Tuberculosis Meningitis

10 April, 2009

Ⅰ Ⅰ overview

TBM is the most serious type in children

with tuberculosis

TBM is an early primary complications in

Primary tuberculosis

the incidence is significantly decreased

after BCG vaccination

Ⅱ Epidemiology

Age of Onset ： More common in 1 ~5 year-old 1180 TBM in Beijing Children's Hospital<3y 56.7% ， <1y 48.5% (half the number) Onset in Season ： common in Winter or spri

ng

Ⅲ Ⅲ PPathogenesis

Hematogenous dissemination ： blood-CSF path main

Brain , meningeal tuberculosis rupture secondly

Tuberculosis in nearly organize direct spread occasionally

Ⅳ Ⅳ Pathology Extensive lesions Lesions in the bases of skull “basilar meningitis”basilar meningitis” (most

obvious) 病变以脑底部脑底部最明显 “脑底脑膜炎” leptomeningeal hyperemia, edema, Inflammatory exudat

e The inflammatory exudate is accumulated in the subarac

hnoid （ cistern in pavimentum cerebri ） cranial nerve lesion cerebrovascular disorder 。 Pyocephalus and Hydrocephalus 。 Tuberculoma

Ⅴ Ⅴ Clinical manifestation

Most typical cases ----slow onset

Generalsymptom

Tuberculosis toxic symptom

meningeal irritation sign cranial nerve lesion irritative or destructive symptoms of encephalon intracranial hypertension spinal cord disorder symptom

nervous systemsymptom

prodromal period（ prophase ）

meningeal irritation period

（ metaphase ）coma period

（ advanced stage ）

•Tuberculosis toxic symptom•Headache•vomiting•Personality change

•intracranial hypertension•meningeal irritation sign•cranial nerve lesion•irritative or destructive symptoms of encephalon•pyramid sign;pyramidal sign•convulsion

•symptom increased •go into coma•spinal cord dysfunction

ⅤⅤClinical manifestation

Ⅵ Ⅵ DiagnosesDiagnoses

(Ⅰ)(Ⅰ)HistoryHistory ：： Age, Seasons, History of exposure and BCG vaccination,History of exposure and BCG vaccination, History of infectious diseasesHistory of infectious diseases

(Ⅱ)(Ⅱ)clinical featureclinical feature ：：

((ⅢⅢ)) CSF ExaminationCSF Examination ：：

1 、 routine ： Appearance ： Like ground-glass ， floccule or membran

e High pressure

Cell count （ Lymphocytes ）： 50 ～ 500×106/L

2 、 biochemistry ： Protein 、 glucose and chloride

3 、 film preparation ： precipitum acid-fast stain positive 30%

(Ⅲ)(Ⅲ) CSF ExaminationCSF Examination ：： 3 、 Others 1 ） tubercle bacillus antigen detection 2 ） anti-tuberculosis antibody （ one of the early diagnosis evidence ） 3 ） adenosine deaminase （ ADA ） activity TBM ： ADA >9μ/L 4 ） immunoglobulin ： IgG 5 ） detect DNA fragment 6 ） tubercle bacillus culture film preparation and cultivation --- may be have a clear diagnosis

((ⅣⅣ)) X-ray examinationX-ray examination Chest X-ray: About 85% have tuberculose focus ((Ⅴ)CT or MRIⅤ)CT or MRI early: normal progression ： Shadow of the basal ganglia enhance

d, cistern density , fuzzy, calcification, ventricular dilatation, cerebral edema or infarct foci

((ⅥⅥ)) PPD-TestPPD-Test

a. Transverse T1W image after contrast administration reveals ringlike enhancement in occipital region and abnormal enhancement of the ependymal of the ventricles

b. coronal T1W image of same patient（同一病人的冠状面 T1W ）

枕区环形强化灶

侧脑室室管膜异常增强

侧脑室明显扩大

Ⅶ Ⅶ Differential DiagnosisDifferential Diagnosis

1 、 purulent meningitis 2 、 Viral Encephalitis 3 、 Cryptococcus neoformans meningi

tis 4 、 cerebral abscess

Ⅷ treatment（Ⅰ） General treatment bed rest Nutrition Nursing Care Coma Patients ： nasogastric feeding 、 pressure sore prevention attention Water-Electrolyte Balance

（Ⅱ） Anti-tuberculosis therapy

Principle ： Early , Complete

Intensificationtreatment

INH+RFP （早、中期）INH+RFP+SMINH+RFP+SM+PZA

3~4M

INH 15~25mg/kg.d RFP 10~20mg/kg.dSM 15~20mg/kg.d PZA 20~30mg/kg.d

Ⅷ treatment

Consolidation treatment INH+RFP

course of treatment≥12Mor when CSF normal, continue treatment 6M

（Ⅱ） Anti-tuberculosis therapy

（Ⅲ） decrease intracranial hypertension

CSF secretion ： lateral ventricles choroid （占 70% ） Ependyma 、 encephalon ----TBM ， Inflammatory stimulation, secretion

absorption ： arachnoid granulations ---- TBM ， absorb disturbance

circulation ： ---- TBM, inflammatory in base of skull, pathway blocked

↑

Ⅷ treatment

（Ⅲ） decrease intracranial hypertension

1 、 dehydrant

20%mannitol ： 0.5~1.0(2.0)g/kg. 次 iv q4h~q6h

2 、 adrenocortical hormone Dx 0.2~0.4mg/kg.d

3 、 lateral ventricular puncture 4 、 lumbar puncture decompression, intrathecal injectio

ns ：

INH 、 Dx

5 、 Surgery ：

Ventriculoperitoneal shunt or external drainage

（Ⅳ） adrenocortical hormone therapy

Dx 0.2~0.4mg/kg.d Prednison 1~2mg/kg.d （ 4 weeks after decreasing ， course ： 8~12 weeks ）

（Ⅴ） others 1 、 Control convulsions 、 Antipyretic 2 、 Water-Electrolyte Balance disturbances Hyponatremia （ dilutional, Cerebral ） Hypokalemia（Ⅵ） follow observation at least 3 ～ 5years

criterion of curecriterion of cure

Symptoms disappearedSymptoms disappeared

CSF normalCSF normal

No recurrenceNo recurrence

((2 years After the end of Treatment)2 years After the end of Treatment)

Ⅸ Ⅸ Prognosis (Relevant factors)

ageTime of therapy--- early or lateThe degree of brain damageTherapeutic method--- correct ？Tubercle bacillus--- resistance ？