. Here edema over the lateral aspects of the eyelids is typical.
VISIBLE VEINS
Patient should be examined for visible veins over limbs (usually lower), abdomen, trunk and neck. With normal venous pressure external jugular vein is invisible or just visible for short distance. Raised venous pressure causes engorgement of external jugular vein. Bilateral engorgement of external jugular vein/neck veins may be due to myocardial infarction or intravenous fluid infusion or retrosternal goiter/thoracic outlet obstruction. Unilateral engorgement of vein is due to compression by lymph nodes, tumor.
In toxic goiter neck veins may be prominent due to increased vascularity.
In SVC (superior vena cava) obstruction, inguino-axillary veins, chest wall veins, neck veins may be prominent with flow of blood from above downwards and through groin veins (across watershed area) to IVC (inferior vena cava) (Figs. 1-58 and 1-59).
In IVC obstruction, veins in the flanks (both sides) will be prominent, with direction of flow from below upwards towards axillary vein along inguinoaxillary vein. Such unilateral flow is observed in unilateral blockage of common or external iliac vein. Caput medusae is visible dilated veins radiating from umbilicus, seen in portal hypertension (Figs. 1-60A and B).
Varicose veins in the leg suggest valvular incompetence in the saphenous system, either congenital nor acquired.
Jugular Venous Pressure/pulse (JVP)
JVP is superficial, wave like pulsation with 3 waves per beat; better visible than felt; alters with position and during phases of respiration. JVP decreases during inspiration but becomes prominent during expiration. Normal jugular venous pressure is 3–4 cm of water (H2O) (Figs. 1-61 to 1-63).
JVP is assessed by observing internal jugular vein on right side with 45° semirecumbent position, with neck turned towards opposite side. Right side is chosen because vein on right side is in direct communication with the atrium. Distance (vertical) from sternal angle to the top of blood column in the internal jugular vein is measured to get the JVP. IJV runs from the medial end of the clavicle up to the level of ear lobule under the sternocleidomastoid muscle. Normal JVP is less than 4 cm. Raised JVP suggests increase in central venous pressure (CVP)—as an indirect evidence. External jugular vein also will be distended in these patients.
Moodley's sign: Radial pulse is felt and simultaneously JVP waveform is observed; the waveform that is seen immediately after the felt arterial pulsation is the ‘v wave’ of the JVP. This sign is used to determine which waveform is viewed.
Internal jugular vein (IJV) if distended with visible jugular pulsation in sitting position also suggests raised JVP.32
Figs. 1-60A and B: Dilatation of abdominal veins including inguino-axillary vein and bilateral varicose veins in IVC (inferior vena cava) obstruction in a patient.
Prominent antecubital vein or superficial veins of the hand (Gaertner's) or veins under surface of the tongue (May's) are all suggestive of raised JVP.
Hepatojugular reflux can be elicited by compression of liver causing raised right atrial pressure and so the distended jugular vein; it is also called as abdominojugular test. Positive abdominojugular test suggests that pulmonary capillary wedge pressure is 15 mm Hg or more.
Elevated jugular venous pressure is seen in cardiac tamponade, right ventricular failure, tricuspid stenosis, increased blood volume, asthma, emphysema, superior vena caval (SVC) obstruction.
Fig. 1-63: Measuring the JVP using two scales. Position of the patient is 45° semirecumbent position with neck turned towards opposite side.
JVP is reduced in shock, dehydration. During normal inspiration, intrathoracic pressure falls and venous blood flow to thorax increases causing inspiratory collapse of jugular venous pressure. In constrictive pericarditis when intrapericardial pressure rises, there will be paradoxical increase in jugular venous pressure during inspiration—Kussmaul's sign.
Nonpulsatile elevation of JVP occurs in obstruction of SVC/brachiocephalic or jugular veins—mediastinal tumors, bronchial tumors, thrombosis of these veins.
Pulsatile elevation of JVP is common; it is seen in congestive cardiac failure (CCF), fluid overload like renal cause or pregnancy, right sided failure, tricuspid regurgitation/stenosis, pericardial effusion, constrictive pericarditis, massive pulmonary embolism, thyrotoxicosis, anemia, high fever.33
EXAMINATION OF PULSE
Pulse means-arterial pulse. It is a waveform felt by the palpating finger over an artery produced by cardiac systole. It gives the overall idea about the status of the heart, circulation, arrhythmias, systolic pressure and condition of the vessel wall. Pulse is an ideal indicator of severity of many diseases. It is increased in sepsis, severe pain, shock, fever, toxic thyroid. It is also altered in all cardiac conditions (Fig. 1-64).
Assessment of Pulse
Pulse is assessed by rate (count the pulse); rhythm (regularity); tension and force; volume; character; condition of arterial wall; radiofemoral delay.
Pulse felt usually is radial pulse (against head of the radius) but when indicated, other pulses in the body also should be examined (dorsalis pedis, posterior tibial, popliteal, femoral, brachial, carotid, superficial temporal; bilateral pulses are compared for rate, rhythm and volume). It is felt using three fingers—index, middle and ring. Ring finger is kept distally to obliterate the retrograde pressure transmission; middle finger is used to feel the pulse; index finger is kept proximally to control and fix the artery to reduce the blood flow while checking the vessel wall thickness. Pulse is counted for full one minute. Counting for few seconds and then multiplying is wrong.
Force of a pulse is the minimum pressure required to obliterate the pulse; which reflects on systolic pressure of the patient.
Pulse volume is the uplift created towards the palpating finger; reflects on the stroke volume. Pulsus parvus is small volume pulse seen in shock and valvular stenosis. Pulsus magnus is large volume pulse seen in heart block, anemia, thyrotoxicosis, high fever. It is the amplitude of the pulse; it can be normal/low/high volume.
Amount of pressure required by the palpating finger to feel the pulse is called as pulse tension; it reflects on diastolic pressure.
Normal pulse rate is 60–100/minute. Tachycardia means increased pulse rate more than 100/minute. Bradycardia (Greek—slow) is decreased pulse rate less than 60/minute. Relative bradycardia (Faget's sign)—Every degree rise in temperature pulse rate will increase by 10 usually (Liebermiester rule); in condition like typhoid fever this rise in pulse rate per degree of rise in fever is less than 10 (less than expected rise, but still having increased pulse rate); it is called as relative bradycardia. It is often also observed in yellow fever, Legionella pneumoniae, Mycoplasma pneumoniae, Brucellosis, drug fever (beta blockers).
Normal Pulse Wave
Normal pulse has got a small anacrotic wave (limb) in the upstroke (which is not felt), a big tidal percussion wave which is felt. During down stroke (catacrotic limb), there is a dicrotic notch with a dicrotic wave (both are not felt) (Fig. 1-65).
Anacrotic wave pulse is felt in severe aortic stenosis.
Pulsus bisferiens is rapid rising, twice beating waves in the systole of the pulse; felt in idiopathic hypertrophic subaortic stenosis, severe aortic incompetence with mitral stenosis.
Dicrotic pulse is twice beating pulse with initial normal percussion wave of systole and eventual abnormal prominent dicrotic wave in diastole. It is seen in reduced peripheral resistance like CCF, cardiac tamponade, typhoid fever. Pulsus alterans is strong and weak beats alternatively; due to alternate contractions of the cardiac muscle; seen in left ventricular failure, toxic myocarditis.
Fig. 1-64: Palpation of the radial pulse. Ring finger is kept distally to block retrograde pressure feel; middle finger is used to feel the pulse and index finger to fix the artery proximally.
Pulsus paradoxus—During inspiration there is increased venous return to right atrium; lung expansion causes pooling of blood in the pulmonary vessels causing decreased venous return to left atrium and ventricle. It causes decreased left ventricular output and arterial pressure during inspiration by 3–10 mm Hg. When this fall in systolic pressure is exaggerated more than 10 mm Hg, it is called as pulsus paradoxus. It is seen in SVC obstruction, airway obstruction, asthma, pericardial effusion. In immobile thoracic cage pulsus paradoxus does not exists.
Pulsus bigeminus with coupling occurs in atrio-ventricular block.
Thready pulse is rapid, small waved pulse is seen in shock, cardiac diseases.
Waterhammer pulse (collapsing/Corrigan's) is large bounding pulse with a forcible jerk and disappearing quickly. It is due to sudden fall in peripheral resistance; seen in thyrotoxicosis, AV fistula, beriberi, aortic regurgitation, PDA.
BLOOD PRESSURE (BP)
BP is essential part of the general examination in all cases. It gives the idea about the general condition of the patient along with other parameters. BP is lateral pressure exerted by the column of blood on the walls of the arteries. Systolic pressure is due to stroke volume of the heart and stiffness of vessels. It is the maximum pressure produced during (cardiac cycle) systole. Diastolic pressure is due to peripheral resistance. BP varies in phases of respiration. It is the minimum pressure exerted during cardiac cycle (diastole). It is related to emotion, exercise, smoking, alcohol, tobacco, relation to meals, temperature, anxiousness, circadian rhythm, age, race, obesity, etc.
Recording the Blood Pressure
BP is recorded by indirect method. Riva Rocci invented sphygmomanometer. It contains mercury manometer, cuff and air pump. Russian surgeon Korotkoff (1905) originated the method of placing of stethoscope over cubital fossa to hear sounds (Korotkoff's sounds) of brachial artery.
Aneroid sphygmomanometer is manual sphygmomanometer with a manometer gauge for measuring blood pressure. It is widely used and is safer than mercury type. Mercury blood pressure apparatus is a desktop model capable of determining blood pressure up to 300 mm of Hg. The complete inflation system is enclosed in an aluminium case.
It is measured by palpatory or auscultatory or oscillatory methods. Usually palpatory and auscultatory methods are used. Palpatory method is done first; then auscultatory; it avoids missing the silent gap observed in hypertension and aortic stenosis.
Procedure of taking BP should be meticulous. Patient should be explained about the procedure. Patient should be in rest for 5 minutes prior to checking of BP. Patient should avoid exertion or meals 30 minutes prior to checking of BP. Clothing of the arm should be removed or kept as it is without folding (folding may cause constriction band). Width of the inflatable bladder cuff should be about 40% of the upper arm circumference (12–14 cm width in average adult); length of the inflatable bladder should be 80% of upper arm circumference, almost long enough to encircle the arm.35
Standard cuff commonly used is 12 × 23 cm size. In the thigh cuff of 18 × 24 cm is used. In obese, 12 × 35 cm sized cuff is used. In children smaller sized cuff (width 3 cm in infants; 8 cm in children) is used. Bladder of the BP cuff should encircle the arm completely; center of the bladder cuff should be over brachial artery; ideally rubber tubes should be placed on the inferior aspect in the line of the brachial artery (even though tubes are commonly placed superiorly to make stethoscope placement over cubital fossa easier); bell of stethoscope gives better sound; but diaphragm of the stethoscope is commonly used as its ability to cover wider area and easier to secure it. Usual position is supine lying down with arm supported to heart level. In sitting/standing position arm should be horizontal at 4th intercostal space of the sternum. If arm is not supported, arm with isometric contraction will elevate the diastolic BP by 10%. In normal individual, there is not much difference in BP in standing, sitting or lying down positions. BP in right arm is higher by up to 10 mm Hg; if BP is more than 10 mm Hg then it should be analyzed carefully. Repeat inflations of cuff will raise the systolic and diastolic BP and give false readings. So cuff should be inflated rapidly and deflated early and completely; further repeat readings are taken with a 15 seconds gap.
Hypertension is persistent raised systolic (above 140 mm Hg) or diastolic (above 90 mm Hg) BP. It is sustained elevation of systemic arterial pressure. It could be due to—essential HT; renal; vascular; endocrinal; neurological; hematological.
Hypotension is diminished BP (systolic pressure less than 90 mm Hg). It could be due to—postural, cardiac, endocrinal like Addison's disease, tuberculosis, malignancy, dehydration, shock, hemorrhage, hypovolemia, anemia, anorexia nervosa.
Figs. 1-69A and B: To check ankle brachial pressure index aneroid manometer is used; along with wave form Doppler; all four limbs are cuffed with separate BP bladder cuffs.
RESPIRATION
Normal respiratory rate is 16–20/minute; in children it is more. It is usually 1/4th of the pulse rate. In male it is abdominothoracic; in females it is thoracoabdominal. Tachypnea is rapid breathing seen in fever, shock, hypoxia, acidosis, tetany, hysteria. Bradypnea is decreased breathing—seen in narcotic poisoning, diabetic coma, uremia and raised intracranial tension.
Irregular respiration often seen in meningitis, coma and shock. Gradual deepening of respiration alternating with short periods of apnea is called as Cheyne-Stokes respiration (John Cheyenne and William Stokes, 1846). It is a periodic breathing; with alternate apnea and hyperventilation; apnea lasts for 30 seconds; hyperapnea lasts for 3 minutes with 30 or more breaths; amplitude of breathing will increase and decrease. It is common in deep sleep, narcotics, left ventricular failure, pneumonia, respiratory infections, uremia, cerebrovascular diseases, severe head injuries, cerebral tumors.
EYES
Eyes are evidence of many diseases. Observation of eyes is very important. Normally eyes blink 3–5 times a minute; infrequent blinking is observed in thyrotoxicosis and parkinsonism.
Orbital margin appears sunken in dehydration/malnutrition; puffiness seen in nephrotic syndrome; sclera looks yellow in icterus/jaundice; red in conjunctivitis, iritis, keratitis. Sclera and conjunctiva looks pale in anemia; grayish white color is seen in limbus (Figs. 1-70 and 1-71).
Arcus senilis is seen in elderly due to atherosclerosis, hypertension; there is deposition of cholesterol in the eyelids. It can also occur in old age commonly. It is asymptomatic common entity seen in 60% of old people. Arcus cornealis is deposition of lipid droplets and cholesterol in superficial and deep layers of cornea forming a yellowish white ring about 2 mm wide with clear space between it and sclerocorneal junction at the limbus. It is seen as bilateral peripheral calcification of cornea.
Argyll Robertson pupil: It occurs in neurosyphilis; unequal, irregular miotic pupil; presence of accommodation reflex but absence of miotic and ciliospinal reflex is seen.
Exophthalmos is bilateral outward protrusion of eyeballs from their normal positions, seen in primary thyrotoxicosis. Proptosis is unilateral/bilateral outward protrusion of eyeball due to condition other than thyrotoxicosis (Fig. 1-72).
Enlargement of lacrimal glands is seen in Sjögren's syndrome.
Figs. 1-70A and B: Sclera should be examined for congestion, redness, discoloration (jaundice); in this patient there is redness and congestion in sclera due to leptospirosis.
Fig. 1-72: Eyes and face should be examined carefully as part of general examination. Note the visible lower sclera—could be due to exophthalmos.
Ptosis: It is inability of upper eyelid to achieve elevation causing drooping (of the upper eyelid). Causes: Congenital is due to weak levator palpebrae muscle. Acquired is due to Horner's syndrome, paralysis of 3rd cranial nerve, myasthenia gravis, multiple sclerosis, edema/trachoma/tumor of the eyelid and trauma. Tabes dorsalis (neurosyphilis) causes pseudoptosis. 3rd cranial nerve (oculomotor) palsy may be due to trauma, ischemia, tumor, aneurysm. It causes unilateral complete ptosis with squint and large pupil. Myasthenia causes bilateral transitory ptosis which is more towards evening due to muscle fatigue.
Horner's syndrome: Enophthalmos due to Müller's muscle weakness; drooping of upper eyelid [partial ptosis (in 3rd nerve palsy ptosis is complete)]; anhidrosis; miosis due to paralysis of dilator papillae; absence of ciliospinal reflex; flushing of face and nasal congestion. Reasons for Horner's syndrome: It is due to interruption of sympathetic nerve supply to head and neck. Preganglionic fibers arise from 1st and 2nd thoracic segments of the spinal cord synapses with three cervical sympathetic ganglia. Any disruption of preganglionic fibers or cervical ganglia or their fibers will cause Horner's syndrome. Causes are: Posterior inferior cerebellar artery thrombosis; often cervical sympathectomy; Pancoast's tumor; secondaries in the neck; advanced thyroid malignancy; carotid artery aneurysm; spinal cord lesions; injuries to lower root of brachial plexus. Unilateral diseases, cervical sympathectomy causes unilateral Horner's syndrome (Fig. 1-73).
Edema of the eyelids: It can be unilateral or bilateral. It is due to drug allergy, physiological (crying, sleeplessness), nephrotic syndrome, part of anasarca, cardiac/liver failure, protein deficiency, etc.
Xanthelasma: It occurs in eyelids as yellow/orange plaques or nodules. It may be single or multiple; unilateral or bilateral. It is seen in old age, diabetes mellitus and ischemic heart disease. Pain, itching or inflammation will not be present.
Other conditions like cataract, eyelid swelling (chalazion), eyelid edema, retinal tumors can occur; conditions should be identified and proper ophthalmic opinion should be sought for (Figs. 1-74 to 1-76).
NOSE
Depressed bridge of the nose is called as saddle nose. It is due to destruction of the nasal cartilage; seen in Hansen's (leprosy) disease, congenital syphilis, cutaneous Leishmaniasis. It can be congenital also. Hypertrophy and adenomatous changes in the sebaceous glands in the tip of nose causing thickened, widened nasal tip is called as rhinophyma.
EARS
Ear is made up of 6 ear tubercles. So dermoid cyst can occur due to sequestration. Bat ear is congenital one which protrudes out from the side of the head. Multiple subperichondrial hematoma in the ear can cause cauliflower ear deformity. Keloid can occur in the ear at the site of ear prick; shows soft or firm nodule hanging down often pedunculated. Accessory auricle may be present in front of the tragus. Hansen's disease (leprosy) can cause ear deformity (Figs. 1-77 and 1-78).
FEVER/RISE IN TEMPERATURE
Normal body temperature is balance between heat gain and loss maintained by hypothalamus. It is the temperature of viscera and body tissues. Normal temperature is 36.7°C–37.5°C (98 to 99°F – 98.6°F). A diurnal variation of 1°C is normal; lowest temperature is during morning 2–4 AM, highest being in afternoon.
Fig. 1-77: Congenital deformity in the ear is not uncommon; it requires reconstructive surgery for correction.
Fever is increase in body temperature more than 1°C or more than the maximum range.
Types of Fever (Fig. 1-79)
Continuous fever: Fever persists throughout the day and temperature does not fluctuate more than 1°C in 24 hours. It is seen in pneumonia, urinary infection, endocarditis.
Remittent fever: Temperature is above normal throughout the day but there is fluctuation of more than 1°C in 24 hours.
Intermittent fever: Fever is present for only few hours a day and reaches to normal. It is observed in malaria, kala-azar. When fever develops daily, it is called as quotidian; when fever develops on alternate days it is called as tertian; when it occurs every third day it is called as quartan.
Pel Ebstein fever: Recurrent bouts of fever and afebrile periods occur at regular alternations. Temperature rises for 3 days, remains high for 3 days, remits in 3 days and goes for an afebrile period of 9 days to develop fever again in the same manner. It is observed in brucellosis; earlier also thought to be due to Hodgkin's lymphoma. It is a cyclical/relapsing fever with a pyrexial period of one or two weeks and then an apyrexial fever period of again one or two weeks.
Relapsing fever: Here febrile episodes are separated by normal temperature for more than one day; like in Borrelia fever; ratbite fever.
Drug fever: It is prolonged fever starts 1–3 weeks after drug intake; persists 2–3 weeks after withdrawal of drug. Drugs which cause fever usually are—sulphonamides, penicillins, iodides, propylthiouracil, methyldopa, anticonvulsants and antitubercular drugs. This fever is associated with rashes, pruritus, arthralgia, eosinophilia, relative bradycardia and hypotension.
Fever with chills and rigors: Fever with chills is sensation of cold with fever. Rigor is profound chill with piloerection (gooseflesh) with teeth shattering and shivering.
Pyrexia unknown origin (PUO): It is defined as—fever with temperature more than 101°F; more than 3 weeks of duration; failure to reach a diagnosis even after one week of inpatient investigation.
TONGUE
It is muscular organ of mastication often red in color, with prominent fungiform papillae at the edge and tip of the tongue; filiform papillae at the dorsum; circumvallate papillae at the junction of anterior 2/3rd and posterior 1/3rd; which help in appreciating various tastes. The color, size, surface, shape, coating, mobility, and any other lesions are to be noted.
Tongue may be large called as macroglossia. It is seen in lymphangioma, hemangioma, acromegaly, myxedema, critinism, amylodosis.
Tongue tremor is observed in thyrotoxicosis (primary). It is checked with tongue kept inside the oral cavity. If tongue is protruded out tongue twitchings may mimic tremor.
Tongue is bright red in color normally—due to rich blood supply through capillary network. Pallor is seen in anemia, hemorrhage. Discoloration can occur after colored food intake, tobacco chewing, Addison's disease, iron tablets intake. Black discoloration is melanoglossia due to iron and bismuth intake; brown discoloration is seen in uremia; scarlet red discoloration—niacin deficiency; white centrally coated tongue is seen in enteric fever and leukoplakia. In central cyanosis, tongue appears blue.
Tongue is moist normally; dry tongue suggests dehydration, shock. Dry brown tongue is a feature of uremia, Sjögren's syndrome, intestinal obstruction.
Furring of tongue is seen in smokers, stomatitis, and poor oral hygiene.
Black hairy tongue is seen in fungal infection.
Bald tongue is due to atrophy of papillae. It is seen in iron deficiency anemia, vitamin B12 deficiency.
Curdy coating is seen in candidiasis infection (Refer chapter 11).
Leukoplakia is a whitish opaque thickened epithelium; it is often associated with superficial glossitis.
Congenital fissuring can occur with irregular folds. Fissuring may also be a presentation of carcinoma of tongue. Lozenge shaped loss of papillae and fissuring is seen in midline in front of the foramen cecum.
Lingual thyroid may be seen posteriorly in midline.
Inability to protrude tongue is seen (ankyloglossia) in tongue tie, advanced carcinoma tongue infiltrating the genioglossus muscle.
Ulcers in the Tongue
Single | Multiple | Recurrent |
Tuberculosis | Aphthous ulcers | Aphthous |
Carcinoma | Herpes | SLE |
Syphilis | Secondary syphilis | Lichen planus |
Dental irritation | Vitamin B deficiency |
Note: One should look for carious tooth, dentition, any artificial dentures, sharp tooth; should observe for the mucous membrane of cheek, palate, floor of the mouth for any ulcers, leukoplakia and pigmentation; should observe for lip pallor, cracks, fissuring, ulcer, and angle of the mouth for cheliosis.
CREPITUS
It is crackling or grating sensation felt on palpation of subcutaneous tissue or joint or bone. Crackling sensation is felt when air is under the palpating fingers. Pockets of air moves in between separated subcutaneous or soft tissues causing crackling feel. Grating sensation is felt in bone or joint as crepitus.
Types
Various types of crepitus is seen depending on the contents (gas/liquid/solid) in the mass felt.
Crepitus in subcutaneous (surgical) emphysema: It is crackling sensation felt under examining fingers with gentle pressure similar like a palpating horse hair mattress. It can often be heard by placing a stethoscope over the surface. Subcutaneous emphysema is better felt (often seen as bull neck) in neck, shoulder and chest wall. Causes of subcutaneous emphysema are—traumatic (injury to lung and pleura following fracture ribs, bronchial/tracheal/laryngeal injury, tracheostomy, fracture skull with air sinus like frontal sinus injury); after surgery (air may get trapped in the subcutaneous plane) prior to closure of skin, after laparoscopic surgery; infective (in gas gangrene); after esophageal rupture (Boerhaave's syndrome—here mediastinal emphysema, subcutaneous emphysema, shock, toxicity occurs).
Crepitus of tenosynovitis: It is seen in de Quervain's tenosynovitis. Here hand is laid upon arm above the wrist, and the patient is asked to close and open the hand. Crepitus is felt at the junction of extensor pollicis brevis and abductor pollicis longus crossing the extensor carpi radialis longus and brevis.
Crepitus of bursitis: It is felt when lining of bursa is rough or contains loose fibrinous particles.
Joint crepitus: It is felt when affected joint passively moved by one hand, and by placing other hand over the suspected joint.
It can be—fine, even crepitations of chronic and subacute joint diseases; coarse, irregular crepitations of osteoarthritis, Charcot's joints; a click due to loose body or displaced cartilage.
Bone crepitus: It is elicited over the fracture segments of the bone when two fragments are moved against each other. A grating sensation is typical. But this should be elicited with utmost gentleness; only when radiological doubt exists. Crepitus is an unmistakable, diagnostic sign of fracture.
LOCAL EXAMINATION
Following rules should always be followed:
- It should be done in the presence of a nurse/ attendant.
- It should be done under good light preferably day light otherwise signs like jaundice may be missed.
- Proper positioning of the patient in relaxed and comfortable manner is a must for a successful examination.Various positions are:
- Supine for abdomen, extremities, chest, and head and neck.
- Prone for back.
- Sitting position for face, eyes mouth, thyroid swellings, neck swellings, back and breast.
- Standing position for hernia, varicosities of lower limb, inguinoscrotal swelling, spine.
- Lateral position for rectal examination.
- Lithotomy for vaginal examination.
- Examination should be carried by the examiner, standing or sitting comfortably on the right side or front of the patient.
- Various parts have to be exposed adequately for proper examination, for example:
- For neck lesion—from chin to nipple.
- For chest lesion—from chin to umbilicus.
- For abdomen—from nipple to thigh.
- For hand—finger to axilla.
- For foot—toes to inguinal region.
- Bilateral examination should be done to compare the disease with normal part.
Local Examination should be Done in a Systematic Way by Observing the Following Steps
Inspection (Look): It is observing the diseased area carefully for clinical features. It should be done with proper complete exposure of the part; compared with normal side.
Palpation (Feel): It is done by feeling of affected part using hand and fingers.
Percussion (Move/Tap): It is tapping of the affected area directly using flexed finger (direct method) or using pleximeter finger and percussion finger (indirect method). Percussion is used over sternum, abdomen (ascites, over mass to find out note, liver dullness,), respiratory system (in pleural effusion, pneumothorax).
Auscultation (Hear): Stethoscope is used to hear abnormal sounds like adventitious breath sounds, altered bowel or absence bowel sounds or loud intestinal sounds (Borboygmi) or succussion splash in pyloric stenosis; bruit over vessel or organ.41
Examination of regional lymph nodes: It is essential as many diseases like inflammation and malignancy may spread to regional nodes. Involvement of regional nodes gives idea about the severity of the disease and staging in case of malignancies.
Movements: Active and passive movements of the joints related are tested to note the abnormal movements; movements are compared to opposite side.
Measurements: Circumferential girth of abdomen is taken for ascites, intestinal obstruction; circumferential girth of upper and lower limb is taken for soft tissue growth/edema; length of limb in case of fracture of long bones.
SYSTEMIC EXAMINATION
Systemic examination is essential in all patients. It includes examination of respiratory and cardiac systems, abdominal examination, central nervous system examination and skeletal system examination.
Respiratory system: Chest wall movements; breath sounds, vocal fremitus, presence of pleural effusion, vocal resonance, tracheal shift, etc.
Cardiac system: Apex beat location, heart sounds, alerted sounds, muffled sounds, murmurs, etc.
Abdominal examination: Inspection of the abdomen for movements, fullness, umbilicus, hernial orifices, visible mass/pulsation, any scars of previous surgeries; palpation for mass and palpable organs like liver or spleen; percussion for the liver dullness (right 5th intercostal space in the midclavicular line), percussion over the mass, percussion for free fluid (ascites); auscultation for bruit around umbilicus; digital examination of the rectum for sphincter tone, rectal ulcers/lesions, prostate enlargement in males, rectal stricture, secondaries in rectovesical or rectouterine pouch.
Skeletal system: Spine should be examined for deformity, tenderness, paraspinal spasm and movements. Rotation movement of the spine should be checked by making the patient to sit in a stool.
FINAL DIAGNOSIS
- It is identification/determination of proper anatomical, pathological and etiological (cause) nature of the disease with its extent, severity based on which proper investigations and treatment can be planned. It is purely analytical. Analysis is based on detailed history, clinical findings and their application towards a disease correlating anatomy, pathology, etc.
- As it happens in many occasions if it is not possible to conclude towards a single disease and features correlate to more than one disease then differential diagnosis is put forward. Each diagnosis listed out in differential diagnosis are analyzed and assessed.
- All positive features in history, symptoms and signs are put together to analyze the anatomical location (tissue of origin), extent and pathological nature of the disease. Sometimes negative features are also important to consider or rule out certain diseases.
Based on the tissue of origin diagnosis can be considered as arising from—skin, fat, fascia, muscles, blood vessels, lymphatics, nerves, bones, joints, lymph nodes, organs like liver/spleen/lungs, etc.
Tissue contents will help to identify anatomical and pathological nature of the disease—solid cellular swelling (firm/hard, nonfluctuant, nontransilluminating); soft/cystic/tensely cystic liquid swelling (soft/firm), fluctuant may be transilluminating (if fluid is clear one) containing serous/purulent (pus)/bloody/lymph fluid; content may be gas (air/hydrogen sulphide/toxic gas) like in surgical emphysema or laryngocele or gas gangrene; or combination of more than one of the above.
Diseases are classified as congenital (begins at birth); acquired which develops at a later period or idiopathic when cause is not identified.
Note: Detailed history taking is essential. First history should be taken with suitable questions; one should wait patiently for right answers; one neither should nor force the answer of our need; leading questions are asked only at the end after complete history is taken. First complaint is noted down; detail of that complaint is elicited; system relevant to that complaint is explored by asking simple direct questions; then history in relation to other systems are asked.
In differential diagnosis most common possible diagnosis should be mentioned first; then in descending order as per correlation of findings.
Investigations are planned depending on the clinical diagnosis; only relevant investigations are to be done. Investigations are done for tissue diagnosis; for system involvement by the disease; relevant for preparation for anesthesia and surgery.
LEVELS OF EVIDENCES
Different levels of evidences are used in clinical practice. It is important to know so that recommendations or strength of evidence is assessed. High quality RCT, systemic reviews, high quality synthesized evidence are evidences beyond reasonable doubt. High quality review of literature is best practice evidence.
LEVELS OF EVIDENCES
Evidence | Level description |
I a I b | Evidence from meta-analysis from randomized controlled studies (RCT) Evidence from at least one RCT |
II a II b | Evidence from at least one controlled study without randomization Evidence from at least one other type of quasi-experimental study |
III | Evidence from nonexperimental descriptive studies, such as comparative studies and case control studies |
IV | Evidence from expert committee reports or opinions or clinical experience of respected authorities or both |
ECOG PERFORMANCE STATUS (EASTERN COOPERATIVE ONCOLOGY GROUP)
This performance status is used as a guide to plan the therapy. It is also important in clinical trials to select the patient.
ECOG (Zubroad) scale | Performance |
0 | Fully active and able to carry out work without restriction |
1 | Symptoms restrict strenuous physical activity but ambulatory and able to carry light sedentary work |
2 | Ambulatory but unable carry out work; up and about >50% waking hours |
3 | Only limited self-care; confined to bed or chair for more than 50% of waking hours |
4 | Completely disabled; confined to bed or chair |
5 | Dead |
KARNOFSKY PERFORMANCE STATUS (KPS)
In 1948 David A Karnofsky devised the scale as a uniform objective assessment of functional status. The KPS is a method of measuring co-morbidity mainly in solid tumors especially in head and neck malignancies as an independent reliable predictor of the outcome.
Karnofsky performance status (KPS) | |
|---|---|
100 | Normal; no complaints; no diseases |
90 | Able to carry on with normal activity; few symptoms and signs of the disease |
80 | Able to carry on with work with effort; some symptoms and signs of the disease |
70 | Inability to do normal activity or active work;’ but can care for self without assistance |
60 | Able to carry out most of basic needs; but occasional assistance is needed |
50 | Frequent medical care and considerable assistance is needed |
40 | Needs special care and assistance—disabled |
30 | Hospitalization is needed with severe disability; but death is not imminent |
20 | Hospitalization, active supports are needed; very sick |
10 | Moribund, rapidly deteriorating |
0 | Dead |
Knows in clinical practice | |
|
|