Paediatric Conditions

Tuberculous Meningitis

Tuberculous meningitis is the inflammation of meninges due to lymphohematogenous spread of the primary infection of tuberculosis to the meninges, found in about 0.3% of untreated primary infection in
children. It is the most dangerous form of extra-pulmonary tuberculosis. 70% of the cases are found in children less than 5 years of age.

Salient features

  • The clinical progression of tubercular meningitis (TBM) may be rapid or gradual. The signs and symptoms progress slowly over several weeks and can be divided into three stages.
      • The 1st stage, which typically lasts 1-2 weeks, is characterized by non-specific symptoms, such as fever, headache, irritability, drowsiness and malaise. Focal neurologic signs are absent.
      • The 2nd stage usually begins more abruptly. The most common features are lethargy, neck-rigidity, seizures, positive Kerning or Brudzinski signs, hypertonia, vomiting, cranial nerve palsies and other focal neurologic signs.
      • The 3rd stage is marked by coma, hemiplegia or paraplegia, hypertension, decerebrate posturing, deterioration of vital signs, and eventually, death.
  • Complications: Survivors may have motor deficits, cranial nerve deficits, mental retardation, learning disabilities, seizures, hydrocephalus, blindness, deafness and diabetes insipidus.
  • The diagnosis is made by analysis of CSF on lumbar puncture, which shows lymphocytic leucocytosis with elevated protein and a low sugar (for details see table 1 in section on meningoencephalitis .

Demonstration of AFB in CSF confirms the diagnosis, but the yield is very poor.Culture of CSF shows growth of M. tuberculosis, takes too much time.Positive tuberculin skin test corroborates the diagnosis but may be negative in severely malnourished/disseminated disease. 20-50% of children have a normal chest radiograph others may show primary disease. CT Scan or MRI of brain may be normal during early stages of the disease. Later, it can show exudates in the basal cisterns of brain, periventricular ooze and hydrocephalus. Some may show tuberculomas even.

Treatment
Treatment consists of proper supportive care, including nonpharmacological treatment, specific antitubercular therapy, treatment of increased intracranial tension and, if required, surgical treatment.

Nonpharmacological

  1. Nutrition: after initial stabilization, nutritional rehabilitation should be done as given in section on protein energy malnutrition.
  2. Skin care and prevention of bedsores.
  3. Care of bowel and bladder.
  4. Physiotherapy and occupational therapy should be instituted early to prevent deformities and contractures..

Pharmacological

  1. Appropriate fluid therapy to correct dehydration due to frequent vomiting and decreased oral intake.
  2. Treatment of SIADH. Fluid restriction to 3/4or 2/3rd of maintenance. Treatment of raised intracranial tension
  3. Inj: Dexamethasone: 0.15 mg/kg IV 6 hourly for 2 weeks followed by
    Tab Prednisolone 1.5 mg/kg/day orally through feeding tube for 4 weeks. This should be tapered over another 2 weeks. A total of 6-8 weeks therapy with steroid is recommended.
  4. Mannitol (20% solution) 1.5 to 2 g/kg or 8-10 ml/kg over 30-60 minutes. Repeated every 6-8 hours for 7 days. Lower doses (0.25 g/kg/dose) can also be tried.
    Or
    Glycerol 1 ml/kg/dose every 6-8 hours, diluted in orange juice or water, given through feeding tube.
    Or
    Tab Acetazolamide 50 mg/kg/day, in 3 divided doses for 2-3 weeks.
  5. Anticonvulsant therapy – presence of seizures necessitates treatment with phenytoin or carbamazepine in appropriate doses.
  6. Specific antitubercular therapy – as given in management of tuberculosis (see section on tuberculosis).
  7. Surgical Treatment Ventriculoperitoneal Shunt (VP Shunt): All TBM show some degree of hydrocephalus by 4 weeks. Obstructive hydrocephalus should be shunted immediately. Non obstructive hydrocephalus with increased intracranial pressure as shown by ventricular tap or CT scan will also be benefited by VP shunt. An early shunt is preferable.

Follow up

  • Patient should be kept under follow up after discharge from the hospital and assessed for neurological deficit and features of increased intracranial pressure (ICP). One of the common cause of increased ICP is untreated hydrocephalus or blocked shunt.
  • Check compliance to drugs and ensure that occupational therapy/physiotherapy is being continued.
  • Assess physical, mental, visual and auditory handicap and take expert opinion for rehabilitation from other specialists.

Patient/parent education

  • Seriousness of disease must be explained.
  • Context survey should be done and any other member in the family found to have active TB should be counselled to attend TB clinic for therapy.
  • Need for compliance should be emphasised
  • Drug toxicity and side effects must be explained.
  • Neurological deficits may appear even in a patient on therapy.

References

  1. Neurotuberculosis with Special Reference to Management of Tubercular Meningitis in Children, 1982, Bull. Int. Union Tuberc, 57, 43-48.
  2. Three Chemotherapy Studies of Tubercular Meningitis in Children. Tubercle 1986, 67: 17-29.
  3. Tuberculosis in Children. A Statement of Scientific Committee of IUATLD, 1991 Bull Int Union Teberc Lung Dis, 66: 61-67.
  4. Treatment of Tuberculosis: Consensus Statement of IAP Working Group. Indian Paediatric 1997, 34: 1093-96.
  5. Jacob RF, Sunokorn P. Tuberculous Meningitis in Children: An Evaluation of Chemotherapeutic Regimens,1990 Ann Rev Resp Dis, 141: (5) A 337.
  6. Dexamethasone Adjunctive Treatment for Tuberculous Meningitis. Paediatric Inf Dis 1993, 39: 361-64.
  7. Mycobacterial Infections. In: Nelson’s Textbook of Paediatrics. Behrman, Leigman, Jenson (eds), 16th Edition, 1999, pp 885-897.

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Acute Meningoencephalitis

Acute meningoencephalitis is an acute inflammatory process involving meninges and brain tissue, due to infectious causes. The common aetiological agents are viruses and bacteria. Children of any age may be affected.

Salient features

Fever, headache, vomiting, irritability altered state of consciousness, signs of meningeal irritation and seizures. Children of any age may be affected.

  • CSF examination differentiates the viral from bacterial cause of acute meningoencephalitis. (Table 1).

Treatment

Supportive treatment is the mainstay of therapy and is started immediately.

  1. Maintain airway, breathing and circulation.
  2. Control of seizures with IV injection of Diazepam 0.2 to 0.4 mg/kg stat followed by Inj Phenytoin 10-20 mg/kg stat followed by 5 mg/kg/day in divided doses.
  3. Increased Intra-cranial tension is treated by proper positioning of patient with head elevated at 15 -30° position, fluid restriction to 2/3rd of maintenance, 20% Mannitol 5 ml/kg over 10-15 min followed by 3 ml/kg every 6 hourly for 48 hours and then SOS.
    Or
    Acetazolamide 50-75 mg/kg/day in 3 divided doses through feeding tube
    Or
    Glycerine 1 ml/kg/day through feeding tube may be added if increased intra cranial tension persists.
  4. Fever is controlled as given in section on fever.
    (CAUTION: Never give aspirin ).
  5. The intravenous fluid is given at 2/3 of the maintenance requirement initially. The electrolyte concentration of the blood is monitored very closely. Any imbalance is treated promptly. Fluid restriction is not done if patient is dehydrate or is in shock.
  6. Feeding: Initially the patient is kept nil orally for first 24-48 hours. Later on the feeding is guided by the level of sensorium. A tube feeding is helpful for feeding as well as for giving medicines.


Table 1. CSF findings in meningoencephalitis.

Pressure (mmH2O) Leucocytosis (mm3) Protein (mg/dl) Glucose (mg/dl)
Normal 50-80 <5, >75% Lymphos 20-45 > 50 or 75% serum glucose
Acute bacterial meningitis Usually elevated (100-300) 100-10,000 PMN’s* predominate 100-500 Decreased (<40)
Acute viral meningoencephalitis Normal or elevated Rarely > 1000 PMN’s early but Lymphos predominate in the most of the course 50-200 Normal rarely decreased
Tubercular meningoencephilitis Usually elevated 100-500 PMN’s early but later lymphocytes predominate 100-3000 <50

*PMN’s = Polymorphonuclear leucocytes

Specific treatment

Until a bacterial cause is excluded, parenteral antibiotic therapy should be administered. The choice of antibiotics depends upon age of the patient and prevalence of organism in the area.

Age 0-3 months

  1. Inj Cefotaxime 200 mg/kg/day IV in 4 divided doses for 14 days.
  2. Inj Ampicillin 300 mg/kg/day IV in 4 divided doses for 14 days.

Age 3 months – 12 years

  1. Inj Ceftriaxone 100 mg/kg/day IV in 2 divided doses for 10 days
    Or
    Inj Cefotaxime 200 mg/kg/day IV in 3 divided doses for 10 days
    Or
    Inj Ampicillin 300 mg/kg/day IV in 4 divided doses for 10 days
  2. Inj Chloramphenicol 100 mg/kg/day in 4 divided doses for 10 days

If meningococcus is suspected/isolated Inj Penicillin G 300,000 – 400,000 IU/kg/day in 4 divided doses for 7-10 days.

Viral meningoencephalitis

Herpex simplex virus: (generally diagnosed by focal encephalitis or CT scan) Inj Acyclovir 30 mg/kg/day in 3 divided doses for 145-21 days. Non HSV viral encephalitis is treated by supportive therapy only.

The lumbar puncture is repeated at 48 hours to see the response. However, if the patient is improving well, a repeat lumbar puncture may not be necessary.

Advise at discharge

  1. Regular follow up for neurological assessment including deafness is advised.
  2. Anticonvulsant therapy to be continued if seizures are recurrent during course of meningitis.
  3. Children with sequated would require assessment of handicap and multidisciplinary management. Occupational/physiotherapy may be taught during hospital stay it self.

References

  1. Central Nervous System. In: Nelson’s Textbook of Paediatrics. Behrman, Leigman, Jenson (eds), 16th Edition, 1999, pp 751-761.
  2. Paediatric Infectious Diseases; 4th Edition pp 457-468.
  3. Acute Viral Encephalitis in childhood. BMJ 1995; 310: 139-140.

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Febrile Seizures

Febrile Seizures are brief (2-5 min), generalized tonic-clonic and self limited seizures followed by a brief post-ictal period of drowsiness, in an otherwise healthy, febrile child of 6 months to 5 years of age, without any evidence of underlying neurological disease. They are the most common seizure disorder during childhood, with a uniformly excellent prognosis.

They occur rarely before 6 months and after 5 year of age. The peak age of onset is approximately 14 -18 months of age, found in 3-4% of young children. There is a strong family history of febrile convulsions in siblings and parents, suggesting a genetic predisposition. Except for the cases at high risk, simple febrile seizures rarely develop into epilepsy.

Salient features

  • Febrile seizures usually occur when the temperature is rising rapidly, to generally 390C (1020F) or more of core temperature.
    They are of two types:

      • Typical (Simple) febrile seizure occurs on day 1 of fever, does not last for more than 10 minutes; generalized tonic-clonic; generally not more than one episode within 24 hours.
      • Atypical or complex febrile seizure may persist for more than 15 minutes; it could be focal in nature; more than one episode of seizure in 24 hours; associated with abnormal neurological findings or deficits. An organic cause such as an infectious or toxic process, should be considered and investigated.
  • Lumbar puncture: A lumbar puncture with examination of CSF is essential to rule out possibility of meningitis in cases with first episode of febrile seizures.
  • EEG is not required in case of simple febrile seizures. However, in cases with atypical febrile seizure or in a child with high risk for developing epilepsy, it may be helpful.
  • High risk for developing epilepsy, include a positive family history of epilepsy, initial febrile convulsion prior to

Treatment

Careful search for the cause of fever and treatment of fever (see section on fever).

Most febrile seizures are brief and would be over by the time a child is brought to the doctor or health facility.

Nonpharmacological

Clear the airway, semi-prone lateral position and oxygen therapy.

Pharmacological

In cases presenting with seizures, the mainstay of management is prompt administration of anticonvulsants.

The best drug is Diazepam in a dose of 0.3 mg/kg by slow intravenous or rectal route. It can be repeated if seizures do not subside (per rectal dose may be given up to 0.5 mg/kg/dose).

Intermittent prophylaxis (during febrile illness)

It is a safe and effective method of prophylaxis. Tab/Syp Diazepam 0.3 mg/kg/dose every 8 hours (1 mg/kg/day) for 2-3 days of febrile illness, started on the day of onset of fever. Dose can be adjusted if over sedation or ataxia noted.

Continuous prophylaxis

Phenytoin and carbamazapine are ineffective for prophylaxis and phenobarbitone has serious effects on cognitive function. Sodium valproate is effective but potential risk do not justify its use.

Patient/parent education

  • The parents and caretaker should be assured of the benign nature of the disease and should be told that no neurological deficit or mental retardation occurs as a result of simple febrile seizure.
  • They should be taught about control of fever at home. They can be taught to give diazepam per rectally at home.
  • Routine immunization as per schedule should be followed. After DPT vaccination, oral paracetamol 15 mg/kg/dose every 6th for 2 or 3 days and similarly, after measles vaccination, oral paracetamol in the same dose started on the 4th day from the day of vaccination and given for 3 to 4 days to avoid precipitation of febrile seizures.

References

  1. Febrile Seizures. In: Nelson’s Textbook of Paediatrics. Behrman, Leigman, Jenson (eds), 16th Edition, 1999, pp 1818-1819.
  2. Protocol for Childhood Neurological Diseases: Manual by Expert Group of SAARC Countries, 1999.
  3. Febrile Seizures: An update, Indian Paediatrics 1995, Vol 32: 566-572.
  4. Long-term Outcome of Prophylaxis for Febrile Seizures. Arch Dis Child 1996, 74:13-16.
  5. Recurrence Risk after First Febrile Seizure and Effect of Short-term Diazepam Prophylaxis. Arch Dis Child 1985; 60:1045-1049.

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Neurocysticercosis

The neurocysticercosis is the disease produced by invasion of the CNS by the cystic stage (cysticercus) of pork-tapeworm ( Taenia solium). It is the most common parasitic cause of CNS disease and is prevalent in every continent except Antarctica. Humans acquire the disease when they ingest the food or water contaminated with the eggs of T. solium.

Salient features
  • The clinical features depend upon site and number of cysts in the CNS, and the inflammatory response of the CNS. It can present as a ‘silent’ case on one hand to encephalitis like symptoms. On the other hand any neurologic, cognitive, or personality disorder in an individual from an endemic area may represent neurocysticercosis. However, the seizures, either focal or generalized, remain the most common form of presentation.
    Less common is the feature of meningeal irritation, hydrocephalus or increased intra-cranial tension. Decreased visual acuity may be seen in ocular cysticersosis. In spinal neurocysticercosis, patients present with evidence of cord compression, nerve root pain, transverse myelitis, or meningitis.
  • Imaging studies (CT & MRI) and serologic tests (ELISA or immunoblot) are the only way to confirm the diagnosis. Cystic lesions with or without enhancement and calcifications are the commonest findings.

Treatment

Issues concerning when and how to treat are not completely resolved. Parenchymal lesions resolve even without treatment. Anticonvulsant drugs may be the only symptomatic therapy required. However, some workers suggest cysticidal therapy because it leads to rapid resolution.

Pharmacological

  1. Tab Albendazole 15 mg/kg/day in 2-3 doses per day for 15 days, taken with fatty meals.
    Or
    Tab Praziquantel 50 mg/kg/day in 3 divided doses for 15 days.
    Albendazole is as effective as Praziquintal.
    Patients should be monitored carefully for development of raised ICP.
    Tab Prednisolone 1-2 mg/kg/day started 2-3 days prior to cysticidal drugs and continued for 5-7 days may prevent these effects.
  2. Anti-convulsants, such as carbamazepine or phenytion should be used in appropriate doses to control the seizures. An optimum duration of therapy has not been settled. However, a seizure free interval for even one year, may be taken as indication to taper off the therapy (for details see section on epilepsy; status epilepticus).
  3. Corticosteroid Currently, the use of corticosteroid is limited to following category of patients only:
    i. For patients who develop signs of increased intra-cranial tension during treatment.
    ii. Large sub-arachnoid cysts. (these cases have risk of developing cerebral infarcts due to occlusive endarteritis).
    iii. Encephalitis like features.
    iv. Cysticercal angitis.

Surgical treatment

  1. A ventricular shunt must be placed if there is evidence of hydrocephalus. This should precede the medical treatment.
  2. Surgical intervention is also required for removal of large solitary cyst for decompression, removal of mobile cysts causing ventricular obstruction, and some cases that fail to respond to medical therapy. (spillage of cyst contents is not seen in these cases as is seen in cases of echinococcosis ).
  3. Ocular cysticercosis should be treated surgically only; enucleation is frequently required.

Patient/parent education

  • Minimising the opportunities for ingestion of facally derived eggs by means of good personal hygiene, effective faecal disposal and treatment and prevention of human intestinal infections.
  • All members of a family of an index case of cysticercosis should be examined for the presence of eggs or signs of disease.
  • Prolonged freezing or thorough cooking of food items, pork in this case, will kill the parasite.

References

  1. Cysticercosis. In: Nelson’s Textbook of Paediatrics. Behrman, Leigman, Jenson (eds), 16th Edition, 1999, pp 1078-1079.
  2. Therapy for Neurocysticercosis. Clin Inf Dis 1993, 17:730-735.
  3. Medical Treatment of Neurocysticercosis. Arch of Neurol 1995, 324: 1137-1139.
  4. Albendazole Versus Praziquentel in the Treatment of Cerebral Cysticercosis. Transactions of Royal Soc Trop Med & Hyg 1991; 85: 244-247.
  5. Dexamethasone with Albendazole. J Neurol 1990; 237: 279-280.
  6. Etiology and Management of Single Enhanced CT lesion. Act Neurol Scand 1991, 84: 465-470.

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Nephrotic Syndrome (NS)

Nephrotic syndrome is an important chronic disorder in children. It can be primary (idiopathic) or secondary (SLE, Henoch Shonlein purpura, amyloidosis etc). About 90% children with idiopathic nephrotic syndrome have ‘minimal lesion’ on renal histology and respond promptly to corticosteroids. Approximately three fourth patients have one or more relapses. Steroid toxicity and frequent serious infection complicate such cases.

Salient features

  • Heavy proteinuria, hypoalbuminaemia (S. Albumin <2.5 g/dl), hyperlipidaemia (S. Cholesterol >200 mg/dl) and oedema. Dipstick or heat coagulation of urine shows 3+/4+ proteinuria.
  • Investigations which help in diagnosis and management are urine analysis, blood counts, S. cholesterol, S. proteins, blood urea, S. creatinine, urine culture, X-ray chest, Montoux, HBsAg

Figure 1. Treatment of nephrotic syndrome without hypertension, haematuria and azotaemia.

Treatment

Definitions useful for guiding treatment are as follows:

Remission - Urine albumin nil or trace (or proteinuria <4 mg/m2/h) for 3 consecutive days.
Relapse - Urine albumin 3+ or 4+ (or proteinuria >40 mg/m2/h) for 3 consecutive days having been in remission previously
Frequent relapses - Two or more relapses in six months of initial response, or more than three relapses in any twelve months
Steroid dependence - Two consecutive relapses when on alternate Day steroids or within 14 days of its discontinuation
Steroid resistance - Absence of remission despite therapy with 4 weeks of daily prednisolone in a dose of 2 mg/kg per day.

Nonpharmacological

  • Avoid saturated fats
  • Adequate proteins, and salt restriction only during oedema, avoid extra salt
  • Good physical activity

Pharmacological

Investigations to rule out infection should be done before starting treatment with steroids i.e. urine culture & sensitivity, Montoux, X-ray chest, Hb, HbsAg.

Treatment of 0edema – in case of moderate to severe edema

  1. Tab Frusemide 1-3 mg/kg/day in 1-2 doses given preferably in the morning. Treatment of nephrotic syndrome without hypertension, haematuria and azotemia is given in Figure I. Presence of the these features points towards nonminimal change. If oedema does not respond Tab Spironolactone 2-4 mg/kg/day as single dose preferably in the morning. A gradual reduction of oedema is better. Patient with refractory severe oedema should be referred to a higher centre.

Monitoring

  1. Urine output, weight record
  2. Blood pressure
  3. Urine albumin daily till remission

Infection in nephrotic syndrome

  1. Patients of nephrotic syndrome with Montoux positive but no evidence of disease should be put on INH prophylaxis for 6 months.
  2. Absence of florid symptoms and signs may delay the diagnosis of serious infections like peritonitis and cellulitis in nephrotics. Systemic antibiotics should be used aggressively if infection is suspected.

Indications for kidney biopsy (to be carried out at tertiary care level)
At onset
<1 year or >15 years persistant microscopic or gross haematuria, low serum C3; substained hypertension; renal failure not attributable to hypovolemia; or suspected secondary causes of nephrotic syndrome

After initial treatment
Proteinuria persisting despite 4 weeks of daily corticosteroid therapy Before starting treatment with cyclosporine-A Frequently relapsing or steroid dependent nephrotic syndrome

Indications for referral to a higher centre

  • Onset <1 year of age
  • Nephrotic syndrome presenting with hypertension, persistent microscopic or gross haematuria, or impaired renal function
  • Complications like refractory oedema, thrombosis, severe infections and steroid toxicity
  • Resistance to steroids: initial or late
  • Frequently relapsing or steroid dependent nephrotic syndrome

Patient/parent education

  • Reassurance that despite a relapsing course progression to end stage renal disease is rare.
  • Urine examination by sulfosalicylic acid (SSA), dipstick or boiling should be taught
  • Maintain a diary showing proteinuria and medication received
  • Ensure normal activity
  • Protection against infection

References

  1. Consensus Statement on Management of Nephrotic Syndrome. Indian Paediatric Nephrology Group, Indian Academy of Paediatrics, Indian Paediatrics, 2001, 38: 975-896.

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Acute Glomerulonephritis (Post-Streptococcal)

It follows streptococcal infection of throat or skin by 1-2 weeks. Complications like congestive heart failure or encephalopathy may occur in a few patients. Diagnosis is clinical with urine showing RBC’s, WBC and mild proteinuria. Serum C3 levels may be low. Disease is self limiting and generally resolves in one month, however, microscopic urinary changes may persist up to one year.

Salient features

  • Sudden onset of gross haematuria, proteinuria, oedema, hypertension, oliguria and other features of renal insufficiency.

Treatment

Child should be admitted for monitoring and treatment, if complications occur.

Nonpharmacological

  • Routine activity need not be restricted unless features of acute renal failure or severe hypertension occur.
  • Diet is restricted like in acute renal failure

Pharmacological

There is no specific treatment
Treatment of hypertension

  1. Inj. Fursemide (40 mg) 1-2 mg/kg/day in 2 divided doses till oliguria lasts
  2. Cap. Nifedipine 0.25 mg/kg SOS
  3. Inj. Procaine penicillin 4 lac units once daily if evidence of sore throat or skin infection

Monitoring and follow up with

  • Regular weight record, strict intake-output chart, blood pressure recording should be done regularly.
  • Refer to a higher centre if hypertension, haematuria or renal failure are not manageable.

Patient/Parent education

  • Parents should be explained the natural course. More than 95% recover within 2-4 weeks. Only a few patients may end up with chronic renal insufficiency.

References

Gross or Microscopic Haematuria. In: Nelson’s Text Book of Paediatrics, Behrman, Liegman, Jenson (eds), 16th Edition, 1999; pp 1581-1584.

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Urinary Tract Infection (UTI)

Urinary tract infection (UTI) is a common bacterial infection in infants and children. One percent boys and 3-5% girls below 14 years develop UTI. Risk of UTI is higher in children with congenital urinary tract anomalies, chronic diarrhoea and malnutrition.

Salient features

  • Symptoms are nonspecific. In neonates, it presents as a part of septicaemia, in infants and young children with fever, diarrhoea, vomiting also pain and poor weight gain.
  • Older children may have burning, urgency, frequency, flank pain, turbid urine and recent onset enuresis. Diagnosis is confirmed by growth of significant number of organisms of a single species in the urine (Table 1).

Treatment

Nonpharmacological

Maintain adequate hydration and encourage liberal fluid intake to alleviate dysuria
(Note: Alkalinization of urine is not necessary)

Pharmacological

Therapy should be started after obtaining urine culture. Patient’s age, degree of toxicity, state of hydration, ability to retain oral intake and the likelihood of compliance with medication help in deciding therapy.

Complicated UTI and/or age less than 3 months

  1. Inj. Ampicillin 100 mg/kg/day IV in 3 divided doses for 10 to 14 days
  2. Inj. Gentamicin 5-6 mg/kg/day in 2 divided doses for 10 to 14 days
    Or
    Inj. Cefotaxime 100-150 mg/kg/day IV in 3 divided doses for 10 to 14
    days
    Or
    Inj. Ceftriaxone 75-100 mg/kg/day IV in 1-2 divided doses for 10 to 14
    days


Table 1. Interpretation of urine culture

Method of collection Colony count Probability of infection
Suprapubic aspiration Urinary pathogen
in any number
99%
Urethral catheterization >50 x 103 CFU/ml 95%
Midstream clean catch >105 CFU/ml 90-95%

CFU: colony forming units.

Definitions:

Significant bacteriuria Colony count of > 105/ml of a single species in a midstream clean catch sample
Asymptomatic bacteriuria Presence of significant bacteriuria on two or more specimens iln a child with no symptoms
Recurrent UTI Second attack of UTI
Complicated UTI Presence of fever > 38.5° C, toxicity, persistent vomiting, dehydration and renal angle tenderness
Simple UTI UTI with low grade fever, dysuria, frequency, urgency but none of the above symptoms

Complicated UTI and age 3-6 months

  1. Inj. Gentamicin 5-6 mg/kg/day IV in 2 divided doses for 10 to 14 days UTI > 3 months.
  2. Syp. Amoxycillin 30-50 mg/kg/day in 3 divided doses for 7 to 10 days.
    Or
    Syp. Cotrimoxazole (Trimethoprim) 6-10 mg/kg/day in 2 divided doses for 7-10 days.
    Or
    Syp. Cephalexin 50-70 mg/kg/day in 3 divided doses for 7-10 days.

(CAUTION: Quinolones should be avoided as first line medication; their use is guided by results of culture and sensitivity)

Nalidixic acid or Nitrofurantoin should not be used to treat UTI since they do not achieve therapeutic concentration in renal parenchyma and blood stream.

Monitoring

An abdominal ultrasound examination and repeat urine culture are necessary in patients who fail to show clinical response (reduction of fever and toxicity) within 48 hours of initial treatment.

Workup of a case of first UTI is shown in Figure 1. Child with more than one episode should be worked up for cause of recurrent UTI. Each episode is treated as mentioned above but child should be investigated in detail with ultrasound, MCU and DMSA scan and prophylaxis for recurrence as in Table 2 and 3.

Figure 1. Workup of a cases of first UTI

Antibiotic prophylaxis in recurrent UTI

Long term, low dose antibacterial prophylaxis is used to prevent recurrent febrile UTI.


Table 2. Antimicrobials for prophylaxis of UTI

Drug Dose (mg/kg/day) Remarks
Cotrimoxazole 1-2 (trimethoprim) Avoid in infants <3 months age and G-6PD deficiency
Nitrofurantoin 1-2 Gastrointestinal upset; avoid in infants < 3 months age, G-6 PD deficiency and renal insufficiency
Cephalexin 10 Drug of choice in first 3-6 months of life


Table 3. Indications and duration for antimicrobial prophylaxis

Findings
First UTI
Age Duration
Reflux and renal scar present All Till 5 years of age*
No reflux but renal scar All Six months and re-evaluate**
No reflux, no renal scar < 2 years
> 2 years
Six months and re-evaluate**
No prophylaxis
Recurrent UTI
(without reflux or scar)
All Six months

* Child >5 years of age at initial evaluation prophylaxis for 12-18 months, reevaluate
**DRCG/MCU to look for vesico urethral reflux (VUR), which might have been missed on initial evaluation. Prophylaxis is stopped if VUR is not detected.
Note: Grade IV (bilateral) and Grade V – prophylaxis given up to 1 year, then surgery is indicated.

References

Consensus Statement on Management of Urinary Tract Infections. Indian Paediatric Nephrology Group, Indian Academy of Paediatircs. Indian Paediatrics, 2001, 38: 1106-1115.

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Hypothyroidism

Hypothyroidism is characterized by decrease in the function of the thyroid glands. Most cases in children are due to congenital hypothyroidism causes such as aplasia, hypoplasia or ectopia of thyroid gland. Common causes of acquired hypothyroidism are iodine deficiency, lymphocytic thyroiditis and following irradiation of cervical region for malignant disorders. Diagnostic studies and treatment are same as that for congenital hypothyroidism.

Salient features

  • Congenital hypothyroidism is difficult to diagnose in neonatal period as the symptoms and signs may not be fully developed.
    However, prolongation of physiological jaundice and feeding difficulty in the form of sluggishness and choking during feeding occur. Infants cry less, sleep more and have constipation, abdominal protuberance and umbilical hernia. Infants with these features should be screened by thyroid function tests to avoid delay in diagnosis. Gradually the features of physical and mental retardation become more obvious which can be severe.
  • The diagnosis is based on demonstration of low serum of T4. Serum T3 levels may be normal and are not useful for diagnosis. In primary hypothyroidism, TSH is elevated. Radionuclide scans are not essential for diagnosis but help to delineate the exact aetiology.

Pharmacological

Initiation of therapy: L-thyroxine (Tab., 50 and 100 mcg).
Initial dose in neonatal period is 10-15 mcg/kg/day (usually 37.5-50 mcg per day), given as a single daily dose half an hour before food. The tablet can be crushed and mixed in expressed breast milk or any other liquid for small infants.

Treatment is required life long and the requirement keeps changing with increasing age. In later part of infancy dose decreases to 5-6 mcg/kg/day then to 3-4 mcg/kg/day in children and the adult dose is 2 mcg/kg/day.

Assessment of response: Early response is evident in initial few weeks and consists of symptomatic improvement in alertness, relief of constipation, improvement in appetite and feeding. Increased linear growth and osseous maturation is seen over next few months.

  • The child should be followed clinically every month for 6 months, 3 monthly till 2 years and thereafter once to twice every year. Recurrence of symptoms such as lethargy, constipation and weight gain suggest undertreatment and diarrhoea, palpitations, increased appetite and weight loss suggest overdosing.
  • Periodic check on thyroid function tests is needed (6 monthly or so).
    Serum T4 level should be maintained in upper normal range and TSH levels suppressed to normal.
  • After few months of starting therapy, sometimes features suggestive of raised intracranial tension such as headache and vomiting may appear. The patient should be immediately admitted and treated.

Patient /parent education

  • Patient should be told about the need for life long administration of the drug.
  • Regular follow up at the interval described above is important for proper monitoring and dose titration.
  • Clinical symptoms of under or overdosage, including the danger signs of pseudotumour cerebri should be explained.

see also Hypothyroidism in chapter-11

References

Hypothyroidism. In: Nelson’s Text Book of Paediatrics. Behrman, Liegman, Jenson (eds), 16th Edition, 1999; pp 1698-1704.

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Diabetes Mellitus (DM)

Most of the cases of DM in children are of insulin dependent diabetes Mellitus (IDDM) and have hyperglycaemia with glucosuria.

Salient features

While some cases present with classical symptoms of polyphagia, polydipsia, polyuria and weight loss, many children at the onset present in the state of diabetic ketoacidosis (DKA).
A minority of cases, while asymptomatic are detected to have glucosuria and hyperglycaemia.
Diagnosis of DM is made by demonstration of hyperglycaemia (random plasma glucose more than 200 mg/dl). Following cut off

 

Time Normal range DM diagnosis
Fasting 70 -105 mg/dl > 115 mg/dl
60 minutes 120 -170 mg/dl > 200 mg/dl
90 minutes 100- 140 mg/dl > 200 mg/dl
120 minutes 70- 120 mg/dl > 140 mg/dl
  • Patients during DKA have moderate to severe dehydration with plasma glucose levels usually more than 300 mg/dl, metabolic acidosis, ketonuria and various electrolyte disturbances.

Treatment

Nonpharmacological

Diet

  • Regularity of eating pattern is very important so that diet and insulin dosing is synchronised.
  • General nutritional guidelines are followed.
  • Calorie mixture should have 55% carbohydrates, 30% fat and 15% proteins.
  • Avoid carbohydrate with refined sugars to prevent metabolic swings. Carbonated drinks should be of sugar free variety.
  • Fats derived from animal sources to be reduced and should be replaced by fats of vegetable origin.
  • Calorie intake should be split as 20% breakfast, 20% lunch, 30% dinner and 10% each for 3 snacks at mid morning, mid afternoon and evening.

Physical activity and fitness

  • Usual exercises advised to diabetic children and adolescents include vigorous walking, jogging, swimming, tennis etc. Though, diabetics can undertake any exercise, but unusual exercise may require modification in insulin dosing. For the schedule day of unusual exercise, insulin dose may be reduced by 10-15%.

Pharmacological

Initial therapy

Treatment is initiated in the hospital with fast acting (regular) insulin.
At the onset of DM (or after recovery from DKA) the dose of insulin is 0.5-1.0 unit/kg/day.
Inj. Regular insulin 0.1-0.25 units/kg subcutaneous injections are given 6-8 hourly before meals.
Simultaneous blood glucose level monitoring is done. One to two days therapy is required to find out total daily insulin requirement. Once the patient stabilises on 6 hourly insulin injections, the patient is switched over to “2 daily injections” schedule.
In “2 daily injections” schedule, the insulin is administered as follows:

  • Combinations of intermediate acting (usually lente) insulin and fast acting (regular) insulin is used in the ratio of 2-3:1. Two third of total daily -dose is injected before breakfast and one third before dinner. Each injection has combination of both types of insulin e.g., total dose of insulin is 30 units -20 units (14 units lente and 6 units regular) are injected before breakfast and 10 units (6 units lente and 4 units regular) are injected before dinner.
  • Blood glucose levels are monitored before each meal and the dose of insulin adjusted accordingly. Blood glucose levels should ideally be 80 mg/dl fasting and 140 mg/dl after meals (acceptable range between 80 -240 mg/dl). Early morning 3 AM blood glucose level should be more than 70 mg/dl.

Following modification in the insulin doses will be required depending upon the blood glucose levels:

Time and blood glucose Type and time of insulin modified
1. High fasting blood glucose Evening lente insulin is increased by 10%
2. High noon blood glucose Morning regular insulin is increased by 10%
3. High pre dinner blood glucose Morning lente insulin is increased by 10%
4. High pre bed time blood glucose Evening regular insulin is increased by 10%
5. Low fasting blood glucose Evening lente insulin is decreased by 10%
6. Low noon blood glucose Morning regular insulin is decreased by 10%
7. Low pre dinner blood glucose Morning lente insulin is decreased by 10%
8. Low pre bed time blood glucose Evening regular insulin is decreased by 10%
  • Any increase or decrease in insulin dose is by 10- 15%. Generally not more than 6 units.
  • After initial stabilisation, newly diagnosed cases may have gradual decline in insulin requirement even upto 0.5 units/kg/day. This may persist for several weeks to several months.
  • Decrease total dose of insulin by 10% at the time of discharge from hospital as the increased activity at home will decrease the insulin requirement.

Assessment of diabetic control or response to therapy

  • Blood glucose estimation should be done before each meal and at bed time in the first few weeks after diagnosis. After stabilisation, it can be reduced to twice a week.
  • Periodically blood glucose estimation at 3-4 AM is required to detect early morning hypoglycaemia.
  • Urine for sugar is also monitored initially 3-4 times daily before meals.

This can be done less frequently after initial few weeks, preferably on the days when blood sugar is not done.

  • Urine for ketones once daily should be done.
  • Glycosylated haemoglobin (HbA1 C) estimation-once every 3 months.
    - HbA1C levels of 6-9% represent very good control of diabetes, 9 -12% show fair control and above 12% represent poor control.
  • Serum lipids -cholestrol, HDL, LDL, VLDL, triglycerides and urine for protein should be done once every year. Serum cholestrol should be less than 200 mg/dl, LDL less than 130 mg/dl and triglycerides less than 140 mg/dl.
  • Thyroid function tests should be done once every year to detect concomitant hypothyroidism.

For management of hypoglycemia and diabetic ketoacidosis see chapter 11 on hormonal disorders.

Patient/parent education

Patient/parents should be taught self diabetic care which should include:

  • Technique of measuring insulin in the syringe.
  • Importance of drawing insulin always in the same sequence (usually regular insulin first) so that same type of insulin is left over in the dead space of the syringe.
  • Explain technique of subcutaneous injections and importance of rotating the injection sites – arms, thighs (upper and lower), buttocks and abdomen.
  • Monitoring urinary sugar – by the double void method (void 30 minutes before the test void).
  • Blood sugar monitoring, maintaining the records of treatment and sugar levels
  • Adherence to diet.
  • Regular exercise.
  • Recognising the symptoms of hypoglycaemia and its home management.

References

Diabetes Mellitus. In Nelson’s Textbook of Paediatrics. Behrman, Leigman, Jenson (eds), 16th Edition, 1999, pp 1767-1791.

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Rheumatic Fever And Rheumatic Heart Disease

Rheumatic fever is a multi system inflammatory disease that occurs as a delayed sequalae to group A Beta haemolytic streptococcal pharyngitis.
The disorder is largely self limited and resolves without sequelae but chronic and progressive damage to heart valves lead to rheumatic heart disease (RHD).

Salient features

  • Presence of two major or one major and two minor criteria in addition to evidence of recent streptococcal infection (raised ASO titer, positive throat swab or recent scarlet fever) is necessary for diagnosis of Rh fever
  • Major criteria: arthritis, carditis, subcutaneous nodules, chorea, erythema marginatum
  • Minor criteria: fever, arthralgia, elevated acute phase reactants (ESR, CRP) and prolong-ed PR interval
  • RHD most frequently affects mitral and aortic valve. Isolated aortic valve involvement is rare and tricuspid and pulmonary valve involvement is unusual.
  • Complications of RHD are cardiac failure and infective endocarditis

Treatment (Acute rheumatic fever)

Nonpharmacological

Avoid vigrous activity till ESR normalizes. In severe CHF, salt restriction, fluid restriction, upright posture. Protect patient from getting injured in chorea.

Pharmacological

  1. In arthritis only:
    Tab. Aspirin 90-120 mg/kg/day in 4 divided doses for 10-12 weeks to be given after meals. During therapy monitor for tinnitus, deafness, respiratory alkalosis/acidosis.
    In carditis without CHF:
    As above.
    In carditis with CHF: Tab. Prednisolone given after meals in dose of 2.5 mg/kg/day 2 divided doses for 3 weeks then tapering over next 3 weeks. During tapering add Aspirin as above and continue it for 4-6 weeks. Monitor blood pressure and blood sugar.
  2. For treatment of CHF see section on CHF.
  3. In Chorea: Tab. Haloperidol 0.05 mg/kg/day divided doses 2-3 divided doses; dose titrated according to response.
  4. Inj. Procaine penicillin 4 lac units IM twice daily for 10 days.
    Or
    Inj. Benzathine penicillin G 1.2 mega units (>27 kg), 0.6 mega units
    (<27 kg) IM single injection.
    Or
    Tab. Penicillin V 125-250 mg twice daily for 10 days.
    Or
    Tab. Erythromycin 40 mg/kg/day 3 times a day for 10 days.

Usually joint pains disappear within 24 to 48 hours, tachycardia settles, pericardial friction rub if present disappears and gradually ESR comes to normal. In established cardiac lesions with CHF not controlled by medical management patient should be referred to a higher centre for surgical intervention.

For secondary prevention (for prevention of recurrences)

Inj. Benzathine penicillin G 1.2 mega units (>27 kg), 0.6 mega units
(<27 kg) IM every 3 weeks.
Or
Tab. Penicillin V 250 mg 2 times a day.
Or
Tab. Sulfadiazine 500 mg once daily.
Or
Tab. Erythromycin 250 mg 2 times a day.
Duration of secondary prevention is individualized. In patients with established valvular lesion prophylaxis should be given for life long or at least till theage of 35 years. In others it is given for atleast 5 years after the most recent attack or till the age of 18 years which ever comes first. In acute rheumatic fever observe for appearance of valvular lesions (most common in the first four weeks of disease) and in RHD for effort intolerance, signs and symptoms of CHF, echocardiographic studies of cardiac functions

Patient/parent education

  • Early and adequate treatment of sore throat.
  • Emphasize the importance of regular prophylaxis with benzathine penicillin.
  • Patients with RHD should avoid contact with sore throat cases and if possible environmental modification e.g., avoid overcrowding.

References

  1. Rheumatic Fever. In: Nelson’s Textbook of Paediatrics. Behrman, Leigman, Jenson (eds), 16th Edition, 1999, pp 754-760.
  2. Eugene Braunwald: Heart Disease 56: 1721,1992.

>> See also Rheumatic Fever in chapter-3

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Cardiac Failure

Cardiac failure is defined as a state in which the heart cannot deliver an adequate cardiac output to meet the metabolic needs of the body. Clinical presentation is dependent on age and degree of cardiac reserve. Common causes according to age of presentation are:
Neonate – Severe anaemia, heart block, congenital heart disease e.g. hypoplastic left heart, co-arctation, left to right shunt and large mixing cardiac defects.
Infant – Left to right shunt, supraventricular tachycardia
Child – Rheumatic fever, myocarditis, cardiomyopathy, acute hypertension e.g., acute glomerulonephritis.

Salient features

  • Exertional dyspnoea, poor weight gain, feeding difficulties, breathes too fast and better when upright, persistent cough and wheezing, excessive perspiration and irritability, puffiness of face and pedal oedema
  • Tachypnoea, tachycardia, small volume pulse, peripheral cyanosis, pedal/facial/ sacral oedema, hepatomegaly, raised JVP (appreciated well in older children), gallop rhythm, cardiomegaly and failure to thrive.

Treatment

Identify and treat the underlying cause.

Nonpharmacological

Restricted activity and bed rest with upright posture depending on cardiac reserve.


Figure 1. Alogrithm for treatment of congestive heart failure

In severe CHF, dietary modifications in infants by increasing calories per feed. Breast-feed supplementation, naso gastric feed to avoid the exertion of active feeding.
No added salt in diet and fluid restriction and cold sponging in case of fever.

Pharmacological

Algorithm for treatment is shown in Figure 1.

  1. Elixir/Tab. Digoxin (Elixir 0.25 mg/5 ml, Tab. 0.25 mg)
    Method of digitalization: 0.5 x digitalization dose initially, 0.25 x digitalizing dose 8 and 16 hours later.
    Digitalizing dose: newborn = IV, IM: 0.010 – 0.030 mg/kg divided or orally: 0.040 mg/kg divided in fractions.
    Infants = IV, IM 0.030 – 0.040 mg/kg or orally 0.050 mg/kg in fractions.
    Childrens = IV, IM, PO: 0.010 – 0.015 mg/kg in fractions
    For maintenance: begin maintenance dosage 24 hours after 1st fraction of digitalizing dose. Newborn = PO: 0.005 – 0.010 mg/kg/24 hours, divided every 12 hours. In infants and children orally 0.002 – 0.005 mg/kg/24 hours divided every 12 hours.
    (CAUTION: Avoid hypokalaemia during therapy with digoxin)
  2. Tab. Frusemide 1-2 mg/kg every 12 hourly. (may need K supplement).
    Or
    Tab. Chlorothiazide 20-50 mg/kg/day in 2 divided doses.
    Or
    Tab. Spironolactone 1-3 mg/kg/day in 2 divided doses.
  3. In cases with regurgitant cardiac lesions like severe MR where reduction in after load is required
    Tab. Captopril 0.1-0.2 mg/kg/dose 8-12 hourly (maximum 4 mg/kg/day)
    Or
    Tab. Enalapril 0.08-0.5 mg/kg/dose 12-24 hourly (maximum 1 mg/kg/ day)
  4. Patients with hypotension and low cardiac output should be referred to a higher center)
    Inj. Dopamine infusion (40 mg/ml) 2-20 mcg/kg/min prepared in normal saline or 5% dextrose. Hypovolaemia should be corrected before infusion is started and BP is monitored during the infusion.
    Or
    Dobutamine infusion (250 mg/5 ml) 2- 20 mcg/kg/min. Both the drugs can be used simultaneously to have added response because of different mechanism of actions.

Patient/parent education

  • Decreased salt intake should be emphasised
  • Sufficient rest and adequate sleep must be emphasised. Strict bedrest is necessary only in severe cases.
  • Semi-upright position during sleep may make the patient more comfortable.

References

  1. Heart Failure. In: Nelson’s Textbook of Paediatrics. Behrman, Leigman, Jenson (eds), 16th Edition, 1999, pp 1440-1445.
  2. Eugene Braunwald: Heart Disease 56: 1721,1992.

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Pertussis (Whooping Cough)

This results from Bordetella pertussis infection leads to this respiratory disorder which can have long term poor effects on health.

Salient features

  • Beginning as a mild upper respiratory tract infection (catarrhal stage), can progress to severe paroxysms of cough, often with a characteristic whoop, followed by vomiting.
  • The child runs out of breath with bulging eyes, flushed face, lacrimation, salivation, protrusion of tongue and distension of the neck veins etc. Such episodes are exhausting and precipitated by yawning, sneezing, eating or even suggestion.

Treatment

Pharmacological

  1. Syp./Tab. Erythromycin, 40-50 mg/kg/day in 4 divided doses orally for 14 days initiated early in the coryzal phase of the disease i.e. first 14 days of the illness may shorten the course of whooping cough, which otherwise may last for weeks or months. Later once the paroxysms start, no antimicrobial have any benefit except for eradication of any secondary pulmonary infection.
  2. In patients with severe coughing paroxysms salbutamol 1-2 mg/kg/ day in 3-4 divided doses for a week or so may be tried.
  3. Severe cases particularly those <6 months of age and those with respiratory distress need to be admitted for intravenous fluids and oxygen therapy.

Supportive therapy

  • Oxygen therapy is required in severe cases with respiratory distress. Hydration should be maintained with intravenous or oral fluids in adequate amounts (cough suppressants are usually not helpful).

Patient/parent education

  • Explain the need to continue feeding during the prolonged period of cough, adequate hydration and nutrition to prevent onset of malnutrition.
  • Antibiotic therapy must be continued for at least 14 days to prevent relapse of the disease, even if they may not be providing any relief in the symptoms
  • All contacts below 7 years of age must be given erythromycin for 14 days.
  • Contact the doctor immediately if the patient develops listlessness, apnea or seizures. This is particularly more common in infants below 6 months.
  • Immunization against pertussis is available in our country as triple antigen (DPT) and 3 primary doses are routinely advised for all infants followed by a booster after 1.5 years and 4.5 years after the primary immunization. The primary immunization is expected to reduce the disease burden by two third.

References

  1. Text Book of Paediatric Infectious Diseases, WB Saunders Co. Philadelphia.
  2. American Academy of Paediatrics. In: Report of the Committee on Infectious Diseases, 25th Edition, Elk Grove Village, Illinois, US.
  3. Pertussis (Bordetella pertussis and B. parapertussis). In: Nelson’s Textbook of Paediatrics. Behrman, Leigman, Jenson (eds), 16th Edition, 1999, pp 838-842.

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Acute Flaccid Paralysis (AFP)

A case of AFP is defined as any child aged <15 years, with acute onset of flaccid paralysis without any obvious cause (e.g. severe trauma or electrolyte imbalance like hypokalaemia). AFP is a notifiable disease and all cases must be reported to District Surveillance Officer (Tel No. 011-2398 3076).

Salient features

  • The paralysis is of acute onset (<4 weeks) and the affected limb(s) are flaccid (floppy or limp). If the AFP is due to polio, then sensation is never affected. Other important differentials to be considered in cases with AFP are detailed in Table 1.
  • Pseudoparalysis due to pain in congenital syphilis, osteomyelitis, abscess, scurvy, unrecognized trauma leading to contusions, slipped epiphysis or fractures etc can also mimic AFP

The following section details the treatment for acute POLIO cases only

Treatment

All cases should be treated as below except patients with isolated single lower limb involvement and reporting after 4 days of onset of paralysis and currently not progressing for more than 48 hours.


Table 1: Important differential diagnosis of AFP (adapted from Field Guide, MO HFW, GOI):

Signs and Symptoms Polio GBS Transverse Myelitis Traumatic or injection neuritis
Age Most cases occur under 3 years of age Usually above 2 years of age Mostly above 4 years of age No age limit
Progression of paralysis 24-48 h onset to full paralysis Hours to days Hours to 4 days Hours to 4 days
Fever onset High always present at onset of flaccid paralysis disappears the following day Not common Rare Commonly present before, during and after paralysis
Flaccidity Acute,
asymmetrical,
proximal
Acute,
symmetrical,
distal
Acute
lower limbs
symmetrical
Acute,
asymmetrical
limb
Muscle tone Diminished Diminished Diminished in lower limbs Diminished in affected limb
Deep Tendon Reflexes Decreased or absent Absent Absent in lower extremeties, later hyper-reflexia Decreased or absent
Sensation Severe myalgia but no sensory deficit Cramps, tingling hypoanesthesia of palms and soles Anesthesia of the lower limbs with sensory loss Pain in gluteal region
Cranial nerve Only in bulbar or bulbospinal cases. Loss of gag reflex most common Often present affecting VII, IX, X, XI, XII Absent Absent
Respiratory insufficiency Only when bulbar and bulbospinal involving respiratory muscles In severe cases Sometimes Absent
CSF WBCs proteins High WBCs.
Normal or slightly
increased
< 10
High
Normal
Normal or
slightly
elevated
Normal
Normal
Bladder dysfunction Absent Transient Present Never
Nerve conduction velocity in 3rd week Abnormal, anterior horn cell disease Abnormal, demyelination Normal of abnormal has no diagnostic value Abnormal in sciatic nerve
EMG 3rd week Abnormal Normal Normal Normal
Sequelae at 3 months and up to a year Severe asymmetrical atrophy, skeletal deformities may develop later Symmetrical atrophy of distal muscles diplegia, atrophy after years Flaccid Moderate atrophy only in affected lower limb

Nonpharmacological

  • Complete bed rest and correct positioning of the affected limbs in the optimal position as follows:
  • Hip – slight flexion, knee – 5 degrees flexion, foot – 90 degrees with support against the soles. Both legs should be supported from the lateral sides with pillows or rolled towels or salt/sand packs to prevent rotation. When pain subsides, passive movements of the joints for about 10 minutes, 2-3 times a day.
  • Warm water fomentation using hot packs with soaked towels wrapped around the affected parts for about 10 minutes, 2-3 times a day help in relieving pain.
  • If transient urinary retention occurs, alternate hot and cold compresses over the suprapubic region.
    CAUTION: Massage or intramuscular injections may further precipitate paralysis. Watch for progression, particularly for the involvement of the respiratory muscles.

Pharmacological

There is no specific drug therapy for polio. For fever and pain use paracetamol or ibuprofen (see section on fever). Referral to a tertiary care level center with a ventilatory support facilities if there is progression of paralysis, respiratory distress, bulbar involvement, paralysis of upper limbs involvement which is <3 days old (there is higher risk of diaphragmatic involvement in such cases), marked drowsiness or any other complication.

Patient/Parent education

  • No dietary restrictions, however, continue breast feeding or other regular feeding.
  • Paralysis progresses usually for about 4-7 days after onset. Recovery may start thereafter over days to weeks with little recovery of strength after 6 months of illness. A regular physiotherapy facilitate recovery of muscles.
    Note: Post Polio Residual paralysis should be referred for rehabilitative services to an appropriate centre.

References

  1. Surveillance of Acute Flaccid Paralysis. Field Guide, 2nd Edition, Child Health Division, Department of Family Welfare, Ministry of Health and Family Welfare, January 2000.
  2. Enteroviruses. In: Nelson’s Textbook of Paediatrics. Behrman, Leigman, Jenson (eds), 16th Edition, 1999, pp 956-964.

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Mumps

Mumps is a disease caused by a virus that can infect many parts of the body, especially the parotid salivary glands.

Salient features

  • The parotid glands become increasingly swollen and painful over a period of one to three days. There is often a fever of up to 1030F (39.40C), with headache and loss of appetite.
  • Mumps can also involve the brain, pancreas and other organs. The involvement of these organs signifies a severe disease and there is usually a recrudescence of high fever in such situations in addition to organ specific symptoms.
  • Meningoencephilitis is the commonest complication (250/100 000 cases). Other complications are orchitis, epididymitis, oophritis, pancreatitis, thyroiditis, myocarditis, deafness, optic neuritis and arthritis.

Treatment

Nonpharmacological

  • Child should be encouraged to drink plenty of fluids. Water, decaffeinated soft drinks and tea are better tolerated than acidic fruit juices (like orange juice, grape fruit juice or lemonade) that make parotid pain worse.
  • Either warm or cold packs – whichever feels better- may be used to sooth the swollen parotid glands.

Pharmacological

  • Most cases are treated symptomatically on OPD basis.
  • Fever when troublesome may be brought down using non aspirin fever medications such as Paracetamol (10-15 mg/kg/day SOS or every 4-6 hours). These medicines will also help relieve pain in the swollen parotid glands.
    (CAUTION: Aspirin is contraindicated in children with viral illnesses due to risk of Reye syndrome)
  • Being a viral illness antibiotics have no role. There is no specific therapy available.
  • Patients with abdominal pain, testicular swellings or signs of raised intracranial tension need to be admitted in the hospital.

Patient/parent education

  • Parents should be explained warning signs e.g.
      • In boys, parents are told to watch for high fever, with pain and swelling of the testicles.
      • Watch for abdominal pain that can mean involvement of the pancreas in either sex, or involvement of the ovaries in girls.
      • Severe headache, stiff neck, convulsions (seizures), extreme drowsiness etc suggest CNS involvement and need for admission to a tertiary level center.
      • Recurrence of high grade fever (above 101oF/38.3oC) often heralds onset of the above complication and can be used as an early referral sign.
  • Children usually recover from mumps in about 10-12 days. First attack of mumps almost always gives lifelong protection against another, therefore, such children do not benefit from any immunisation later.
  • Mumps can be prevented by a vaccine which can be given alone, or as part of the mumps-measles-rubella (MMR) vaccine given at the age of 15 months. Mumps vaccine is effective in 75 to 95% of immunized persons.

References

  1. Text Book of Paediatric Infectious Diseases, WB Saunders Co. Philadelphia.
  2. American Academy of Paediatrics. In: Report of the Committee on Infectious Diseases, 25th Edition, 2000, Elk Grove Village, Illinois, US.
  3. Mumps. In: Nelson’s Textbook of Paediatrics. Behrman, Leigman, Jenson (eds), 16th Edition, 1999, pp 954-955.

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Measles

Measles is an acute viral disease of childhood, associated with high rates of morbidity and mortality. It directly or indirectly contributes to 7% of the under five deaths in the developing world.

Salient features

  • Fever, cough, coryza, conjunctivitis, an erythematous maculopapular rash appearing on the 4th day of the illness, and a pathognomonic enanthem (Koplik spots) characterize it.
  • Rash starts from behind the ears, along the hairline, involve the face and then the trunk and the limbs.
  • Fever usually subsides after the appearance of the rash unless there is some complication such as otitis media, bronchopneumonia, laryngotracheobronchitis (croup), and diarrhoea. Acute encephalitis, which frequently results in permanent brain damage, occurs in approximately 1 of every 1000 cases.
  • Another cause of persistence of fever could be flairing up of Koch’s.

Treatment

Nonpharmacological

  • The patient should be isolated from other susceptible individuals particularly unimmunised children for atleast four days after the appearance of the rash.
  • Bed rest is usually required and cold sponging may be required for febrile patients.
  • Small frequent feeds and plenty of oral fluids should be continued.

Pharmacological

No specific antiviral treatment is available.

  1. Fever is managed with oral Paracetamol (see the section on fever ).
  2. If there is persistent coryza or nasal itching which is disturbing the child, oral Syp. Promethazine 1 mg/kg/day in 3-4 divided doses can be used

Treatment of other co-existing problems

  1. Inj. Vitamin A 100,000 IU is given intramuscularly for 2 consecutive days or else high dose oil based preparations containing 50,000 units per ml may be given. A third dose may be given 4 weeks later particularly if there are manifesting signs of vitamin A deficiency.
  2. Treat appropriately the secondary bacterial infection like bronchopneumonia and/or gastrointestinal infection

Patient/Parent education

  • The disease leads to marked anorexia and also often precipitates protein energy malnutrition (PEM) and other deficiencies, Regular frequent feeds must continue. Extra meal should be added to provide for increased requirement during convalescence.
  • The disease usually lasts 10-12 days and the maximum risk of infectivity is 5 days prior to and 4 days after the appearance of rash. The rash usually heals by desquamation and often leaves some hyperpigmented stains on the body which disappears over weeks subsequently.
  • The parents must report to the hospital in case the child develops any of the following warning signs:
      • Stiff neck, facial twitching or convulsions (seizures), extreme drowsiness, loss of consciousness or altered behaviour.
      • Rapid and or laboured breathing, difficulty in feeding, cyanosis. Significant dehydration as evident by sunken eyes or fontanels, loss of skin turgor, dryness of tongue or lack of tears etc.
      • Blood in stools
  • Vaccination against measles is recommended at 7- 9 months of life and a subsequent booster with measles or MMR is mandated at 15 months of age particularly if the primary immunisation was done at less than 9 months of age. There is no role of giving measles vaccination to a child who has already suffered from the disease.
  • In case any other susceptible (unimmunised child below 5 year) has been in contact with the patient of measles then it may be worthwhile to immunise this individual. Measles vaccine is useful if used early as it can prevent or decrease the severity of the disease in the secondary contacts (for details see appendix IX and immunization schedule).

References

  1. Measles Virus. In: Text Book of Paediatric Infectious Diseases, Feigin and Cherry (eds.), 4th Edition, 1998, WB Saunders Co. Philadelphia, pp 2054-2074.
  2. American Academy of Paediatrics. In: Report of the Committee on Infectious Diseases, 25th Edition, Elk Grove Village, Illinois, US.
  3. Measles. In: Nelson’s Textbook of Paediatrics. Behrman, Leigman, Jenson (eds), 16th Edition, 1999, pp 946-949.

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Chicken Pox Or Varicella

Varicella is the primary infection caused by Varicella-zoster virus. It is highly infectious and is transmitted by droplet infection. The incubation period is about 14 days.

Salient features

  • Begins as crops of small red papules over the trunk appearing within 1 day of fever and systemic symptoms which quickly develop into clear, often oval vesicles on an erythematous base.
    Contents become cloudy in about 24 hours and than scab. Many such crops may appear for 3-4 days.
  • Bacterial superinfection, thrombocytopenia, arthritis, hepatitis, encephalitis or meningitis can complicate the disease.
  • The disease is severe in adolescents and adults as well as immune compromised individual. Reactivation disease results in herpes zoster or shingles (for details see skin section)

Treatment

Nonpharmacological

  • Itching is bothersome and scratching effect may be minimised by making the patient wear mittens, daily change of clothes and good personal hygiene may decrease the risk of secondary infection.

Pharmacological

Symptomatic therapy

  1. For management of fever (see section on fever). Aspirin and other salicylates are contraindicated due to risk of Reye’s syndrome and should not be used.
  2. Local anti-pruritic agents like Calamine lotion may alleviate itching. If itching is not relieved with above Tab. Pheniramine 25 mg 2 times a day
    In children Syp. 0.5 mg/kg/day every hours
    Or
    Tab. Cetrizine 10 mg once a day
    In children (2-6 years) 5 mg; (>6 years) 10 mg once a day.
  3. In case of immuno-compromised children on long term treatment with steroids, those on anti-cancer drugs or other immunosupressive therapy, HIV positive patients, children older than 12 years of age, those with chronic cutaneous or pulmonary disorders who are at increased risk of the severe disease oral acyclovir if started within few hours (<24 h) of the onset of rash may decrease the duration, magnitude of fever as well as the number of skin lesions. Not recommended routinely for a healthy child
    Tab. Acyclovir is 20 mg/kg/day given 6 hourly for 5 days.
    In case the patient is severely immuno-compromised, viral encephalitis or severe disease in adults Inj. Acyclovir should be started as soon as possible in all cases at the dose of 10 mg/kg 8 hourly IV for 7 days.

Assessment of response to therapy

Most cases will stop having fever after the initial 3-4 days when new crops of vesicle stop appearing. The vesicles normally heal by scabbing in about a week’s time. Persistence of fever may suggest secondary infection.

The disease can be complicated by: secondary bacterial infection of skin lesion, thrombocytopenia, pneumonia – particularly in adolescents and adults, Reye’s Syndrome, Post infectious encephalitis and if develops, should be treated appropriately.

Patient/Parent education

  • The disease commonly is self limiting in healthy children. Child should be excluded from day care or school till after 6th day of the rash or till scabs are formed.
  • Do not use over the counter fever medicines as they may contain aspirin or other salicylates.
  • An expensive but potent vaccine is available for protection against the disease and can be recommended only for those at risk of severe form of the disease but are immunocompetent.
  • Post exposure prophylaxis with VZIG (specific immunoglobulins) is recommended for the contacts who are severely immunocompromised or pregnant (particularly in the first trimester).

References

  1. Cutaneous Manifestations of Systemic Infections. In: Text Book of Paediatric Infectious Diseases, Feigin RD, Cherry JD (eds), 4th Edition, WB Saunders Co. Philadelphia, 1998, pp 713-737.
  2. American Academy of Paediatrics. In: Report of the Committee on Infectious Diseases, 25th Edition, 2000, Elk Grove Village, Illinois, US.
  3. Varicella-Zoster Virus. In: Nelson’s Textbook of Paediatrics, Behrman, Leigman, Jenson (eds), 16th Edition, 1999, pp 973-977.
  4. Viral Infections. In Textbook of Dermatology. Champion RH et al (eds), 6th Edition, Blackwell Science Ltd., pp 1015.
  5. Varicella and Herpes Zoster. In: Dermatology in General Medicine. Fitzpatrick TB et al (eds), 5th Edition, the McGraw Hill Company Inc., New York, pp 2427.

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Acute Viral Hepatitis

Acute viral hepatitis is a systemic infection affecting liver and is caused by a number of viruses like Hepatitis A, B, C, D, E viruses etc. Commonest causes for infective hepatitis among children are Hepatitis A and Hepatitis E. Both of these are spread by faeco-oral route. Hepatitis B and C are more common in children requiring blood product for certain chronic illnesses.

Salient features

  • The illness may vary from asymptomatic infection, anicteric hepatitis to icterus, and even hepatic coma.
  • Prodrome constituted by fever, malaise, nausea, emesis, anorexia and abdominal discomfort may preceed the appearance of jaundice. It may go unnoticed or may be severe mimicking malaria or typhoid fever.
  • LFTs may be done only if the course of disease is unusual or when obstructive jaundice is suspected.

Treatment

Nonpharmacological

  • Rest if the patient feels exhausted or fatigued (forced rest does not help and does not shorten the time to recovery).
  • Regular small frequent meals with high caloric content. High carbohydrate diets are acceptable but should be hygienic. Traditionally sugarcane juice is used as home therapy though it has no established benefit.
  • Maintain adequate hydration in case of vomiting and avoid fatty meals.

Pharmacological

There is no specific treatment for simple acute viral hepatitis. Uncomplicated cases can be treated at home.

  • If patient has frequent vomiting Syp./Tab. Metoclopramide 0.1 mg/kg/dose can be given as and when required but not to be repeated before 6 hours.
  • Usually fever abates after jaundice appears. Occasionally if the situation requires, paracetamol may be used sparingly (see section on fever).

Persistent high grade fever suggests alternative diagnosis. Hospitalization required only in clinically severe illness e.g. alteration in sleep pattern, altered behaviour, abnormal movements, persistent vomiting, dehydration, decreased urinary output, bleeding from any site or any other complication.

Patient education

  • Continue breast feeding or other regular feeding
  • Observe carefully for any danger signs listed above
  • Usually a self limiting disease and fever subsides after the jaundice is evident clinically. Most patients start recovering in 7-14 days time. Total duration of illness is 3 weeks.
  • Hepatitis A and B are two different diseases. Getting your child vaccinated with hepatitis B vaccine will not protect you against Hepatitis A (see immunization schedule and appendix IX and X for details).
  • Hepatitis A spreads through contaminated food and water and close person to person contact
  • Raw or insufficiently cooked food (fruits, vegetables, salads) or cooked food handled by an infected individual can be the source of hepatitis A infection.

References

  1. Viral Hepatitis. In Nelson’s Textbook of Paediatrics. Behrman, Leigman, Jenson (eds), 16th Edition, 1999, pp 768-776.
  2. Acute Viral Hepatitis. In: Harrison’s Principles of Internal Medicine. Braunwald, E, Fauci AS, Kasper DL,et al (eds), 15th Edition, 2001, McGraw Hill Company Inc: New York, pp 1721-1737.

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Acute Diarrhoea

Acute diarrhoea is defined as increase in frequency, fluidity or volume of stools. It is caused commonly by Rotavirus, E. coli, V. cholera, Giardia or parenteral infections and invasive diarrhoea by Shigella, Salmonella and E. histolytica

Salient features

  • Clinical features of diarrhoea are frequent stools, vomiting, fever and dehydration
  • Dehydration is categorized into some dehydration and severe dehydration.

In some dehydration child is thirsty and drinks voraciously, active and alert but irritable, with sunken eyes, depressed fontanelle, absent tears, loss of skin turgor and some decrease in urine output.
In severe dehydration all these are more severe except that child is lethargic and does not want to drink water.

Following investigations may be done if indication exists:

Investigations Indications
Stool microscopy Dehydration or high fever, Diarrhoea persisting beyond 7 days, Blood persisting in stool after 48 hour of treatment
Blood urea

S. electrolytes (SE) and arterial blood gas
(ABG)

All 3 investigations in moderate to severe dehydration,

SE in persistent vomiting or signs ofdyselectrolytaemia
ABG in respiratory distress and no chest signs and sepsis (correct it only if pH <7.25).

Infection screening byTLC, DLC, band cellcount, ESR and CRP Fever persisting >72 hours,PEM > grade III or age <3 months.
Blood culture
Chest X-ray, CSFand others
Stool culture
Suspected sepsis, Before starting antibiotics.
As and when required
No role

Treatment

Nonpharmacological

  • Maintain hydration by home available fluids in place of or along with ORS. These are rice, kanji, butter milk, dal soup, coconut water or weak tea etc.
  • Maintain nutrition: continue breast feeding. Continue normal light diet e.g. khichri, dalia, banana or mashed dal etc. Do not dilute or stop milk as there is not much role of lactose intolerance or milk protein allergy. Give extra food during recovery.

Pharmacological

1. Oral rehydration solution (ORS) is used in some dehydration

  • 75 ml/kg in 4 hours under observation.
  • After 4 hours if dehydration is corrected, or if child was not dehydrated at presentation, send home with instructions to give ORS in 2:1 dilution as accepted by the child. Asked to report back if vomiting persists or urine is not passed for >8 hours. As a rough guideline 10 ml/kg of ORS may be added for each large stool.
  • If dehydration is not corrected after 4 hours, same amount of ORS may be repeated in next 4 hours and if dehydration is corrected send home.
  • If dehydration does not improve in 8 hours or if it worsens abandon oral rehydration therapy (ORT) and give IV fluids.

Principles of ORT

  • Give in small sips.
  • Vomiting is not a contraindication unless persistent.
  • Contraindicated in altered sensorium or paralytic ileus.
  • Stop as soon as diarrhoea stops

2. IV fluid therapy in case of severe dehydration or shock or contraindications or failure of ORT. N/2 saline is given over 8 hours (1:100 ml KCl after child passes urine), as follows:

  • Some dehydration- 75 ml/kg.
  • Severe dehydration- 150 ml/kg (half in first 2-3 hours)
  • Shock- push 20 ml/kg of Ringer’s lactate or normal saline over 15 minutes and can repeat twice more if shock persists use central venous pressure monitoring for further management if shock present after pushing 60 ml/kg.

Specific therapy with following, if indicated:

Frank blood and mucus in the stool or >10 pus cells/HPF
Syp. Nalidixic acid 55 mg/kg/day in 3 divided doses for 5 days
Or
Syp. Ciprofloxacin 15-20 mg/kg/day in 2 divided doses (Shigella strains are largely resistant to ampicillin and cotrimoxazole)

Giardiasis (only if trophozoites are seen on stool microscopy),
Syp. Metronidazle 20 mg/kg/day in 3 divided doses for 7 days
Or
Syp. Tinidazole 20 mg/kg/day for 7 days

Cholera (suspect in any child with severe watery diarrhoea)
Mainstay of treatment is fluid therapy, following antibiotic may be used to prevent spread:
Syp. Doxycycline 5 mg/kg in single dose
Or
Syp. Furazolidone 6 mg/kg/day for 3 days
Or
Syp. Cotrimoxazole (TMP) 8 mg/kg/day for 5 days.
Or
Syp. Erythromycin 30 mg/kg/day for 3 days.
Parenteral infections to be treated by appropriate antibiotics. There is not much role of antiemetics in a child with vomiting. Rule out meningitis, URI and dyselectrolytemia and give ORS in sips. If vomiting persists give intravenous fluids. However, occasionally 1 or 2 doses of metoclopramide (0.5 mg/kg) or domperidone (0.5 mg/kg) may be tried before giving intravenous fluids. Binding agents e.g., Kaolin pectin etc. are not useful.

Following drugs are contraindicated:

  1. Antimotility agents e.g. diphenoxylate, atropine etc.
  2. Antisecretory agents e.g., loperamide, salicylates etc.

Keep record of vitals e.g. pulse, BP, capillary filling time (CFT), respiratory rate (l hourly) and temperature (6 hourly). Monitor for improvement or worsening of signs of dehydration. Record urine output and stool frequency and consistency.

Modifications or step up treatment

  • Admit if PEM grade III or age <3 months (as higher chances of complications e.g. shock, hypoglycaemia etc.), anxious mother, associated severe systemic infections e.g. septicaemia, meningitis or pneumonia.
  • Investigate for lactose intolerance, incipient infections e.g., Urinary tract infection (UTI) or rare gut organisms, if diarrhoea persists for >7 days.
  • Exclude parenchymal renal failure, if child has not passed urine after hydration. Give a fluid challenge (20 ml/kg of normal saline) followed by frusemide injection (1-2 mg/kg). If urine is still not passed then parenchymal renal failure considered and managed accordingly.

Patient/Parent education

  • Information on natural course of diarrhoea to avoid dissatisfaction and that ORS only prevents dehydration i.e. purge rate and consistency usually improves by 3-7 days
  • Explain that most of the complications in diarrhoea are because of dehydration and thus ORS is the mainstay of therapy.
  • Explain preparation of ORS and method of administration.
  • Nutritional advise as mentioned earlier in nonpharmacological section.
  • Education about food and water hygiene.

References

  1. Major Symptoms and Signs of Digestive Tract Disorders. In: Nelson’s Textbook of Paediatrics. Behrman, Leigman, Jenson (eds), 16th Edition, 1999, pp 1102-1108.
  2. Acute Diarrhoea. In: Management of Acute and Chronic Diarrhoea in Children. SK Mittal (ed.), 2nd Edition, 1999, pp 1-44.

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Typhoid Or Enteric Fever

Salmonella typhi causes a variety of illnesses including asymptomatic carriage, gastroenteritis, enteric fever etc.

Salient features

  • The onset of fever is typically gradual with constitutional symptoms like malaise, anorexia, lethargy etc. which may be associated with abdominal pain and tenderness, hepatomegaly, splenomegaly, and/ or change in mentation. Usually the patient is sick and toxic looking with a coated tongue and has a soft splenomegaly.
  • Complications like hepatitis, peritonitis, meningitis, pneumonitis, myocarditis can occur, usually after the first week.

Treatment

Pharmacological

  • Management of fever (see section on fever)
  • Antipyretics can cause precipitous fall in temperature and even shock, in enteric fever. They should be used judiciously. Therefore, hydro therapy is preferred for fever management in such patients.
  • Adequate nutrition and hydration should be maintained ensuring adequate intake either orally or with Intravenous fluids (in severely ill) l In-patient treatment is recommended if the patient is very sick, not accepting orally with inadequate urine output, has altered sensorium/drowsiness or is having very high pyrexia particularly in the second week of illness when the risk of complications increases or if the complications have already ensued.

Pharmacological

Specific therapy: Multi drug resistance is prevalent among S. typhi. So the antibiotics are recommended on the basis of available resistant pattern or epidemiological data and sensitivity pattern is as below:

  1. Inj. Ciprofloxacin 15-20 mg/kg/ day in 2 divided doses given as IV infusion/Oral. Oral drug should be taken about an hour after meals and not empty stomach or with meals.
    Or
    Inj./Tab. Oflaxacin 5-8 mg/kg/day in 2 divided doses given as IV infusion or oral
    Or
    Tab. Cefixime 10-20 mg/kg/day in 2 divided doses
    Or
    Inj. Ceftriaxone 75-100 mg/kg/day IV in 2 divided doses
  2. In patients with shock, obtundation, stupor or coma short course of dexamethasone may be used Inj. Dexamethasone 2 mg/kg initial dose followed by 4 mg/kg every 6 hours for 48 hours.

The usual duration of antibiotic treatment is 10-14 days or atleast 7 days after the patient has become afebrile. Intravenous therapy is used during acute phase among the admitted patients. Less sick patients can be treated with oral drugs on an outpatient basis.

Assessment of response to therapy

  • The toxic look of the patient decreases and appetite starts returning in 72-96 hours of treatment and gradually the fever also starts responding, touches the baseline for increasing duration. The fever can take as long as 7 days to respond.
  • Some times the patient may apparently appear to have responded whereas patient may be developing impending shock due to complications. So a careful clinical assessment should be done particularly if there is a precipitous fall in temperature.

Modification or step up therapy if required

  • The patient should be monitored for complications and usual indications for inpatient treatment are: myocarditis (fall in perfusion and BP, arrhythmias), altered sensorium, shock (tachycardia, cold clammy skin, diaphoresis, hypotension), perforation peritonitis (acute pain in abdomen, guarding, rigidity, hypotension, billious vomiting).
  • In case the patient worsens or fails to show any response to therapy in 4 -7 days or so, as discussed above, then a change of antibiotics is suggested, preferably on the basis of the culture sensitivity report, where available.

Patient/parent education

  • Small frequent feeds should continue. Give plenty of oral fluids and compensate for increased fluid loss from the body due to high grade fever.
  • Fever usually lasts 5-7 days even after starting effective treatment in most cases. Frequent change of therapy should therefore be avoided.
  • The treatment should be completed till the patient has been afebrile for atleast 7 days as incomplete treatment increases the risk of relapse and emergence of resistance.
  • The caregivers of the patients should be informed about the complications as described above.
  • Ciprofloxacin and Ofloxacin are very bitter and cause severe nausea and gastritis. Patient should be asked to report any missed doses due to vomiting.
  • Three types of vaccines are available to prevent this disease (see section on immunization and appendix IX and X for details).

References

  1. Text Book of Paediatric Infectious Diseases, WB Saunders Co. Philadelphia.
  2. American Academy of Paediatrics. In: Report of the Committee on Infectious Diseases, 25th Edition, 2000, Elk Grove Village, Illinois, US
  3. Salmonella. In: Nelson’s Textbook of Paediatrics. Behrman, Leigman, Jenson (eds), 16th Edition, 1999, pp 842-848.

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Recurrent Abdominal Pain Of Childhood (RAP)

Three or more bouts of abdominal pain occurring over a period of not less than three month and severe enough to interfere with child’s normal activities. It is most common in the age group of 5-15 years and in 90% cases it is functional.

Salient features

  • Paroxysmal – Child appears well in between the episodes or sometimes dull continuous ache may be present.
  • Mostly periumblical, epigastric or suprapubic.
  • Episodes last for generally less than one hour.
  • Not related temporally to activity, meals, stress or bowel habits.
  • Rarely awakened from sleep
  • Normal physical examination and growth.

Warning signs pointing towards organic pain

  • Well localized pain away from midline (Apleys law – farther the pain from midline, more likely to be organic).
  • Repeated vomiting
  • Pain awakening the patient from sleep.
  • Radiation to shoulder, back, scapula, lower extremities.
  • Age less than 2 years
  • Associated fever, arthralgias, rash, rectal bleeding.
  • Consistent sleepiness following pain attacks.
  • Intermittent faecal incontinence
  • Weight loss or growth deceleration
  • Recurrent isolated episodes of pain that come on suddenly and last for several minutes to few days.
  • In case of any warning sign patients should be investigated accordingly, otherwise treat as functional. However, basic investigations e.g. urine, stool, Montoux and ultrasound examination might be done. Upper gastrointestinal endoscopy is generally not required.

Treatment

Nonpharmacological

  • Treat organic cause if found.
  • Environmental intervention to avoid painful stress, change in parent reaction to avoid secondary gain. Common psychogenic factors responsible for RAP are complaint modelling (parents with abdominal pain), school phobia, learning problems, anxious over achiever, ridicule by peers, teacher incompatibility, attention seeking (attention withdrawal after an illness, over busy parents, single child, sibling rivalry, eating time conflict, forceful toilet training), family psychopathology (parental conflict, single parent).
  • Visit to doctor and placebos often help
  • Child is asked to maintain pain chart (help in assessment of improvement as well as etiology).
  • If required, help from a psychologist may be taken.

Pharmacological

  • Nothing more than placebo are required.
  • Constipation, if present may be treated.

Patient/parent education

  • Explain the outline of the work up and treatment for the child before starting treatment. Doing so after negative work up makes family feel that the physician is making excuses. Explain that cause of RAP in most children is nonorganic.
  • Discovery of cause may lessen the family’s concern but may not alleviate the symptoms. There is no way to be certain that abdominal pain is because of identified disease entity. Pain may continue and its persistance does not mean serious organic disease.

References

  1. Recurrent Abdominal Pain. In: Pain in Infant, Children & Adolescents. Neil L. Schhechter, Leonard A, Rappaport, Alan M. Leichtnr (eds), pp 561-569.
  2. Recurrent Abdominal Pain in School Children. Paediatric Clinics of North America, Vol. 31. No. 5., October 1984, pp 969-991.
  3. Recurrent Abdominal Pain of Childhood. In: Nelson’s Textbook of Paediatrics. Behrman, Leigman, Jenson (eds), 16th Edition, 1999, pp 1176-1178.

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