Respiratory distress may follow due to aspiration of fluid elsewhere in the lungs

(c) Jaundice due to pressure on the bile ducts. (d) Severe systemic reaction following rupture into peritoneal cavity, gut itself or pleural cavity. (e) Cholangitis from rupture into biliary tree. 2. LUNG - Pulmonary hydatid cyst can present as - (a) Solitary or at times multiple cysts, on plain radiograph. (b) Shortness of breath or chest pain if cyst is large. (c) Haemoptysis following ulceration into a bronchus. (d) Expectoration of watery. fluid and daughter cysts ( grape skin' expectoration) following rupture into the bronchial tree. Respiratory distress may follow due to aspiration of fluid elsewhere in the lungs, and may be associated with urticaria and anaphylactic shock. (e) Fever, cough and purulent sputum, if secondary pyogenic infection occurs. 3. OTHER ORGANS - Presence of cysts in - (a) Brain - Epilepsy or hemiplegia. (b) Long bones - Pathological fractures. (c) Spleen -Splenomegaly. (d) Kidneys - Hematuria. (e) Spinal cord - Seizures or signs of increased intracranial pressure of subacute onset and progressive course. Root pains-and motor or sensory deficits. (f) Thyroid - Goitre (g) Behind the eye - Exophthalmos (h) Abdomen - Pseudocycesis from rapidly growing cysts. Diagnosis - 1. DEMONSTRATION OF HYDATID CYSTS - (a) Chest radiograph - various signs are - (a) Classical appearance of a circular shadow sharply defined with no reaction in surrounding lung parenchyma. The cyst may change shape on maximum inspiration an expiration (Escudero nimerove sign). (b) Crescent sign or pulmonary meniscus sign - If the cyst communicates with a bronchus, a cap of air may be seen above the cyst (also seen in lung abscess partially filled with ins pisated pus or blood clot, tuberculous cavity containing a Rasmussen aneurysm, and in intracavitary fungal ball). (c) Double arch (Cumbo's) sign - As more sir enters between pericyst and endocyst, the shrinking cyst ruptures with resultant air fluid level within the endocyst capped with crescent of air between pericyst and endocyst. (d) Water lilly sign - With further separation of endocyst and evacuation of fluid, a wavy endocyst membrane floats on top of remaining abscess exudates and seen microscopically on wet mount. (b) Adult worm - Remnants of adult worm cuticle surrounded by granulomatous tissue or calcification may be seen in surgical specimens from deep tissues. (c) Serological tests - EL ISA can detect antibodies in patients with cryptic or prepatent infections. Management - Minor surgical enlargement and firm massage along the tract of the worm can facilitate removal of emerging worms. The worm is wound on a rod, few centimeters each day, avoiding excessive tension. Septic abscesses and anaphylaxis require appropriate therapy. 20. TROPICAL SPRUE Definition -It is an alimentary dysfunction characterised by deficiency in gastric secretion and inability to absorb adequately fat, glucose, calcium and certain other food constituents and characterised by morning diarrhoea, bulky gaseous stools, sore tongue, megalocytic anemia and wasting. Etiology - Age - usually middle age. Sex - more in females especially when pregnant. Geographical distribution - Tropics and subtropics and mainly in hot, damp coastal climates. Season - Onset usually after rains. Race - mostly amongst Europeans Other predisposing causes - Prolonged residence in endemic area and hills, chronic dysentery, mucous colitis or hill diarrhoea Cause- An alimentary dysfunction in which a series of interlocking pathophysiologic events occur. Clinical features and Diagnosis - See Malabsorption syndromes. Course - Sprue relapses are uncommon after adequate treatment (unlike idiopathic steatorrhoea) and where they do occur, ultimately respond to treatment. Fatal cases are rare Differential Diagnosis - 1. Other megaloblastic anemias. 2. Idiopathic steatorrhoea- Long history. In sprue onset and course often more rapid, diarrhoea almost invariable, anemia tends to be more severe and is commonly normochromic or hypochromic. Hypocalcemia and cramps uncommon, stomatitis more marked, anorexia and abdominal pain more common. No specific response to folic acid or antibiotics 3. Chronic pancreatitis- Faeces contain high percentage of neutral fat but split fat content. low, the reverse is true in sprue 4 Giardiasis - may cause steatorrhoea. Diagnosis made by finding cysts of the parasite in formed stools and vegetative forms in fluid stools. 5. Intestinal strictures - e.g. due to TB Management - Aims - (i) Rest to alimentary canal by dietary regime (ii) Correction of anemia and gross deficiency conditions. 1. Diet - High protein, low carbohydrate and low fat - (a) Milk diet -Skimmed milk or proprietary dried milk; or protein hydrolysates and concentrates, 2 hourly feeds. Fruits and glucose. (b) Mixed diet - Skimmed milk, eggs, meat, bread, green vegetables, fresh fruits, and milk pudding. 2. Folic acid - Effect most marked in cases with prominent megaloblastic anemia. 30 mg. day p.o. or 15 mg I M for 3 weeks controls diarrhoea and causes improvement in stomatitis and glossitis. Maintenance dose of 5 mg b d The effect on fat absorption defect is minimal 3 Antibiotics - Short course treatment with broad spectrum antibiotics such as oxytetracycline 250 mg. q. d.s. by mouth can be effective. 4. Corticosteroids- if folic acid therapy fails. Prednisolone 50 mg. /day for 7 days, dose gradually reduced to 15

predominance of lymphocytes. Sugar normal. 2. Isolation of virus - from nasopharyngeal swabs

rises to 100-200 mg. per 100 ml. during second week. Sugar normal. Cells 50-100, mostly polymorphs at first, later lymphocytes Rarely normal fluid. Signs - (a) Pulse fast and out of proportion to rise of temperature. (b) Excessive perspiration. (c) Patient is alert. 3. Paralytic stage - usually develops between 2nd and 5th days after onset of signs of involvement of nervous system. May set in without initial symptoms. Characteristics are - (i) Usually appears while there is still fever. (ii) Maximum at onset (iii) Distribution often asymmetrical. (iv) Usually begins within 1 to 5 days after onset of illness, progresses for 1 to 3 days, remains stationary for about a week and then shows rapid improvement for some weeks and then slower. (v) Absence of sensory loss DISTRIBUTION OF PARALYSIS - usually patchy, may produce monoplegia, paraplegia and quadriplegia. (a) Lower limbs - more frequently affected Usually quadriceps, tibialis anterior and peroneal group. (b) Upper limbs - most commonly deltoid. (c) Trunk -abdominal muscles, muscles of back, intercostals or diaphragm. (d) Respiratory disturbances - due to paralysis of diaphragm and intercostal muscles, or affection of respiratory centre in bulbar type - anxiety, increasing weakness of voice, cough, sucking in of epigastric or intercostal spaces with increasing use of accessory muscles of respiration, diminution in the numbers a patient can count after one inspiration, and cyanosis. 4. Convalescence - Initial paralysis usually diminishes to some extent after two or more weeks, and improvement may continue for several months. The affected muscles become flaccid whilst contraction will tend to produce severe deformities unless these are prevented. When chronic stage is reached six months to a year after initial infection, no further spontaneous improvement can be expected. Clinical types - Infection of a susceptible individual may result in one of 3 clinical manifestations - 1. Inapparent infection - in majority of cases. Does not progress beyond involvement of regional lymphnodes. However replication of virus in lymphoid tissue stimulates the immune system. 2. Abortive illness- occurs in 4-8% cases. Infection reaches viremic phase and foreign protein from virus is released into blood stream, as also endogenous pyrogens and other toxins from necrotic cells. This results in: (a) Abortive poliomyelitis - Presumptive diagnosis during epidemic Brief influenza-like illness with one or more of the following symptoms - malaise, anorexia, nausea, vomiting, headache, sore throat, constipation and localised abdominal pain. Fever seldom more than 103°F Coryza and cough uncommon. (b) Non-paralytic poliomyelitis - Subjective symptoms as in abortive type but headache, nausea, vomiting more intense, and soreness and stiffness of posterior muscles of neck, trunk and limbs. Fleeting paralysis of bladder not uncommon. 3. Paralytic poliomyelitis - (a) Spinal form - Paralysis of flaccid type usually asymmetrical and scattered in distribution, though more severe in one extremity Legs most frequently involved. Respiratory paralysis may result from involvement of diaphragm and intercostal muscles Transient bladder involvement in some. (b) Bulbar form - Muscles supplied by bulbar nuclei involved alone or with spinal musculature. Facial, palatal and sometimes pharyngeal paralysis causes change in voice, difficulty in swallowing, nasal regurgitation and choking when attempting to drink. Respiratory paralysis is the usual cause of death. Diagnosis: 1 CSF -Increased white cell count (usually below 500/mm3), often with high polymorph count in first few days followed by predominance of lymphocytes. Sugar normal. 2. Isolation of virus - from nasopharyngeal swabs during the first 5 days of illness only, but from stools and rectal swabs containing faecal material upto 5 weeks after onset. 3. Serology - A fourfold rise in level of antibody to the strain of virus isolated. Differential Diagnosis - Initial prodromal phase - (a) Infections of respiratory tract - Coryza, tonsillitis, bronchitis, influenza. (b) Gl disorders - Gastro-enteritis, rarely acute appendicitis. Preparalytic phase - 1. Viral (aseptic) meningitis - Rigidity more marked and persistent. Headache more severe Consciousness not clear. Hyperaesthesiae not prominent. Paralysis of limbs rare and occur late. C.S.F. clear or slightly turbid with upto 1000 cells per c. mm. usually lymphocytes 2 TB meningitis - Insidious onset. Previous ill health. Slow respiration. Flaccid paralysis uncommon. Ocular palsies. 3. Encephalitis - (Refer). 4. Conditions with tenderness of limbs - e. g. acute rheumatic fever and infection of bones, joints and muscles. No abnormal nervous signs. CSF normal. No true paralysis Paralytic stage - 1. CONDITIONS CAUSING PSEUDOPARALYSIS - (a) Rickets - enlarged epiphysis, beading of ribs, frontal bossing., diagnostic X-ray. (b) Scurvy - Swelling of limbs with extreme tenderness. Swollen and bleeding gums. (c) Syphilitic epiphysitis - occurs early in life. Other signs of congenital syphilis. Positive serology. X-ray changes. (d) Acute osteomyelitis - child may not move limb because of pain Diagnosis by X-ray. (e) Unrecognised trauma - e.g. contusion, sprain, fracture. 2. CONDITIONS CAUSING MUSCLE WEAKNESS - (a) Guillain-Barre syndrome - Paralysis commences in legs and rapidly ascends. No hyperaesthesia, often

impaired Serial estimations of plasma creatinine provide the best indication of the state of renal function

lupus erythematosus, anaphylactoid purpura. 2. Infections - Chronic pyelonephritis, renal tuberculosis. 3. Obstruction - Bilateral renal calculi, prostatic obstruction, urethral valves, retroperitoneal fibrosis. 4. Renovascular disease - Atheroma of renal arteries causing renal ischemia. 5. Interstitial nephritis. 6.Polycystic kidneys. B. SECONDARY RENAL DISEASE (Renal complication of systemic disease) 1. Diabetes mellitus. 2. Hypertension. C. IDIOPATHIC Pathogenesis-of clinical syndrome of CRF -1. Uremic toxins - Fall in glomerular filtration rate and reduction in renal tubular secretory capacity prevent certain substances from being excreted by the kidney and these probably produce their adverse effects on every organ of the body. However studies of the effects of dialysis, dietary modifications and transplantation have not identified the toxins involved. 2. Electrolyte and water excretion - Limited ability of diseased kidney to manipulate electrolyte and water excretion appropriately may lead to either salt and water retention with oedema and circulatory congestion, or to salt depletion. 3. Erythropoietin and 25-hydroxycholecalciferol -There is impaired production of erythropoietin and reduce hydroxylation of 25-hydroxycholecalciferol xycholecalciferol, the most active metabolite of vitamin D, a step which normally occurs in the kidney. 4. Renin - Impaired perfusion of remaining renal tissue may stimulate the inappropriate release of renin. 5. PTH - One of the principal disturbances of endocrine function in CRF is marked hyperplasia of parathyroid glands with very high levels of PTH. This contributes to renal oesteodystrophy, soft tissue calcification and bone necrosis in CRF, and also probably to pruritus, anemia, hypehipidemia, neurological disturbances and sexual dysfunction. However patients with primary hyperparathyroidism manifest few of these disturbances and the role of PTH in uremic toxicity is still uncertain. 6. 'Middle molecules' - The middle molecule hypothesis is based on the apparent absence of neuropathy in patients on chronic peritoneal dialysis (which is less efficient than hermodialysis in removing small molecules, but more efficient for middle molecules), and the high risk of neuropathy in patients treated with small surface area dialysers. Also the observation that when weekly hemodialysis time was markedly reduced, neuropathy did not appear provided a membrane highly permeable to middle molecules was used. While the identity of uremic toxins is largely unknown, it is suggested that some dialysis schedules permit accumulation in body fluids of molecules in the range 1,000 to 2,000 daltons, and these cause some of the uremic problems encountered by patients on regular dialysis. Stages - of chronic renal failure - 1 Diminished renal reserve -About 50-70% of kidney function has to be lost before the effect, on blood chemistry becomes readily detectable, e. g. , by rise of blood urea. 2. Renal insufficiency - from loss of further kidney function. There is moderate nitrogen retention (blood area 50-100 mg/100 ml., plasma creatmine 1.5-2.5 mg./100 ml.) and mild acidosis, may occur. Usually no symptoms except nocturia Hypertension may dominate the clinical picture. 3. Stage of renal failure - Further kidney damage produces considerable nitrogen retention, derangement of plasma electrolytes, anemia and usually marked symptoms. The term 'uremia' is reserved for the clinical syndrome resulting from advanced renal failure, when glomerular filtration rate is Management - 1. Monitoring renal functions - (a) Blood urea and creatinine - levels always raised. However normal levels cannot be taken to indicate that renal function is not impaired Serial estimations of plasma creatinine provide the best indication of the state of renal function in patients with CRF. Use of reciprocal plots of serum creatinine against time has shown that the decline in renal function is linear with time. An abrupt decline or acceleration in the slope demands a search for the cause (hypertension, UTI, hypovolemia or fluid overload, urinary tract obstruction particularly in elderly males, drugs or pregnancy). Hypercatabolic renal failure refers to rise of urea of more than 6.5 mmol/litre per day. (b) Ultrasound - to ascertain renal size and to monitor renal function regularly in patients with CHF who are prescribed ACE inhibitors (which may cause acute deterioration in renal function). 3. Plasma sodium -Hyponatremia is common. 4. Potassium - Normal values until terminal stages when hyperkalemia occurs. 5. Calcium, phosphate and magnesium - Increased plasma phosphate and decreased calcium levels. Magnesium levels normal or slightly raised. 6. Uric acid - increased. 7. Hypehipidemia - Raised plasma levels of triglycerides and pre-beta lipoproteins 8 Anemia - Normochromic normocytic anemia almost constant. Contributing factors - (a) Decreased production of erythropoietin by diseased kidney (ii) Direct marrow suppression by uremic toxins. (iii) Shortened red cell survival (iv) Increased blood loss 2 Conservative management of uremic syndrome - (a) Diet - Low protein diet of 40pg of protein (0.6g/kg). The diet must be high in essential amino acids and total caloric intake must exceed 35 kcal/kg/day, sing carbohydrate supplements if necessary. (b) Treatment of hyperkalemia - has already been described. 3. Salt and water intake - Salt overload and salt depletion are both hazards. The

Diabetes mellitus, amyloidosis, SLE, Henoch-Schonlein Purpura, cryoglobulinemia, polyarteritis nodosa

as dipyridamole because of involvement of coagulation process in crescent formation, 3, CHRONIC GLOMERULONEPHRITIS CLINICAL FEATURES (a) Persistent proteinuria - After an apparent recovery from attack of acute nephritis or asymptomatic proteinuria discovered at routine examination. After a variable period of upto 20 years, hypertension and renal failure supervene (b) Nephrotic syndrome - About half the patients who develop chronic glomerulonephritis pass through a nephrotic phase with hypoalbuminemia, oedema and massive proteinuria. (c) Persistent hematuria - Hematuria begins with onset of sore throat and may last several weeks No oedema or hypertension. In between attacks patient is well. Many patients also have persistent proteinuria. (d) Chronic renal failure - Final stage. In majority the symptoms of advanced chronic renal failure, hypertensive cardiac failure, or malignant hypertension are the first indication of its presence. Symptoms and signs of uremia - nausea, vomiting, hiccough, fatigue, anaemia (normochromic, normocytic); dyspnoea, pruritus, pericarditis, bloody diarrhoea, nocturia Often the only symptom before the onset of uremia is nocturia for a period of months or years. DIFFERENTIAL DIAGNOSIS -1 Essential hypertension - No history of AGN, patient not pale or inert. No anemia, no oedema of feet. B.P. more labile No or slight impairment of renal function. 2. Chronic pyelonephritis - (a) Urine culture shows organisms though these may appear intermittently. (b) History of recurrent rigors and fever, often with loin pains. (c) Urinary excretion of white cells much more than of red cells. (d) Pyelography will show distortion of the pelvicalyceal pattern. 3. Renal tuberculosis - should be considered in any patient with unexplained genitourinary symptoms or persistent symptomless albuminuria, pyuria or microhaematuria Positive culture or other diagnostic techniques. Excretory urograms may be normal in the presence of minimal disease or may reveal changes suggestive of tuberculosis such as incomplete visualization of one or more calyces, a fuzzy outline of a calyx, a cavity, hydronephrosis or nonvisualization of the entire kidney. Cystoscopy may demonstrate diffuse cystitis, tubercles, ulcerations or 'golf-hole1 ureters. 4. Polyarteritis nodosa - Hypertension and renal failure with often arthropathy, neuropathy and pyrexia 5 Systemic lupus erythematosus - may present with renal involvement. The commonest finding is persistent symptomless proteinuria usually accompanied by microscopic haematuria. 6. Polycystic kidneys - Hypertension, cardiac hypertrophy, haematuria and renal insufficiency simulate chronic nephritis. Palpable kidney tumours and diagnosis by radiology MANAGEMENT - (i) Control of hypertension with suitable hypotensive agents. (ii) Treatment of anaemia by blood transfusion (iii) Low protein diet. (iv) Dialysis (See treatment of chronic renal failure). SALT-LOSING NEPHRITIS - As the glomerular filtration rate (GFR) falls, the remaining living nephrons undergo osmotic diuresis and the loss of sodium in urine causes salt-wasting' or salt-losing nephritis' The common causes of salt-losing nephritis are: (a) Chronic renal failure. (b) Pyelonephritis. (c) Addisons disease. This can be treated by careful resalination by giving 250 ml. of 3 percent sodium chloride. 4. NEPHROTIC SYNDROME (NS) - Definition - A clinical condition in which there is oedema, proteinuria and hypoproteinemia irrespective of etiology or any other additional abnormal clinical features. Over 80% of patients with nephrotic syndrome have idiopathic glomerular lesions Causes - 1. Primary glomerular diseases - (a) Minimal change nephropathy (b) Mesangioproliferative glomerulonephritis (c) Membranous nephropathy. (d) Focal and segmental glomerulosclerosis. (e) Crescentic glomerulonephritis. 2. Idiopathic 3 Secondary to other diseases - (a) Infections - Malaria, hepatitis B, herpes zoster, streptococcal and staphylococcal infections, syphilis, leprosy, schistose miasis. (b) Drugs - Heavy metals such as gold, anticonvulsants (especially phenytoin andtroxidone), penicillamine, ACE inhibitors, heroin, rifampicin NSAIDs, tolbutamide and probenecid. (c) Tumours - Carcinoma, leukemia and lymphoma, multiple myeloma. (d) Systemic diseases - Diabetes mellitus, amyloidosis, SLE, Henoch-Schonlein Purpura, cryoglobulinemia, polyarteritis nodosa. (e) Familial disorders - Congenital (neonatal) nephrotic syndrome. Airports syndrome, Fabrys disease. (f) Miscellaneous conditions - Reflux nephropathy, renal vein thrombosis, toxemia of pregnancy, allergic reactions to insect bites, pollens and vaccines, renal artery stenosis. Pathology - The kidneys are large, pale and soft. Biopsy studies show a wide variety of histopathological changes - (a) Minimal change nephropathy is common in very young children (b) Focal glomerulosclerosis. (c) Membranous nephropathy. (d) Proliferative glomerulosclerosis - accounts probably for the largest group of adults with idiopathic nephrotic syndrome. Clinical features - 1. Age and sex - Two to three times more common in childhood with peak incidence at 2-3 years In this age group there is a male female ratio of 2.5:1, in adults, sex incidence is equal. 2. Oedema - Oedema is peripheral involving the limbs, particularly lower limbs. In children oedema may be more obvious in

-ROCKY MOUNTAIN SPOTTED FEVER

rises steadily to maximum on 5th day. (b) Stage of eruption and nervous excitement - (i) Rash - usually on 5th day. Pink macules varying in size and shape, disappearing on pressure. Generalised but face rarely involved In a day or two lesions become dull red and finally slate blue or grey before disappearing. Petechiae may occur. Following eruption of macules, paler subcuticular lesions appear between the macules - subcuticular mottling or mulberry rash. (ii) Temperature - high till the 6th day. (iii) Delirium -replaces headache and stupor. Mostly at night. (iv) Spleen may be palpable. (c) Stage of prostration -Patient appears exhausted and stuporose, this may progress to delirium or coma. Hypotension may result from myocarditis and peripheral vasodilatation. Features of grave prognostic significance include -progressive fall of B. P. , gangrene of fingers or toes, pressure areas and genitalia, urinary and faecal incontinence, renal failure and secondary infection. (d) Stage of defervescence- In favourable cases about the 12th or 14th day striking improvement occurs. Patient becomes quieter. Fever becomes remittent and drops to normal in a few days. Complications - (a) Bronchopneumonia. (ii) Myocarditis. (iii) Thromboembolic complications. (iv) Peripheral failure. (v) Suppurative parotitis. (vi) Gangrene of areas of skin. 2. BRILL-ZINSSER DISEASE - is a recrudescent form of epidemic typhus. Intense frontal headache and low B. P. are prominent features. Scrub typhus - caused by R. tsutugamushi and transmitted by larval mites. Eschar at site of mite feeding. Lymph nodes draining the eschar swollen and tender with generalised lymphadenopathy, fever, chills, headache, malaise and orbital pain. Maculopapular rash in about 50% may appear between 3rd and 7th day. Lymphocytosis in blood (large lymphocytes). Convalascence prolonged Diag. - (a) Serology: Detection of antibodies by microimmunofluorescence (MIF). A titre of 1:128 in diagnostic. (b) Weil Felix reaction- Louse and flea or tick borne typhus agglutinate with strain OX-19 and OX-2, scrub typhus with OX-K alone. Tr. - Doxycycline 200 mg/day for 10 days. II. Spotted fevers-ROCKY MOUNTAIN SPOTTED FEVER - is the most severe form. Caused by R. ricketsii and carried by ticks. Abrupt onset of fever with chills, severe headache, photophobia, prostration and muscle and joint pains Temperature 40°-41 °C with irregular morning remissions. Rash on 3rd or 4th day, maculopapular, first on extremities then spreading to the trunk; the rash becoming petechial. In severe cases rash becomes confluent, deep red or purple and may necrose. CNS manifestations include restlessness, confusion and delirium. In severe cases coma and peripheral vascular collapse precede death. BOUTONNEUSE FIEVRE - Milder than Rocky Mountain spotted fever. Primary cutaneous lesion or eschar at the site of tick bite. Regional lymphadenopathy in glands draining the eschar. Maculopapular rash Fever subsides by lysis in 2nd week. RICKETTSIALPOX - caused by R akari, transmitted to man by blood-sucking mite. Fever, eschar and papulovesicular eruption. Recovery in 1-2 weeks without sequelae. Diag. -Serology: MIF. Rickettsia of the spotted fever group are antigenitically cross-reactive and the same antigen may be used to detect all species. A titre of 128 is diagnostic. Tr. - Doxycycline 200 mg/day, for 1 -7 days depending on severity. Q-fever - Casual organism coxiella burnetti. Transmission - is

Tracheostomy undertaken early in patients whose disease is not controlled with conservative sedative regimen

periosteal - calcification and myositis ossificans. Wedge fracture of thoracic vertebrae can also result from spasms. 3. Complications due to tracheostomy and prolonged respiratory support. 4. Multiple organ dysfunction - In severe fulminant tetanus. Besides respiratory system, CVS (hypotension requiring inotropic support), Gl system (ileus and massive bleeds), liver (rise in serum enzymes and bilirubin), renal insufficiency (rise in serum creatinine, rarely acute renal failure). 5. Sudden death - from cardiovascular instability, excessive vagal tone giving rise to bradycardia and cardiac arrest, hypoxia due to prolonged laryngeal spasm or continuous seizures, hyperpyrexia, massive pulmonary embolism, heart block. Prognosis - can be assessed from -1. Type of infection - Neonatal and puerperal tetanus carry a very bad prognosis. 2. Type of patient - Prognosis bad in elderly and drug addicts. 3. Frequency and severity of spasms. 4. Incubation period - Mortality higher if incubation period is short. 5. Period of onset - Interval of less than 48 hours between the first symptom (usually trismus) and the first spasm, carries double or treble the mortality. 6. Severity of tetanus - as described above. Management - AIMS OF TREATMENT - 1 .Neutralize existing toxin before it gains access to the nervous system. 2. Reduce further production of toxin. 3. Control neuromuscular and autonomic manifestations. 4. Sustain the patient until effects of the toxin resolve. 1. Neutralization of unbound toxin - Hyperimmune human anti-tetanus immunoglobulin 1000-3000 units IM/IV as a single dose or anti-tetanus serum 10,000 units IV after testing for sensitivity. Intrathecal HITG 1000-3000 units given before onset of major spasms may prevent disease progress .2. Reduction of further toxin production - (a) Care of the wound - Removal of foreign material and debridment of non-viable tissue of entry wound. (b) Antibiotic - Benzyl penicillin GOO mg G-houhy IM or IV, or Erythromydn 500 mg G-houhy for 10 days to minimize risk of bacterial infection Metronidazole can be used in patients allergic to penicillin. 3. Control of rigidity and tetanic seizures (a) Avoidance of provocative stimuli -such as noise, unnecessary movement, and keeping injections to minimum minutes 2-G hrly. Note - Respiratory depression can occur when using combinations and the doses above are for single dose regimens. If drug treatment cannot control muscle spasm and seizure without impairing consciousness or respiration, muscle paralysis and assisted ventilation become necessary. (c) Tracheostomy undertaken early in patients whose disease is not controlled with conservative sedative regimen, because inadequate control of muscle spasms results in asphyxia and depression of swallowing reflex. (d) Induced paralysis with ventilator/ support - Neuroparalytic agents pancuronium 2-4ng bolus 1/2-1 hrly initially or gallamine 20^1-Oml iv., the dose being so adjusted that the neuromuscular paralysis achieved allows or efficient ventilator/ support (PaO2 should be maintained >70mm Hg and PaCO2 at 35-40mmHg. ) When spasms abate, pancuronium or gallamine is stopped; but ventilatory support is continued till the patient is fit to be weaned 4. Autonomic circulatory disturbances - (a) Hypotension (systolic BP<70)>200, diastolic >110) - propranolol 5-1 Omg p. o. or 5mg sublingual nifedipine or both. Morphine 2-5mg as infusion may be

picture - Onset - Sudden with fever, chilly sensations, and prostration, catarrhal

viruses circulating in the population: Influenza virus has thus been described as an unvarying disease caused by a varying virus. Incubation period - 1 to 3 days. Clinical picture - Onset - Sudden with fever, chilly sensations, and prostration, catarrhal symptoms, headache, pains and dry cough. Sometimes erythematous rash. CLINICAL TYPES - 1. Febrile type - Only constitutional symptoms - fever, malaise, headache, severe bodyache, catarrh, congestion of eyes and throat; rapid prostration. Dry cough with few or no signs in chest. Fever lasts for 4 to G days, there may be relative bradycardia. 2. Respiratory type - (a) Bronchitis and bronchopneumonia. (b) Pleurisy; empyema not uncommon. (c) Pneumonia - (i) Fulminating rapidly fatal form in which pneumonia is present from the onset. (ii) Progressive form in which on the 2nd or 4th day signs of pneumonia begin to develop with copious fine crepitations usually basal. The sputum may be pinkish, frothy and copious, or tenacious mucus of several hues. (iii) Late form in which often after apparent recovery from the primary influenza, pneumonia suddenly supervenes on the 4th to 10th day after the onset. 3. Gl type -Temperature rarely above 37.5°C, severe anorexia and vomiting, abdominal discomfort and general prostration Tympanitis, diarrhoea and continued fever may simulate typhoid fever. 4. Malignant type - Severe toxemia, cyanosis and rapid cardiac failure. Always fatal. 5. Nervous type - Headache sometimes very severe, delirium, intense depression which may continue after the acute illness. A true meningitis may occur. Complications and sequelae - 1. Respiratory - Bacterial bronchopneumonia or lobar pneumonia, less often pure viral pneumonia. These may be concurrent with initial viral infection or follow after an interval. Staphylococcal pneumonia is a serious sequel and may be fatal, less severe infections may result in lung abscess. 2. Nervous system - Post influenzal psychoses, insomnia, irritability, polyneuritis, neurasthenia, meningitis and hemorrhagic encephalitis. 3. Circulatory system - Cardiac dilatation, irregularities, pericarditis, endocarditis. 4. Suppuration - Otitis media, mastoiditis, sinusitis. 5. Miscellaneous - Thrombophlebitis, arthritis, orchitis, myositis, nephritis, intestinal hemorrhage. Management - 1. Complete rest in bed. 2. Analgesics and sedatives. 3. Nose drops and throat gargles, or steam inhalations for congestion of nose and throat. Cough suppressive such as codein. 4. Antibiotics for secondary infections such as otitis media and pneumonia 5 Antiviral drug - Amantadine or rimantadine 200 mg/day orally useful for influenza A PREVENTION - (a) Vaccines - Polyvalent influenza virus vaccine 1 ml subcut; or 0.1-0.2 ml. intradermally given 1-2 weeks apart gives moderate temporary protection against current strains. (b) Anti-viral agents - Ribavirin 100-200 mg as effective as vaccination against Influenza A strains and may be started at the same time as vaccination to provide protection until immunity develops. 5. MEASLES Epidemiology - Age - mostly children between ages of 3-5 years, rare during first G months of life because of transferred passive immunity from mother. Causative agent - RNA paramyxovirus group. Transmission - Highly infectious and spread by direct contact or droplet infection. Patients suffering from measles shed virus from their respiratory tract during the prodromal period and for 24-48 hours after the rash appears Immunity - Immune response is not fully competent in early infancy, intercurrent infection or malnutrition further reduce these responses, increasing severity of the disease. Transplacental material IgG