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Acute bacterial meningitis
Bacterial meningitis is the disease process of inflammation of the leptomeninges caused by bacterial infection. Varying degrees of parenchymal involvement may also be present.
INCIDENCE
Varies from 3.0 cases per 100,000 population in United states to 45.8 cases per 100,000 population in Brazil.
AETIOLOGY
Agents causing ABM -
Neonatal age group- E. coil, streptococcus beta haemolyticus, streptococcus fecalis, staphylococcus aureus, salmonella spp. and Pseudomonas aeruginosa
3 months to 2 years age- H. influenzae, pneumococci and meningococci
3 years onwards- Pneumococci
N.B.- Neisseria meningitis infection can occur at all ages.
Host factors -
Increased susceptibility in
Diminished host resistance e.g. Diabetics, malignancy, patients on immunosuppressive drugs, infections (Listeria monocytogenes, Mycoplasma pneumoniae) & HIV.
Infants and young children (due to immature immune mechanisms and phagocytic functions)
Other immunosuppressive conditions- Splenectomy, burns, congenital deficiencies, sickle cell anaemia, etc.
Other predisposing conditions -
Upper respiratory tract infections, otitis media, pilonidal sinus, pyodermas and head injuries (all act as primary foci of infection)
PATHOGENESIS -
Foci of infections -
Distant foci- Pneumonia, empyema, pyoderma, and osteomyelitis
Contiguous septic foci- in skull and spine, infected paranasal sinuses, mastoiditis, and ostemoyelitis of the skull
Extension of bacteria from the nasopharynx to the meninges through a linear fracture in the base of skull in cases of minor head injury
Recurrent meningitis occurs in cases of
Immune deficiency disorders
Pilonidal sinus
CSF fistula associated with rhinorrhoea and otorrhoea following lesions of the cribriform plate and ethmoidal sinus & congenital fistulae
Causes of cerebral oedema -
1)Vasogenic oedema- Increased permeability of the blood brain barrier.
2)Cytotoxic oedema- Swelling of cellular elements of the brain caused by toxins released by bacteria and neutrophils.
3)Interstitial oedema- Obstruction of CSF outflow from the subarachnoid space.
4)Antidiuretic hormone induced hyponatremia and hypotonicity of EU.
Cerebral oedema is a major contributor to increased intracranial pressure in ABM.
Other pathologic processes in ABM -
Vasculitic changes- which narrow/obstruct the lumen of vessels and lead to ischaemia or infarction of the brain.
Loss of autoregulation of cerebral blood flow.
PATHOLOGY
Cloudy opaque fluid is filled in the subarachnoid space.
Leptomeninges are infiltrated with inflammatory cells.
Purulent exudate collection at the base of the brain which can block the foramina of Luschka and Magendie leading to a hydrocephalus.
Cerebral vessel thrombophlebitis with infarction of cerebral tissue.
Exudate can later organise into fibrosis leaving behind neurological sequale of infarction, necrosis & hydrocephalus.
Fulminating course progressing to death occurs in meningococcal meningitis.
CLINICAL FEATURES -
A) In older children and adults -
Onset- acute and fulminant.
Features of meningeal irritation
Irritability, headache and photophobia.
Headache is frontal or diffuse, bursting in quality and spreading to neck and eyeballs.
Projectile vomiting may occur.
Acute shill cries common.
Fever - 39° to 400c with constitutional symptoms.
Respiration may become periodic/Cheyne Stoke's type in later stages.
Generalised flexed posture
Drowsy/stuponts.
Hypertonia with marked neck rigidity (i.e. painful restricted flexion of the neck).
Kernig's sign is positive- The thigh is flexed on the abdomen to 90° and the flexed knee is extended.
Extension of knee is limited with pain in back or thigh or spine (Normal extension to 135° and beyond).
Brudzinski's sign- Knees get flexed on flexing the neck.
Fundus- NormaVcongestion & papilloedema.
Extrinsic ocular palsies-Squint, diplopia & ptosis.
`Tache cerebrale'- If the skin of the abdomen is lightly scratched, flushing is seen.
Neurological deficits- Hemiparesis & hemianopsia can develop.
Later stages- Deep comatose stage.
B) In neonates and young infants -
Difficult to diagnose
Neck rigidity and Kerning's sign may not be positive.
Anterior fontanelle may/not be bulging. High risk neonates & infants -
Prematurity
Low birth weight
Complicated labour
Premature rupture of membranes
Maternal sepsis
Babies requiring extensive resuscitation
Following are the ominous signs in the infants (which should be looked for) -
Vacant stare
Alternating irritability and drowsiness
Persistent vomiting with fever
Refusal to feed
Poor tone
Poor cry
Circulatory collapse
Fever or hypothermia
Tremors, convulsions
Neurological deficits of varying degrees
C) Special features of clinical picture of varying aetiology -
A.Meningococcal meningitis -
Petechial hemorrhages on the skin or the mucosa
Adrenal insufficiency
'Waterhouse Friderichsen syndrome': Hypotension, shock & coma (occurs due to hemorrhage & necrosis of adrenals). Septicaemia.
B.Pneumococcal meningitis -
Follows otitis media, sinusitis, pneumonia or head injury. Subdural effusion is common.
C.Staphylococcal meningitis -
Umbilical infection, pyoderma or septicaemia is the cause.
In older children it follows otitis media, mastoiditis, cavernous sinus thrombosis, and septic lesions of the scalp.
D. H. influenzae meningitis -
Common in age of 3-12 months.
Subdural effusion occur (Neurological sings & fever may persist after clearance of the CSF- biochemically & microbiologically).
Convulsions are common.
Residual auditory deficit also common.
COMPLICATIONS -
Encephalomyelitis
Ventriculitis
Internal hydrocephalus
Mental deterioration
Spinal cord compression due to arachnoiditis
Cerebral infarction
Subdural empyema/effusion
SEQUALE -
Mental retardation and cognitive impairment
Cerebral palsy
Epilepsy
Neurological deficits - e.g. hemiplegia, aphasia, ocular palsies, hemianopsia, blindness, deafness, etc.
SIADH- Syndrome of inappropriate secretion of ADH DIFFERENTIAL DIAGNOSIS -
Meningism- Apical pneumonia, typhoid
Generalised infection associated with toxaemia
Partially treated bacterial meningitis
Aseptic meningitis --
Tuberculous meningitis
Cryptococcal meningitis
Lymphocytic choriomeningitis
Viral encephalitis
Poliomyelitis
Subarachnoid haemorrhage
Brain tumor/abscess
Lyme disease
INVESTIGATIONS -
Lumbar puncture -
CSF is turbid
Cell count- over 1000/m0 with polymorphonuclears predominance
Proteins- above 100 mg/di (Normal - 5-35 mg/di)
Sugar- Significantly reduced (CSF sugar less than half of blood sugar or <40 mg/di)
CSF lactic acid is higher than 35 mg/di (elevated in suppurative meningitis as compared to viral/TB meningitis).
Gram stain- organisms can be identified & culture establishes the diagnosis. Antibiotic sensitivity- to decide the appropriate antibiotic to be given.
Lumbar puncture should be done cautiously in patients with papilloedema using a small bore needle allowing the fluid to drain very slowly to prevent coning of brain stem.
Predicted number of WBC in CSF (P) is calculated as
P= CSF(RBC) x Blood (WBC)/Blood (RBC)
In Bacterial meningitis P is >100
RoIe of CT and MRI -
Not routinely required
Done in cases of neurological deficit or patients with papilloedema before doing LP
Also useful to diagnose subdural effusion, pus or brain abscess.
Rapid diagnostic methods — Not routinely available
Antigen demonstration using -
Counter current immunoelectTophoresis
Latex particle agglutination
Limulus lysate test
Other special tests -
C-reactive protein test (differentiates between viral and bacterial meningitis)
Lactate dehydrogenase
Tumor necrosis factor is raised in CSE
Recent advances -
Polymerase chain reaction of CSF to diagnose infection with herpes simplex, enteroviruses, tuberculosis, etc.
Other investigations -
WBC count - Leucocytosis
ESR - raised
LFT, RFT
X-ray chest - To diagnose TB/pneumonia (focus of infection)
MANAGEMENT -
Principles -
1)Specific antimicrobial therapy
2)Symptomatic
3)Supportive
4)Diet and Nursing
5)Treatment of complications
6)Follow up and rehabilitation
1) Antimicrobial therapy -
When organisms are not identified-
Ampicillin (300 mg/kg/day) in 4 divided doses for 10 days or Benzyl Penicillin (50,000 units/kg/day in 4 divided doses) with Chloramphenicol (100 mg/kg/day) or
Gentamicin (2.5 mg/kg/dose TDS) OR Cefotaxime (200 mg/kg/day, QDS) with amikacin (7.5 mg/kg/dose TDS)
Streptococci and strept. pneumoniae -Benzyl Penicillin or Cefotaxime or Ceftriaxone (100 mg/kg/day, BD)
Staphylococci - Cloxacillin (200 mg/kg/day, QDS) or Vancomycin (20-40 mg/kg/day TDS) with Gentamicin or Amikacin
H. influenzae Cefotaxime or ceftriaxone (100mg/kg/day) or chloramphenicol
Meningococci Penicillin or Cefotaxime or ceftriaxone
Rifampicin is used to eradicate the carrier stage
Pseudomonas Ceftazidime or Cefaperazone
Discontinuation of therapy with antimicrobials -
Usually for 14 days
Cell count in CSF less than 30/me
CSF protein and sugar return to normal levels
2) Symptomatic therapy -
Treatment of increased intracranial pressure
Cortisone/ dexamethasone
Osmotic diuretic- e.g. Mannitol 0.5 gm/kg of 20% solution iv every 4 hours.
Antipyretics for fever
3) Supportive therapy -
Fluid and electrolyte balance- Frequent ABG and electrolyte monitoring required.
Hypotension- Use of fluids and vasopressors (Dopamine)
4)Diet and nursing care -
Protein rich; adequate calories and vitamin. Feeding through nasogastric tube is required in an unconscious child.
5)Treatment of complications -
Subdural empyema- Drainage of subdural space and irrigation with dilute solution of penicillin or aminoglycoside with simultaneous antimicrobial therapy.
Hydrocephalus- Ventriculoperitoneal shunt
Convulsions- Diazepam 2-5 mg IV followed by phenobarbitone 5 mg/kg/day in divided doses.
6) Follow up and rehabilitation -
Follow up for detection of the residual neurological deficits or mental retardation
Rehabilitation of neurologically handicapped by appropriate physiotherapy and occupational therapy
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