Most central nervous system infections in infants and young children are meningoencephalitis, although one or the other aspect (meningitis or encephalitis) may be more marked. Acute infection of the meninges may be bacterial (Acute purulent meningitis), or viral (aseptic meningitis). Meningitis may also be due to tuberculosis and rare pathogens such as fungi and protozoa.
The term meningitis denotes an inflammation of the mcninges, which overlies the brain and the spinal cord. It is one of the most serious paediatric emergencies. Correct and appropriate therapy is life saving. Inadequate therapy, increases mortality and morbidity, particularly long-term neurological sequelae.
Meningitis can be classified into two broad groups, depending on aeliological agents:
1. Bacterial or pyogenic meningitis
2. Aseptic
a. Viral meningitis
b. Tuberculous meningitis.
Acute Pyogenic Meningitis:
Acute purulent meningitis in infants and children remains a serious threat to life and neurologic squeal in the survivors irrespective of etiology. The clinical presentation does not allow the physician to distinguish among the various etiological agents. Initial empiric therapy and supportive management is standard regardless of the specific pathogens.
Pyogenic meningitis accounts for around 5-8% of paediatric admissions. It results from either primary infection of the meninges or spread from a nearby focus.Age-specific isolation of bacteria from CSF in pyogenic meningitis:
Under 2 months : Ecoli.,Streptococcus.,Staphylococcus.,Listcria , monocylogenes
2 months to 6 years : H influenza ,Pncumococcus.,Meningococcus.
Beyond 6 years : Pneumococcus. Meningococcus.
There are many causative agents. The most commonly encountered organisms are, H. influen/a, Pncumococcus, Staphylococcus, Streptococcus, and Meningococcus. E. coli mostly effects neonates.
Clinical manifestations:
The signs and symptoms of purulent meningitis varies greatly with age. Many are nonspecific like fever, anorexia and poor feeding, URTI, myalgia, arthralgia, tachycardia, hypotension, and various cutaneous signs such as purpura which is usually associated with meningococcal sepsis and meningitis. Seizures are common with altered mental status and a reduced level of consciousness.
Clinical manifestations in meningitis depend upon the age of the child and the severity of infection. It may be of insidious or acute onset. In older children there may be sudden rise of body temperature, irritability, vomiting and convulsions (grand mal or focal seizures). Headache Is rarely complained by children. There may he photophobia, restlessness, drowsiness or coma. Signs of mcningcal irritation such as neck rigidity, Kernigs sign and Brud/inski's sign may be present. Bulging of the fontanel may be present if it has not been closed.
The characteristic signs of meningial irritation are neck stiffness, Kernig sign and Brudzinski sign but these are often absent in children under 18 months of age and the child may have bulge fontanel .Many of these signs may also be present with meningismus. Meningismus refers to meningial irritation especially nuchal rigidity, not due to central nervous system infection. Meningismus may be due to pneumonia, pharyngeal abscess, and rheumatoid arthritis with cervical spine involvement.
In neonates, there may be vacant stare, vomiting, reluctance to fed, fever or hypothermia, hypolonia and poor cry. The newborn child may be jittery or frank convulsions may occur. Signs of mcningcal irritation are usually absent in neonates and infants. The corner-stone of diagnosis is clinical suspicion.
The diagnosis of acute pyogenic meningitis is confirmed by analysis of the CSF obtained by Lumber puncture (LP). The diagnosis should he confirmed by lumbar puncture. The CSF should be sent for cytology. Gram and acid fast stains, biochemical and culture and sensitivity tests. Blood culture may also help in identifying the causative organism.
In pyogenic meningitis the CSF is usually under increased pressure and turbid. Cell count is greatly increased with polymorphonuclear leucocylosis. The CSF sugar is markedly reduced, whilst protein is raised.
A blood culture should be performed in those patients who started treatment empirically prior to LP. Additional diagnostic methods include culture and staining of purpuric lesions and CSF C-reactive protein.
Complication:
During the treatment the common complications are, seizures, syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and subdural effusion. Symptomatic subdural effusion should be treated by aspiration. Persistent fever may complicate the management and may be due to subdural effusion, drug reaction, nasocomial infection, phlebitis, pneumonia, pericarditis or arthritis. Disseminated intravascular coagulation (DIC) is most often common in patients with shock and purpura.
The neurological sequalae are recurrent seizures, sensoryneuronal hearing loss,hydrocephalus, hemiparesis and mental retardation.
Recrudescence is the reappearance of infection during therapy with appropriate antibiotics and is usually due to development of bacterial resistant. Relapse occurs between 3 days and 3 weeks after therapy and represent persistent bacterial infection in the CNS (subdural empyema, ventriculitis, cerebral abscess or mastoiditis, cranial osteomyelitis, orbital infection).
Recurrence is a new episode of meningitis due to reinfection with it or another pyogenic pathogen and suggests presence of anatomic communication and in immunocompromised subjects.
Treatment
The choice of antibiotic depends on the isolation of the organism and its sensitivity pattern. Prior to its isolation, a combination of antibiotics covering both Gram negative and Gram positive organism is given.
1. Penicillin 300,000 units/kg/day in divided doses or Ampicillin 300- 400 mg/kg/day/IV or IM in divided doses.
2. Chloramphenicol 100 mg/kg/day I.V. or I.M. 4 divided doses (orally) during recovery.
3. In neonates Chloramphenicol should not be given, the drug of choice is Gentamicin in a dose of 4-8 mg/kg in divided doses.
The appropriate drug should be selected on the basis of the culture and sensitivity result of the spinal fluid. Second and third generation cephalosporin may be selected .Duration of treatment is 10-14 days or until the patient is afebrile for at least for 3 days. It is preferred to do a second lumbar puncture before stopping the treatment.
Indications to Stop Therapy:
I. No fever for three days
2. Cell count in CSF is less than 50/cumm (and most are mononucleai ).
3. Gram stains show no organism
4. Culture gives no growth.
Intrathecal administration of antibiotics may be considered initially. In advanced cases, convulsions should be controlled first by intravenous or rectal diazepam followed by Phenobarbitone orally.Adequate hydration and nutrition of the patient should be maintained. As there is a danger of fluid overload due to inappropriate ADH secretion, fluid should be restricted.
Prevention :
a) Vaccines:
Haemophillus influenzae type b (Hib) vaccines should be given to all children, and Pneumococcal vaccine and meningococcal vaccine should be given to high risk children .
b) Chemoprophylaxis:
Recommended for household contact which means one who lives in the residence of the index case or who has spent a minimum of 4 hours with the index case for at least 5 of 7 days preceding the patients hospitalization. In case of H.influenzae tybe b infection, the patient and the household contact should receive Rifampicin 20mg/kg/dose every day for 4 days. In case of meningococcal infection, the close contacts should receive 10 mg/kg/dose every 12 hours for two days and ceftriaxone 250mg IM for one dose is an effective alternative for pregnant women.
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