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G.ERIC™ MD4 MENINGITIS PEDIATRICS
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ACUTE BACTERIAL MENINGITIS Acute bacterial meningitis, a major cause of morbidity and mortality in young children, occurs both in epidemic and sporadic pattern.
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Epidemiology Age. Acute bacterial meningitis is commoner in neonates and infants than in older children because of poorer immunity and phagocytic functions. The common organisms in neonates are Escherichia coli, Streptococcus pneumoniae, Salmonella species, Pseudomonas aeruginosa, Streptococcus fecalis and Stap hylococcus aureus. Three months to 3 yr, the infection is most often due to Haemophilus
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Host. Patients with diminished host resistance (complement, immunoglobulin or neutrophil function defects), malignancies, on immunosuppressive drugs are more susceptible to develop meningitis, by fungi, Listeria and Mycoplasma.
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Pathogenesis The infection spreads hematogenously to meninges from distant foci, e.g. pneumonia, empyema, pyoderma and osteomyelitis. Purulent meningitis may follow head injury. Rarely, the infection may extend from contiguous septic foci, e.g. infected paranasal sinuses, mastoiditis, osteomyelitis and fracture of the base of skull.
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Clinical Features The onset is usually acute and febrile. The child becomes irritable, resents light, has bursting headache either diffuse or in the frontal region, spreading to the neck and eyeballThe infant may have projectile vomiting, shrill cry and a bulging fontanelSeizures are a common symptom and may occur at the onset or during the course of the illness.Varying grades of alterations in sensorium may occur. Photophobia is marked. There is generalized hypertonia and marked neck rigidity. Flexion of the neck is painful and limited. Kernig
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The muscle power in the limbs is preserved. Reflexes are normal, diminished or exaggerated. Neurological deficits like hemiparesis, cranial nerve palsies and hemianopsia may develop. Respiration may become periodic or Cheyne-Stokes type often with shock in the late stages of illness
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Meningitis in neonates and young infants. Neck rigidity and Kernig sign are seldom prominent. Symptoms and signs, which arouse suspicion of bacterial meningitis are: (i) sepsis; (ii) vacant stare; (iii) alternating irritability and drowsiness; (iv) persistent vomiting with fever; (v) refusal to suck; (vi) poor tone; (vii) poor cry; (viii) shock, circulatory collapse; (ix) fever or hypothermia; (x) tremor or convulsions; and (xi) neurological deficits of varying types. The following are risk factors for neonatal meningitis:
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Special Features Meningococcal meningitis. Epidemics of meningococcal meningitis are generally caused by serotype A and less commonly by type C. Type B generally cause sporadic disease. Children living in overcrowded houses are specially predisposed. Carrier state is common in children. Besides features of meningitis, children show petechial hemorrhages on the skin or mucosa. Meningococcemia may be associated with acute fulminant illness with adrenal insufficiency, hypotension, shock and coma.
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This is called Waterhouse Friderichsen syndrome and occurs due to hemorrhage and necrosis in the adrenal glands. Chronic meningococcemia may occur with intermittent fever, chills, joint pains and maculopapular hemorrhagic rash lasting for several days. Meningococci are very fragile
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Pneumococcal meningitis. While pneumococcal meningitis occurs at all ages, it is uncommon in the first few months of life. Usually follows otitis media, sinusitis, pneumonia or head injury. Exudates are common on the cortex and subdural effusion is a usual complication. Staphylococcal meningitis. Neonatal staphylococcal meningitis is often associated witpyoderma or septicemia. In older children it follows otitis
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Haemophilus influenzae type B meningitis. Is frequent between the ages of 3 and 12 months. Subdural effusion should be suspected in infants in whom focal neurological signs and fever persist even after the CSF clears biochemically and microbiologically. Convulsions are common. Residual auditory deficit is a common complication. HiB vaccine is recommended to reduce the
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Complications Empyema Ventriculitis arachnoiditis, brain abscess hydrocephalus. hydrocephalus.
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CNS complications should be suspected if infants and children fail to respond to treatment, or if fever, focal neurological signs and constitutional symptoms recur after a lapse of few days. Longterm neurological deficits include hemiplegia, aphasia, ocular palsies, hemianopsia, blindness, deafness, sensorineural auditory impairment
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Diagnosis Acute bacterial meningitis should be suspected in children presenting with a brief history of fever, irritability, photophobia, headache, vomiting, convulsions and altered sensorium. Diagnosis should be substantiated by examination of the cerebrospinal fluid.
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The CSF should be examined promptly for cellular response and sent for culture for bacteria and stained to identify morphology. The CSF has elevated pressure, is turbid with an elevated cell count, often >1,000/mm3 with mostly polymorphonuclear leukocytes. Proteins are elevated above 100 mg/ dl and sugar is reduced below 50% of blood sugar or below
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CT scan is not necessary for diagnosis, but is useful to exclude the presence of subdural effusion, brain abscess, hydrocephalus, exudates and vascular complications. It is also useful to distinguish partially treated pyogenic meningitis from tuberculous meningitis. Rapid diagnostic tests may be used to distinguish between
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DDX Meningism. Partially treated bacterial meningitis Aseptic meningitis. Tuberculous meningitis. Cryptococcal meningitis. Viral encephalitis Subarac/moid hemorrhage Lyme disease.
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Treatment Initial Empiric Therapy Initial therapy recommended is a third generation cephalosporin such as ceftriaxone or cefotaxime. A combination of ampicillin (200 mg/kg) and chloramphenicol (100 mg/ kg/24 hr) for 10-14 days is also effective as initial empiric choice. If fever or meningeal signs persist after 48 hr of therapy, a lumbar puncture should be repeated and the
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Specific Antimicrobial Therapy Meningococcal or pneumococcal meningitis. Penicillin 400- 500,000 units/kg/ day q 4 hr. Cefotaxime (150-200 mg/ kg/ day q 8 hr IV) or ceftriaxone (100-150 mg/kg/day q 12 hr IV) are also effective. H. influenzae meningitis Ceftriaxone or cefotaxime IV is used as a single agent. The combination of ampicillin (300 mg/kg/ day IV q 6 hr) and chloramphenicol (100 mg/kg/ day) is less preferred. Staphylococcal meningitis. Vancomycin is the treatment of
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Listeria. Ampicillin (300 mg/kg/ day IV q 6 hr) and aminoglycoside (gentamicin, amikacin or netilmicin) are preferred. Gram-negative bacilli. Cefotaxime, ceftazidime or ceftriaxone, or a combination of ampicillin and aminoglycoside may be used. Pseudomonas. A combination of ceftazidime and an aminoglycoside is used. Ceftazidime may also be
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Duration of Therapy Generally, patients with bacterial meningitis show quick improvement within days. The treatment is for 10- 14 days. except for staphylococcal meningitis and Gram- negative infection, where it is extended to 3 weeks. Routine lumbar puncture at the end of therapy is not recommended. In delayed or partial clinical response, a repeat CSF examination is indicated. Therapy is stopped if child is
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Steroid Therapy Dexamethasone at a dose of 0.15 mg/kg IV q 6 hr for 2-4 days is recommended. The first dose of corticosteroids is best given shortly before or simultaneously with the first dose of antibiotic. This helps to reduce the incidence of residual neurological complications, such as sensorineural deafness, hydrocephalus and behavioral
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Symptomatic Therapy Increased intracranial pressure. Lumbar puncture should be done very carefully in the presence of increased intracranial pressure. Osmotic diuresis with 0.5 g/kg of mannitol as a 20% solution is administered intravenously every 4- 6 hr for a maximum of 6 doses Convulsions. These are treated using diazepam 0.3 mg/kg (maximum 5 mg) IV, followed by phenytoin 15-20 mg/
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Fluid and electrolyte homeostasis. Maintenance fluids are given, hypotonic fluids should be avoided. ADH secretion occurs in some patients. If unconscious, child may be fed through the nasogastric tube. Hypotension. The patients are treated with intravenous fluids and vasopressors such as dopamine and dobutamine
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TUBERCULOUS MENINGITIS Meningitis is a serious complication of childhood tuberculosis. It may occur at any age, but is most common between 6 and 24 months of age. There is usually a focus of primary infection or miliary tuberculosis. Mortality rate has reduced but serious disabling neurological sequelae may occur
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Pathogenesis The tuberculous infection usually reaches the meninges by hematogenous route, less commonly through the lymphatics. Tubercle bacilli affect end arteries and form submeningeal tubercular foci. The tubercle bacilli discharge into the subarachnoid space intermittently, proliferate and cause perivascular exudation followed by caseation, gliosis and giant cell formation. Tuberculous
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The meningeal surface and ependyma are inflamed, covered with yellow grayish exudates and tubercles. These are most severe at the base, in the region of the temporal lobes and along the course of the middle cerebral artery. The subarachnoid space and the arachnoid villi are obliterated resulting in poor reabsorption of cerebrospinal fluid and dilation of the ventricles, resulting in
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Clinical Manifestations The clinical course of tuberculous meningitis is described in three stages. This differentiation is arbitrary as one- stage merges into the other. Prodromal stage or stage of invasion. The onset is insidious and vague with low grade fever, loss of appetite and disturbed sleep. The child who was active and playful earlier becomes peevish, irritable and restless. Vomiting is frequent and the older children may complain of headache. Child may exhibit head banging and resents
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Stage of meningitis. During this stage, neck rigidity may be present and Kernig sign may be positive. Fever may be remittent or intermittent, pulse is slow but regular. Breathing may be disturbed. The patient may be drowsy or delirious. Muscle tone may be increased. As the disease progresses, convulsions and neurological deficits may occur; sphincter control is usually lost.
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Stage of coma. This stage is characterized by loss of consciousness, rise of temperature and altered respiratory pattern. Pupils are dilated, often unequal, with nystagmus and squint. Ptosis and ophthalmoplegia are frequent. With the progression of the disease, coma deepens; episodic decerebration is observed which progresses in severity. The respiration becomes Cheyne-Stokes or Biot type, bradycardia is common. Untreated illness is lethal in about four weeks. Hemiplegia, quadriplegia, cranial nerve palsies and decerebrate rigidity are common findings. Some patients show monoplegia, hemiballismus, tremors, cerebellar sings and decorticate rigidity
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Diagnosis Lumbar puncture. Lumbar puncture should always be done in children with low grade pyrexia, unexplained recurrent vomiting, unusual irritability and lassitude. The cerebrospinal fluid pressure is elevated to 30-40 cm H20 (normal 3-4 cm H20). Cerebrospinal fluid does not confirm the etiological diagnosis, but provides adequate evidence for starting antitubercular therapy. Demonstration
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 X-ray of the chest may provide supportive evidence for tuberculosis. Negative Mantoux test does not exclude the diagnosis Computerized tomography is useful in tubercular meningitis and may reveal basal exudates, inflammatory granulomas, Serological tests for the diagnosis of tuberculous meningitis are not very sensitive. Bactec and PCR for tuberculosis
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DDX Purulent meningitis. Partially treated purulent meningitis Encephalitis Typhoid encephalopathy Typhoid encephalopathy Brain tumor. Prognosis The prognosis is poorer in younger children. Early diagnosis, adequate and prolonged therapy improves the prognosis. Untreated cases die within 4 to 8 weeks.
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Treatment Antitubercu lar therapy. The treatment of tuberculous meningitis should be prompt, adequate and prolonged for at least 12 months. Short course chemotherapy is not recommended. At least 4 antitubercular drugs should be used for initial 2 months comprising (i) isoniazid (5 mg/ kg/ day, maximum 300 mg per day); (ii) rifampicin (10 mg/kg/ orally, once empty stomach in the morning, maximum dose 600 mg/ day); (iii) ethambutol (15-20 mg/ kg/day); and (iv) pyrazinamide (30 mg/kg/day PO).
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Steroids. Parenteral dexamethasone (0.15 mg/kg/dose q 6 hr) is preferred in acute phase of illness and switched over to oral prednisolone. Oral corticosteroids may be continued for 6 weeks and tapered over next two weeks. Steroids reduce the intensity of cerebral edema, risk of development of arachnoiditis, fibrosis and spinal block.
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Symptomatic therapy of raised intracranial pressure, seizures, dyselectrolyternia should be done. The patient should be kept under observation for development of papilledema, optic atrophy or increasing head circumference. Decerebration is common in advanced cases in the acute phase. Ventriculocaval shunt may be required
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CRYPTOCOCCAL MENINGITIS. It usually occurs in an immunocompromised host. There is low-grade fever, mild cough and pulmonary infiltration. Meningeal involvement has a gradual onset with a protracted course. The clinical features are not specific. The CSF shows the fungus as thick walled budding yeast cells, surrounded by a large gelatinous capsule in India ink preparation. The organism grows well on Sabouraud medium.
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