A Patient with Fever 1 Fever is a very common symptom that brings a patient to a physician. Fever is encountered in numerous and diverse clinical situations. Indeed, at times it may be very difficult to establish the cause for fever. It is worthwhile at this point to define a few terms. Normal Body Temperature Normal body temperature in adults is in the range of 36.8 o C + 0.4 o C with a diurnal variationlowest at 6 AM and highest at 4-6 PM. Any AM temperature > 37.2 o C (98.9 o F) or PM temperature > 37.7 o C (99.9 o F) is abnormal. The normal daily variation in temperature is 0.5 o C. Fever Any elevation of body temperature that exceeds the normal definition along with an increase in the set point of the hypothalamus constitutes fever. Hyperpyrexia Any fever of > 41.5 o C (106.7 o F) is defined as hyperpyrexia. Hyperthermia An increase in the body temperature in the presence of a normal hypothalamic set point is defined as hyperthermia. Important causes of hyperthermia are enumerated in Table 1.1.

A Patient with L ymphadenopathy 2 Enlargement of lymph nodes is referred to as lymphadenopathy. Lymphadenopathy may be noticed by the patient himself as small lumps or masses or may be detected by the physician during a physical examination. The important thing is to be able to assign as to whether the lymphadenopathy is a minor aberration or, whether it is a marker of a more serious underlying condition. In certain circumstances palpable lymph nodes may be overlooked as innocuous. This is especially true in case of: 1 . Soft submandibular nodes 2 . Lymph nodes of size < 1 cm especially in children and young adults 3 . Isolated inguinal nodes < 2 cm size. However, it is important to remember that when multiple groups of nodes are palpable, the palpable submandibular and inguinal lymph nodes also become significant findings. Lymphadenopathy can be classified as: Localised Generalised involvement of 3 or more non-contiguous lymph node regions. Causes of Lymphadenopathy The main causes of lymphadenopathy are summarised in Tables 2.1 and 2.2. In assessing a patient with lymphadenopathy, the medical history will give important clues to the cause. History TakingAsk About History of fever: Fever is a very prominent symptom especially in patients with infections.

A Patient with Splenomegaly 3 The spleen is a part of the reticuloendothelial system of the body. It is composed of a red pulp and a white pulp made up of RBC filled sinuses and reticuloendothelial cell lined cords and lymph follicles. The spleen serves the following important functions in the body: 1 . Destruction of senescent and abnormal erythrocytes 2 . Destruction of bacteria and bacterialaden cells 3 . Extramedullary haematopoiesis 4 . Functions as a part of the immune response system of the body. The spleen is usually not palpable in normal persons and lies entirely within the thoracic cage. The spleen enlarges in the direction of its long axis from the left subcostal area towards the right iliac fossa. The presence of an enlarged spleenSplenomegaly, is an important physical sign and clues to its cause can be obtained if one remembers the function the spleen serves. HISTORY TAKING Though splenomegaly is a sign that is elicited on physical examination, an enlarged spleen itself may produce certain symptoms of its own. Pain The presence of an enlarged spleen is usually suggested by a sense of heaviness or a dragging pain felt in the left upper abdomen. This pain is usually of a dull nature and rarely it may be sharp and acute, e.g. in the infarction of the spleen. Abdominal Distension Patients may notice an abdominal distension or at times may have palpated a lump in the abdomen.

A Patient with Generalised Oedema (Anasarca) 4 Oedema is defined as a state of increased interstitial fluid volume. Gross, generalised oedema is referred to as anasarca. Pathogenesis of Oedema The Starlings forces govern the rate of interstitial fluid collection. The hydrostatic pressure within the vasculature and the colloid oncotic pressure in the interstitial fluid promote movement of fluid from the vessels into the interstitium. Opposing this movement, is the colloid oncotic pressure of the plasma and the hydrostatic pressure of the interstitial fluid, that promote the movement of fluid into the vessels. The fine balance between these forces maintains the fluid balance in the vascular and extravascular compartments. Any alteration in pressures, shifts the balance, and promotes interstitial fluid accumulation or oedema. Oedema could be: Localised, e.g. restricted to a limb Generalised. The causes of localised oedema are listed below in Table 4.1. The main causes of generalised oedema are enumerated in Table 4.2. Table 4.1: Causes of localised oedema 1. Inflammation of the limb, e.g. cellulitis 2. Venous obstruction, e.g. deep vein thrombosis 3. Lymphatic obstruction - Lymphangitis - Filariasis - Resection of draining lymph nodes - Malignant invasion of nodes Whenever a patient presents with complaints of oedema a thorough history must be taken to identify the cause.

A Patient with Ascites 5 Ascites is the term used for the collection of excessive free fluid in the peritoneal cavity. It is an important physical sign and is the indicator of a number of underlying conditions. The pathogenetic mechanisms responsible for the development of ascites include: 1 . Increased transudation due to portal hypertension 2 . Avid sodium retention by the kidneys 3 . Decreased plasma oncotic pressuredue to hypoalbuminaemia 4 . In some cases, it a combination of two or more of these mechanisms. The important causes of ascites are listed in Table 5.1. History The clinical presentation of ascites depends upon: 1 . The volume of fluid collected 2 . The rate of collection of fluid Hence Mild to moderate ascites may go completely unnoticed, and the patient may remain asymptomatic With increasing fluid volume, patients become symptomatic and give a history of: i . Abdominal distensionalways ask about the duration for which distension has been noticed and the rate of development of distension i i . Abdominal heavinessdue to the large volume of fluid collected in the peritoneal cavity, a sense of heaviness and a dragging type of pain are important features. With increasing abdominal distension, breathing difficulty is a prominent symptom. This is primarily because the diaphragm is pushed up.

A Patient with Jaundice 6 Jaundice (icterus) is the yellowish discolouration of the sclera and other tissues due to deposition of bilirubin. The jaundice could vary from a pale yellow discolouration limited to the sclera to a deep yellow discolouration of even the whole skin. The normal serum bilirubin is 0.2-0.8 mg/dl and icterus in the sclerae usually becomes evident at serum bilirubin levels of 3.0 mg/dl or more. A rise in serum bilirubin manifesting as jaundice is due to any of the following three conditions: 1 . Increased production of bilirubin due to excessive destruction of erythrocyteshaemolytic jaundice 2 . Impaired uptake, conjugation and/or excretion of bilirubin by the liverhepatic causes of jaundice 3 . Impaired excretion of bilirubin through the biliary tree obstructive jaundice. The important causes of these are listed in Table 6.1. Haemolysis produces predominantly unconjugated hyperbilirubinaemia as the production of bilirubin far exceeds the ability of the liver to process this bilirubin. Hepatic causes and obstructive causes produce a predominantly conjugated hyperbilirubinaemia. In the evaluation of any patient who presents with jaundice (noticed by the patient himself, his relatives or attendants, or by the examining physician) a detailed history and physical examination is very important to arrive at the diagnosis of the cause of jaundice. HISTORY TAKING Ask about the onset, the duration and progress of jaundice. Also ask about the colour of urinehigh coloured or normal.

A Patient with Abdominal Pain 7 One of the most common complaints that brings a patient to a physician is abdominal pain. Acute abdominal pain is an emergency situation where prompt, urgent action is warranted. Many a times a surgical consultation and intervention will be required. Often a diagnosis of Acute Abdomen is made this is however, incomplete and should be avoided, as it does not clearly identify the disease condition responsible for the abdominal pain. The abdomen is vast with many organs within it. Also, pain may originate from within the abdomen itself or, be referred to the abdomen from other organs. It is very vital to take a detailed history especially focusing on the duration, nature, character, site, radiation of the pain and the presence of associated factors. A detailed physical examination will provide vital clues to the diagnosis. However, it must be remembered that in patients who present with severe abdominal pain and/or in shock, the haemodynamic resuscitation of the patient should be the primary focus of attention. The important causes of abdominal pain are enumerated in Table 7.1. HISTORY TAKING A detailed history should focus on the various aspects in relation to the abdominal pain. 1. Duration Ask about the duration of painacute, subacute or chronic. Ask the patient to describe in terms of hours, days, weeks, etc. 2. Frequency How often does the pain occurmany times in a day, daily, once in a while, etc. 3. Site The site of origin of the abdominal pain is very important to determine.

A Patient with Anaemia 8 Anaemia is a common clinical condition that results in a reduction in oxygen delivery to the tissues. Anaemia is a manifestation of a variety of clinical syndromes. The clinical presentation of anaemia can be very varied from largely asymptomatic, detected only on laboratory investigations to dramatic, serious consequences for example, hypoxic encephalopathy. It is important to recognize anaemia and then to identify its cause. The clinical features of anaemia depend upon: 1 . The severity of anaemia 2 . The rate of development of anaemia 3 . The underlying cause of anaemia Anaemia that develops acutely Anaemia that develops acutely or over a short period of time, for example after severe, sudden blood loss, can present very dramatically with features of hypovolaemic shock. If acute haemolysis has led to the development of anaemia, there may be clinical evidence of jaundice and acute renal failure. Insidiuous development of anaemia Anaemia that develops more slowly over a long period of time allows for the compensatory haemodynamic mechanisms of the body to get activated. These haemodynamic alterations compensate for the tissue hypoxia in the early stages and hence may mask the symptoms and signs of anaemia. However as the anaemia persists and becomes more severe, its clinical features become manifest. HISTORY While eliciting a clinical history in patients with anaemia, the focus should be directed towards: Clinical symptoms pertaining to anaemia Features that help to identify the underlying causes.

A Patient with Chest Pain 9 Chest pain is one of the most common symptoms that brings a patient to a physician. The complaint of chest pain invokes a sense of urgency in most patients and physicians primarily because ischaemic heart disease, (that can be life-threatening), presents with chest pain. Chest pain is produced by numerous diseases that vary from benign conditions to life-threatening, emergency situations. It is very important to carefully assess any patient who presents with chest pain so as to identify its cause. This is especially true for the identification of potentially fatal situations so that prompt, appropriate therapy can be instituted. It is equally vital to exclude serious causes of chest pain and allay the fear and anxiety of the patient. The chief causes of chest pain are summarised in the Table 9.1. The first step in the assessment of a patient with chest pain is to take a detailed history. It is very important to remember that patients with chest pain may present acutely with cardiorespiratory collapse. The first intervention in these patients is cardiopulmonary resuscitation. A brief history taking and physical examination may be performed initially. A more detailed clinical evaluation may be performed after ensuring haemodynamic stability. HISTORY Always ask the patient to describe the: 1. Character of pain It is important to ask the patient to describe the quality of pain. Varied descriptions of pain may be obtainedtearing pain, ache, heaviness, burning pain, ripping pain. Patients also have very varied perceptions of pain and the pain threshold varies from individual to individual. 2. Duration of pain Ask about the time of onset of chest pain. It will provide many vital clues to the aetiology of chest pain.

A Patient with Shortness of Breath 10 Shortness of breath, also called dyspnoea, is defined as an abnormal awareness of breathing. Dyspnoea occurs whenever the work of breathing is excessive. It is important to remember that moderate exertion, can make normal persons aware of their breathing. However, this awareness is transient and will settle down after some time. Dyspnoea is a cardinal symptom of cardiorespiratory disease. It can vary in severity from mild, exertional dyspnoea to very severe dyspnoea during which the patient feels extremely distressed and restless. Any patient who presents with shortness of breath or dyspnoea, needs to be evaluated very diligently to identify the cause. HISTORY TAKING A detailed history taking is very valuable in assessing any patient who presents with dyspnoea. The following points must be addressed carefully: 1 . Firstly, ask the patient to describe the shortness of breath. Patients have very varied perceptions and indeed are very varied in their description of dyspnoea. They may describe it as breathlessness, air not entering the chest, air being stuck in the upper airways or having to take deep breaths or sighs while breathing. In whatever way the patient describes it, it is very essential to establish the presence of dyspnoea. Occasional sighs does not comprise dyspnoea. Dyspnoea may be the only presenting symptom of a very serious underlying cardiac or pulmonary disease and hence it is important to ask the patient to describe it in detail. 2. Onset of dyspnoea It is essential to establish the mode of onset of dyspnoea.

A Patient with Pneumonia 11 Pneumonia is a common clinical disorder that physicians come across. The clinical presentation of pneumonia may vary from a typical scenario with fever, chills, characteristic respiratory findings and radiological signs to a very subtle or atypical presentation seen especially in elderly patients. Based on the setting in which it occurs, pneumonia is classified into Community acquired pneumonia (CAP) Hospital acquired pneumonia (HAP) or nosocomial pneumonia (NP) The need to categorise pneumonia into the two categories is because- i. The environmental setting in which the two conditions develop is entirely different. i i . The pathogens responsible for the two diseases are very different (Table 11.1). iii. The clinical presentations are not similar i v . The disease severity and prognosis is very dissimilar. v . Disease pathogens are likely to be more virulent and resistant to treatment in hospital acquired pneumonias. v i . Treatment protocols are very different. Table 11.1: Aetiological agents of pneumonia Community acquired pneumonia Hospital acquired pneumonia 1. Streptococcus pneumoniae 1. Pseudomonas aeruginosa 2. Hemophilus influenzae 2. Acinetobacter sp. 3. Mycoplasma pneumoniae 3. Klebsiella pneumoniae 4. Chlamydia pneumoniae 4. Enterobacter sp. 5. Staphylococcus aureus 5. Staphylococcus aureus 6. Aerobic gram negative bacteria 7.

A Patient with Pleural Effusion 12 Excessive accumulation of fluid in the pleural space is referred to as a pleural effusion. The condition is termed: Empyema when the collection consists of pus Haemothorax when the collection consists of blood Chylothorax when the collection consists of chyle The genesis of pleural effusion depends upon the alterations in Starlings forces that govern movement of fluid between the vascular compartment and the pleural space. An increase in the hydrostatic pressure in the vascular compartment and a reduction in the plasma oncotic pressure both favour a movement of fluid into the pleural space. In contrast an increase in hydrostatic pressure in the pleural cavity and a decrease in pleural fluid oncotic pressure promote movement of fluid from the pleural space into the vascular compartment. HISTORY TAKING The symptoms with which patients of pleural effusion present depend upon and reflect the Rate of collection and volume of pleural effusion Underlying disease condition Small pleural effusions may not produce any symptoms of their own. The patients may present only with symptoms due to the primary disorder. However, large volume pleural effusions frequently produce symptoms. The common complaints of patients are 1. Breathlessness Breathlessness is a prominent complaint in patients with a pleural effusion. It varies in intensity from mild to very severe depending upon the amount of pleural effusion.

A Patient with Pneumothorax 13 Pneumothorax is the collection of air in the pleural space. Pneumothorax can be classified into: 1 . Spontaneous pneumothorax a . Primary spontaneous pneumothorax b. Secondary spontaneous pneumothorax 2 . Traumatic pneumothorax (including iatrogenic pneumothorax) Pneumothorax is a fairly common problem and its presentation is very varied. In many patients, a pneumothorax may produce no or minimal symptoms and be detected only on radiological investigations. On the other hand, at times a pneumothorax may present with acute onset dyspnoea, chest pain and cardiovascular collapse to an emergency room. The main causes of pneumothorax are summarised in Table 13.1. Table 13.1: Causes of pneumothorax 1. Primary spontaneous penumothorax 2. Secondary spontaneous pneumothorax - Chronic obstructive airway disease - Interstitial lung disease - Pulmonary tuberculosis - Sarcoidosis - Pneumocystis carinii pneumonia - Other pulmonary infections 3. Traumatic - Direct chest injury - Iatrogenic CLINICAL FEATURES History The main symptoms associated with a pneumothorax are: 1. Chest pain Chest pain may vary from a mild chest discomfort to very severe, excruciating chest pain.

Mitral S tenosis 14 The cross-sectional area of the mitral valve in normal adults is 4-6 cm 2 . When the size of the mitral valve orifice is reduced to 2c m 2 it represents mild mitral stenosis (MS). When the mitral valve area is reduced to 1 cm 2 it is considered as critical MS. MS is predominantly rheumatic in origin and infrequently, MS is due to some other causes. The causes of MS are enumerated in Table 14.1. Pathophysiology of MS With narrowing of the mitral valve area, the blood flow from the left atrium (LA) into the left ventricle (LV) can occur only when it is propelled by an increase in the LA pressure. Any increase in heart rate increases the gradient across the mitral valve and further elevates the LA pressure. This can explain why with the onset of atrial fibrillation (AF), there may be a sudden development of dyspnoea and acute pulmonary oedema. Another important pathophysiological change is the development of pulmonary hypertension. Pulmonary hypertension in MS, develops due to a combination of: 1 . Passive transmission of the elevated LA pressure to pulmonary circulation. 2 . Increase in LA pressure that triggers pulmonary arteriolar constriction. 3 . Organic obliterative change in pulmonary vasculature. Table 14.1: Causes of mitral stenosis 1. Rheumatic heart disease commonest 2 . Congenital 3. Carcinoid syndrome 4 . SLE 5. Rheumatoid arthritis 6. Mucopolysaccharidoses 7.

Mitral Regurgitation 15 Mitral regurgitation (MR) or mitral incompetence or mitral insufficiency may develop under two conditions acute MR resulting from an acute insult to the mitral valve apparatus, and chronic MR due to a more slowly progressive disorder. The important causes of acute MR and chronic MR are summarised in Table 15.1. It is important to recognise these two patterns as the pathophysiologic mechanisms and hence the clinical presentations of the two conditions are very diverse. Table 15.1: Causes of mitral regurgitation (MR) Acute MR Chronic MR 1. Acute rheumatic fever 1. Rheumatic heart disease 2. Trauma 2. S L E 3. Infective endocarditis 3. Prolapse mitral leaflet 4. Papillary muscle dysfunction 4. Marfans syndrome myocardial infarction/ischemia 5. Ruptured chordae tendinae 5. Prosthetic mitral valve secondary to MI, trauma, endocarditis dysfunction 6. Dilated cardiomyopathy 7. Ehlers Danlos syndrome PATHOPHYSIOLOGY OF MR The compliance of the left atrium (LA) and the pulmonary venous bed are important determinants of the clinical picture of MR. In patients with acute MR, the LA compliance is normal. Hence, there is little enlargement of the LA but marked elevation of LA pressure. This manifests as acute pulmonary oedema. In contrast, in patients with chronic MR, the LA compensates over the time by dilating and enlarging, and hence LA pressures are only mildly elevated, at the expense of a reduced cardiac output.

Aortic Stenosis 16 Obstruction to the left ventricular outflow tract may be caused by: 1 . Valvular aortic stenosis 2 . Supravalvular stenosis 3 . Subvalvular aortic stenosis 4 . Hypertrophic obstructive cardiomyopathy Of these, the commonest is valvular aortic stenosis (AS). The important causes of aortic stenosis are enumerated in Table 16.1. Of all the causes of valvular aortic stenosis, degenerative aortic stenosis, also called senile or sclerocalcific AS is the commonest cause in the west. In India, rheumatic AS is a major cause of acquired AS. Table 16.1: Causes of valvular aortic stenosis 1. Congenital aortic stenosis Malformation of aortic valve: Unicuspid aortic valve, bicuspid aortic valves 2. Acquired aortic stenosis Rheumatic aortic stenosisdue to adhesion and fusion of cusps and commissures Degenerative aortic stenosisdue to mechanical stress on the valve and calcium deposition Rheumatoid arthritis (rare) Pathophysiology of AS Whatever the cause, obstruction to the left ventricular (LV) outflow produces a systolic pressure gradient between the LV and the aorta. The most important compensatory mechanism to maintain LV output, is LV hypertrophy. The cardiac output may be normal at rest, but fails to rise normally with exertion. Late in the course of the disease, the cardiac output and stroke volume decline and the mean pressures in the left atrium (LA), pulmonary capillaries, pulmonary artery, right ventricle (RV) and right atrium (RA) rise.

Aortic Regurgitation 17 Aortic regurgitation (AR) can be due to: 1 . Disease of the aortic valve 2 . Disease of the aortic root 3 . Combination of both The important causes of valvular AR are enumerated in Table 17.1. The chief causes of aortic root disease are summarised in Table 17.2. Table 17.1: Causes of valvular aortic regurgitation 1. Rheumatic heart disease 2. Infective endocarditis 3. Congenital bicuspid aortic valve 4. Trauma 5. Associated with Marfans syndrome Ehlers Danlos syndrome 6. Rare causes SLE Rheumatoid arthritis Ankylosing spondylitis Ulcerative colitis Table 17.2: Important causes of aortic root disease 1. Cystic medial necrosis of aorta (with Marfans syndrome) 2 . Syphilis 3. Associated with Behcets disease Ankylosing spondylitis 4. Osteogenesis imperfecta 5 . Hypertension PATHOPHYSIOLOGY OF AR AR may develop two settings acute AR and chronic AR.

Multivalvular Heart Disease 18 Involvement of more than one valve simultaneously is common in patients with rheumatic heart disease. Multivalvular involvement could be: Functional or secondary for example, dilatation of the tricuspid annulus due to pulmonary hypertension in mitral valve disease. Organic simultaneous involvement of valves by the same disease process. It is important in multivalvular heart disease to: Identify all the involved valves and valvular lesions. Identify the dominant valvular lesion. This is necessary for planning future corrective surgeries. It is also important to remember that: The presence of a specific valve lesion may mask the clinical manifestations of another valve lesion. The severity of one valve lesion may be modified by the presence of another valve lesion. A proximal regurgitant lesion worsens a distal regurgitant lesion and both are poorly tolerated. The progress of symptomatic heart disease and the prognosis are directly related to the number of valves involved, types of valvular lesions and the effect they have on one another. Some Typical Combinations of Valve Involvement Mitral Stenosis (MS) and Aortic Regurgitation (AR) The presence of MS will mask the signs of AR. Many of the clinical manifestations and peripheral signs of AR may be absent. Hence, even though severe and significant AR may be present, it may be missed in the presence of severe MS, unless diligently looked for.

Approach to a Patient with Coma 19 One of the more challenging clinical situations is the evaluation of a patient with alteration in sensorium in order to arrive at a clinical diagnosis. It is even more difficult when no history is available, as for example in patients who are found unconscious in public places and are brought to the emergency room by concerned citizens or the police who do not know anything about the patients medical history. The reticular formation of the brainstem maintains arousal responses and, coma represents a disorder of this activity. Many descriptive terms are in existence to define altered mental status delirium, confusion, stupor, encephalopathy, precoma, coma. It is important to remember that there are very diverse conditions that can present with coma and a very detailed clinical evaluation is required. The important cause of coma are outlined in Table 19.1. History Coma is a medical emergency and it is always important to bear in mind that immediate resuscitative measures may be needed in some patients, following which a detailed evaluation may be performed. Many vital clues are evident in the patients medical history. In most situations the patient themselves cannot provide a history and the medical complaints must be obtained from family, attendants or neighbours who bring the patient to the hospital. Always ask about: 1. The onset: Ask specifically about the onset of unconsciousness whether it happened suddenly, over a period of a few hours or couple of days or more slowly over days. The onset may offer vital information regarding underlying disease conditions. For example, a sudden onset loss of consciousness may be seen in a cerebrovascular accident.

A Patient with Motor W eakness 20 A very important complaint related to the neurological system is motor weakness or weakness of one or more limbs. It can be very distressing and traumatic for patients who may suddenly find one or more limb to have loss of motor function. Motor weakness is defined as a decrease in the power of muscles. If it is near complete or a complete absence of power a suffix of plegia is added. So, a patient who has complete loss of power of: Both lower limbs has Paraplegia All four limbs has Quadriplegia One half of the body has Hemiplegia. The suffix paresis is added to refer to a more milder muscle weakness that is incomplete. Hence similarly, patients can have paraparesis, quadriparesis or hemiparesis. Muscle weakness or motor weakness needs to be clearly differentiated from generalised weakness or asthenia. Motor weakness signifies neurological disease. Generalised weakness or fatigue does not have a neurological cause and may be due to a number of other systemic disorders.

A Patient with Paraplegia/Paraparesis 21 Weakness that affects both the lower limbs is called Paraplegia or paraparesis. Most of the cases of paraplegia are due to diseases that affect the spinal cord, though on occasion, other conditions, e.g. cerebral lesions and acute neuropathies may produce paraplegia. The cerebral causes of paraplegia are enumerated in Table 21.1. Whenever, a patient presents with complaints of para- plegia or paraparesis, a detailed history and neurological exami- nation is mandatory. Table 21.1: Cerebral causes of paraplegia 1. Superior sagittal sinus thrombosis 2. Parasagittal meningioma 3. Thrombosis of an unpaired anterior cerebral artery 4. Cerebral diplegia 5. Hydrocephalus HISTORY The Onset Ask the patient about the onset of the muscle weakness. This provides a useful insight into the disease aetiology as different diseases have different modes of presentation. The cause of paraplegia as determined by the onset of symptoms can be grouped into acute, subacute, and chronic onset (Table 21.2). The Extent Ask specifically about the extent of the muscle weakness. If the patient describes a horizontal level on the trunk below which all muscle power is lost, it is highly suggestive of a spinal cord lesion (myelopathy). Ask patient what all functions he can do and always assess for truncal weakness.

A Patient with Muscle Disease 22 Diseases of the muscle may also produce muscle weakness. Since the muscle is a component of the motor unit, disorders of the muscle present as a lower motor neuron disease. Muscle diseases present with a classical pattern of muscle weakness that is unmistakable and readily evident on history and physical examination. HISTORY Prominent symptoms of muscle disease include: Muscle Weakness Motor weakness is a very prominent presenting complaint. Whenever a patient complains of muscle weakness, enquire about a. Age of onset of muscle weakness: It is important to identify the age of onset of the muscle weakness. Many diseases of muscles, e.g. muscle dystrophy have a chronic, insidious onset over years, starting at childhood or adolescence. Certain muscle dystrophies are congenital and manifest at a young age in childhood for example, Duchenne muscle dystrophy. Certain other forms of muscle dystrophy, for example, Facio-scapulo-humeral dystrophy, oculopharyngeal dystrophy may present well into adulthood. b. Pattern of muscle weakness: It is very important to establish the extent and pattern of muscle weakness. Muscle diseases have characteristic patterns of involvement which could be Predominantly involving proximal muscles The proximal muscle predilection is very typical of muscle diseases. Most muscle diseases begin in the proximal group of muscles.

A Patient with Neuropathy 23 Neuropathy is a lower motor neuron disease. Neuropathy can present in one of the following patterns: MononeuropathyIt is due to the involvement of a single nerve. Mononeuritis multiplexIt is the involvement (simultaneous or sequential) of more than one non-contiguous nerve trunks. PolyneuropathyIt is the involvement of multiple widespread nerves. CLINICAL FEATURES 1 . In mononeuropathy, since a single nerve is involved, the presentation is focal and the deficit is restricted to the loss of function of end organs supplied by the nerve motor, sensory, autonomic. The deficit is always in a particular distribution. For example, median nerve involvement in carpal tunnel syndrome. Trauma, entrapment and extrinsic compression are frequent causes of mononeuropathy. 2 . Mononeuritis multiplexmononeuritis multiplex presents with patchy, random nerve involvement, e.g. leprosy, sarcoidosis. POLYNEUROPATHY History The following points in history should be elicited. 1. Onset of symptoms Always enquire about the onset of symptoms acute, subacute or chronic. Specific diseases have different onset and hence knowledge of the onset of symptoms can help identify disease aetiology. Acute onset neuropathy is characterized by rapid onset and progress of symptoms over a matter of days or weeks, e.g.

Outline of Paediatric History T aking 24 First Obtain i. Name, age (date of birth, if possible), sex of the child, details of informant, educational status of informant and reliability, place of residence i i . Presenting complaintsAll presenting complaints should be listed in chronological order. iii. History of present illnessThis should include the following a . Details of presenting complaints in chronological order b. Relevant negative history c . Details of treatment taken d . Effects of current treatment i v . History of past illness Details of relevant past illness includ- ing details of hospitalization, treatment v . Antenatal historyThis includes a . Details of pregnancy, birth order, maternal age, any maternal illness, antenatal care, mode of delivery, place of delivery, history of asphyxia b. Any significant neonatal illnesses v i . Developmental historyDetailed developmental history in each of the following domains should be presented in chrono- logical order. Physical Development Gross motor Fine motor General Understanding Linguistic development (speech) Bladder and bowel control. vii.

Approach to a Newborn 25 Fetal and extrauterine life forms a continuum during which human growth and development are affected by genetic, environmental and social factors. It is important to know the following terminology in relation to the newborn. GESTATIONAL AGE Gestational age is calculated from the first day of the last menstrual period till the date of birth and is expressed in completed weeks. PERINATAL PERIOD This is most often defined as the period from 28th week of gestation till the 7th day after birth. NEONATAL PERIOD The neonatal period is defined as less than 28 days of life. LOW BIRTH WEIGHT These are infants weighing 2500 grams or less at birth. VERY LOW BIRTH WEIGHT These are infants weighing 1500 grams or less at birth. PRETERMS Preterm is defined as a baby with a gestation of less than 37 completed weeks.

Developmental History 26 Assessing a childs development is an integral part of paediatric history and examination. A detailed history is important because there are numerous factors prenatal, perinatal and postnatal, which profoundly affect development (Table 26.1). A full physical exami- nation is important to determine whether there are conditions such as visual or auditory defects, cerebral palsy or hypotonia which will greatly affect development (Fig. 26.1, Plate 9). An accurate Table 26.1: Important history to be elicited before a developmental assessment i . Educational status, socioeconomic status and IQ of parents i i . History of any hereditary conditions in parents, e.g. CNS anomalies iii. Any siblings previously affected with any malformations like hydrocephalus, spinal bifida i v . History of epilepsy in parents v . Hereditary metabolic defects like phenylketonuria v i . Endocrine problems in mother, e.g. diabetes mellitus vii. Unwanted pregnancy viii. Twin pregnancy i x . Antenatal radiation exposure x . Drug intake during pregnancy smoking, alcohol x i . Maternal infections in pregnancy xii. Advanced maternal and paternal age xiii. Maternal malnutrition xiv. History of maternal infertility x v . Disorders of pregnancy, e.g. placental insufficiency, hydramnios, hypertension, toxaemia of pregnancy, antepartum haemorrhage xvi. Prematurity, low birth weight xvii. Post maturity xviii. Birth asphyxia xix. Severe malnutrition in infancy and childhood x x . Child abuse and emotional deprivation xxi. CNS infections, e.g. meningitis xxii. Craniospinal irradiation xxiii.

Approach to a Child with Acute Diarrhoea 27 Diarrhoea is the passage of stools of increased frequency, fluidity and volume. It is defined as the passage of three or more liquid or watery stools in a day. However, it is the consistency of the stools rather than the number that is more important. Frequent passage of formed stools is not diarrhoea. Babies fed only breast milk during the initial 2-3 months of life may pass many formed or semi formed stools daily, if they are gaining adequate weight, this should not be taken as diarrhoea. Acute diarrhoea: Most episodes of acute diarrhoea terminate within 7 days. Only 3-12 per cent of acute diarrhoeal episodes last beyond two weeks. Persistent diarrhoea: This is defined as diarrhoea that starts acutely and lasts 14 days or more. Two clinical types of acute diarrhoea can be recognised Acute watery diarrhoea: This is characterised by passage of loose watery stools and lasts several hours or days. The main danger is dehydration; weight loss also occurs if feeding is not continued. Acute bloody diarrhoea: This is also called as dysentery. The clinical syndrome of dysentery is characterised by the presence of blood and pus in the stools, abdominal cramps and fever. Gross blood in the stools is the most reliable sign (Table 27.1). Table 27.

Appr oach to a Child with Anasar ca 28 Oedema is the excess accumulation of interstitial fluid. It may occur as a result of increased capillary pressure (congestive heart failure) or decreased plasma protein concentration. Decreased plasma proteins may be due to increased losses (nephrotic syndrome) or due to decreased intake (malnutrition). The history and physical examination are very important to determine the specific system affected. Note the presenting complaints. Ask about the duration of oedema. Next determine the following: Mode of onset : Was the onset of oedema sudden or gradually increasing Sudden oedema local or generalised may be angioedema. It often involves the lips, dorsum of the hands and feet, scalp, scrotum and periorbital tissues. It may be recurrent. Oedema of renal or cardiac disease appears and gradually progresses. Site of first occurrence : Oedema of renal disease starts as periorbital puffiness and later progresses to involve the whole body. Cardiac oedema occurs in dependent parts of the body, e.g. feet first and later progresses. Oedema of liver disease characteristically starts on the abdomen and is disproportionate to peripheral oedema. Diurnal variation : Renal oedema appears first in the morning on awakening and later decreases as the day progresses. Cardiac oedema is more in the later parts of the day on the dependent parts, e.g. legs.

Approach to a Child with Protein Energy Malnutrition 29 Malnutrition is the syndrome that results from the interaction between poor diets and disease and leads to most of the anthropometric deficits observed among children in the worlds less developed countries. A large percentage of the worlds children grow and develop while experiencing malnutrition. The consequences of children becoming and remaining malnourished are increased risk of morbidity and mortality, delays in motor and mental development and decreased work capacity. Malnutrition potentiates the threat of infection and contributes to more than half of the deaths of children under five years of age. The methods available for assessment of malnutrition may be broadly classified as anthropometric parameters and clinical methods. Anthropometric Parameters The measurements to be taken include weight, length/height, head circumference, chest circumference, mid arm circumference. Weight: An electronic or Salter spring machine can be used (Figs 29.1 and 29.2, Plate 11). Technique: Leave a cloth in the weighing pan to prevent chilling the child. Adjust the scales to zero with the cloth in the pan. Place the naked child gently on the cloth in the weighing pan. Wait for the child to settle and the weight to stabilise. Measure the weights (to the nearest 10 g) and record immediately. Standardisation of the scales should be performed weekly or whenever the scales are moved. Head circumference: Correct measurement of the head circumference is important.

Approach to a Child with Congenital Heart Disease 30 Congenital heart disease refers to a structural abnormality of the heart or intrathoracic great vessels. It affects 1 per cent of newborns and accounts for 10 per cent of all congenital anomalies. Children with congenital heart disease may present any time from the neonatal period till late childhood. The diagnosis is not always easy as physical findings, ECG and chest X-ray are difficult to interpret especially in the newborn period and manifestations of heart disease may be quite different from those of older children. First determine as usual the age and sex of the child. Importance of Age Some congenital heart diseases present in the first week and some in later neonatal period and some in later infancy and childhood. Next determine the presenting complaints. In the history of presenting illness determine the following. History Suggestive of Congestive Heart Failure Rapid Breathing In infants with congestive heart failure the respiratory effort is more and resting ventilation is more rapid. Poor Feeding Feeding may be laboured or impossible because of rapid breathing. These neonates may take 45 to 60 minutes to finish feedings that should take only 10 to 15 minutes. Decreased urine output and periorbital puffiness are signs of CHF. Weak Crying The cry may be weak and feeble.