Tuberculous MeningitisCHCUMSCHCUMSDIVISION OF INFECTIOUS DISEASE AND DIVISION OF INFECTIOUS DISEASE AND GASTROENTEROLOGYGASTROENTEROLOGYNovember 24th, 20041EPIDEMIOLOGY - TBMTuberculous Meningitis (TBM)u The younger the children, the more readily to develop TBM. u 60% in Children aged 1-3 yearsu Death rate: 15-30%2TBM (Tuberculous meningitis)u TBM is the most serious complication of tuberculosis in children and is usually fatal without treatment.u TBM always be a part of systemic disseminated tuberculosis.u TBM often occurs within 1 year of initial infection, especially in the first 2 to 6 months of infection.3Tuberculous BacilliPrimary ComplexBacteremiaRich FociSubarachnoid SpaceBrain or Spinal Cord PerenchymaTuberculomasMeningitisPATHOPHYSIOLOGYTrauma/Diseases measles, pertussis Miliary TB4PATHOLOGICAL EFFECTSMeningesuDiffuse HyperemiauEdemauInflammatory Exudates uConformation of Tubercles 5PATHOLOGICAL EFFECTSSubarachnoid SpaceuA large amount of thick gelatinous exudates concentrate to the pavimentum cerebri, optic chiasma, bridge of varolius, bulbus rhachidicus and Sylvian fissure. u Basal meningitis accounts for the frequent dysfunction of cranial nerves III, VI, and VII.6PATHOLOGICAL EFFECTSCerebral Parenchyma Tuberculous meningoencephalitisuswelling and hyperemia of the parenchyma contribute to the intracranial hypertension, then ischemia of parenchyma occur, finally lead to the foci of encephalomalacia and necrosis. Hemiplegia may be present because of this change. uMeninges, spinal, and spinal nerve root also involvement. The later always leads to paraplegina.7PATHOLOGICAL EFFECTS Cerebral VesselsuThe bacteria invade the adventitia directly in the early stage and initiate the process of acute vasculitis. uProgressive destruction of adventitia, disruption of elastic fibers, and finally intimal destruction (endoarteritis), lead to the obliterative vasculitis, which may facilitate the ischemia, encephalomalacia and necrosis of parenchyma. 8Circulati on of CSFChoroid plexusLateral ventricleInterventricular foramenthe 3rd ventricleCerebral aqueduct4th ventricle2 Lateral foramina1 Medial foramenSubarachnoid spaceArachnoid granulationsDural sinusVenous drainage9PATHOLOGICAL EFFECTSHydrocephalus Hyperemia of choroids overproduction of CSF Inflammatory adherence of Meningedefective absorption of CSF Communicating hydrocephalus CSF flow is obstructed on the route before the cerebral aqueduct and the 4th ventricleNoncommunicating hydrocephalus 10In tuberculous meningitis there is a tendency for the exudate to be primarily located on the under surface of the brain, particularly over the ventral surface of the brain stem. 11CLINICAL MANIFESTIONSA. Prodrome (1-2 week) uFever, fatigue, malaise, myalgia, drowsiness, headache, vomiting uMental status changes uFocal neurologic signs are absent uCSF abnormity 12CLINICAL MANIFESTIONS B. Meningeal Irritation Stage (1-2 week) uMore serious TB toxic symptoms uIntracranial hypertension: severe headache, irritation, projectile vomiting, seizures; Bulging of anterior fontanelle, widening of cranial sutures in infant uMeningeal Irritation : nuchal rigidity, hypertoniaKernig sign or Brudzinski sign uCranial nerve abnormalities: 3, 6, 7 uSome children have no evidence of meningeal irritation but may have signs of encephalitis: disorientation, abnormal movements and speech impairment 13CLINICAL MANIFESTIONS C. Coma Stage (1-3 week) uFrequent convulsion, progressive altered state of consciousness: lethargy, confusion, semicoma, deep coma, decerebrate or decorticate posturing uDepletion: extremely maransis, constipation, urinary retention uprogressive abnormalities of vital signs, and eventual die from cerebral hernia 14Characteristics of TBM in infants and young childrenuA rapid onset with convulsion, abruptly high fever uAtypical miningeal irritation uIntracranial hypertension manifests as bulging of anterior fontanelle and widening of cranial sutures in infant 15PROGN OSISu The prognosis of tuberculous meningitis correlates most closely with the clinical stage of diagnosis and treatment. u Age: infants or younger children are generally worse than that of older childrenu Drug resistant strain u Variation of host immunityu Appropriate therapeutic regimenu Completion of the antituberculor agent regimen16It is imperative that antituberculosis treatment be considered for any child who develops basilar meningitis and hydrocephalus, cranial nerve palsy, or stroke with no other apparent etiology.17DIAGNOSIS History Clinical Symptoms and Signs Auxiliary Examinations18DIAGNOSIS - HistoryElucidate the following: uMedical and social history, including recent contact with patients with TB uNegative history for Bacille Calmette-Guerin (BCG) vaccination uHistory of immunosuppression from a known disease or drug therapy19DIAGNOSIS Symptoms and signs uA gradual onset uFever, headache, alternant