结核性脑膜炎(英文)PPT课件.ppt

1、 1Tuberculous MeningitisNovember 24th, 2004 2EPIDEMIOLOGY - TBM Tuberculous 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% 3TBM (Tuberculous meningitis)u TBM is the most serious complication of tuberculosis in childre

2、n 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. 4Tuberculous BacilliPrimary ComplexBacteremiaRich FociSubarachnoid SpaceBrain or Spinal Cor

3、d PerenchymaTuberculomasMeningitisPATHOPHYSIOLOGYTrauma/Diseases measles, pertussis Miliary TB 5PATHOLOGICAL EFFECTSMeningesuDiffuse HyperemiauEdemauInflammatory Exudates uConformation of Tubercles 6PATHOLOGICAL EFFECTSSubarachnoid SpaceuA large amount of thick gelatinous exudates concentrate to the

4、 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. 7PATHOLOGICAL EFFECTSCerebral ParenchymaTuberculous meningoencephalitisuswelling and hyperemia of the parenchym

5、a 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. 8PATHOLOGIC

6、AL EFFECTSCerebral 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 ma

7、y facilitate the ischemia, encephalomalacia and necrosis of parenchyma. 9Circulation of CSFChoroid plexusLateral ventricleInterventricular foramenthe 3rd ventricleCerebral aqueduct4th ventricle2 Lateral foramina1 Medial foramenSubarachnoid spaceArachnoid granulationsDural sinusVenous drainage 10PATH

8、OLOGICAL EFFECTSHydrocephalusHyperemia 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 11In tuberculous meni

9、ngitis 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. 12CLINICAL MANIFESTIONS A. Prodrome (1-2 week)u Fever, fatigue, malaise, myalgia, drowsiness, headache, vomitingu Mental status changesu Foca

10、l neurologic signs are absent1. CSF abnormity 13CLINICAL MANIFESTIONSB. Meningeal Irritation Stage (1-2 week) uMore serious TB toxic symptomsuIntracranial hypertension: severe headache, irritation, projectile vomiting, seizures; u Bulging of anterior fontanelle, widening of cranial sutures in infant

11、 uMeningeal Irritation : nuchal rigidity, hypertonia Kernig sign or Brudzinski sign uCranial nerve abnormalities: 3, 6, 71.Some children have no evidence of meningeal irritation but may have signs of encephalitis: disorientation, abnormal movements and speech impairment 14CLINICAL MANIFESTIONSC. Com

12、a Stage (1-3 week)uFrequent convulsion, progressive altered state of consciousness: lethargy, confusion, semicoma, deep coma, decerebrate or decorticate posturinguDepletion: extremely maransis, constipation, urinary retention 1.progressive abnormalities of vital signs, and eventual die from cerebral

13、 hernia 15Characteristics of TBM in infants and young childrenuA rapid onset with convulsion, abruptly high feveruAtypical miningeal irritationuIntracranial hypertension manifests as bulging of anterior fontanelle and widening of cranial sutures in infant 16PROGNOSISu The prognosis of tuberculous me

14、ningitis 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 regimen

15、 17It 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. 18DIAGNOSIS History Clinical Symptoms and Signs Auxiliary Examinations 19DIAGNOSIS - History Elucidate th

16、e following:uMedical and social history, including recent contact with patients with TBuNegative history for Bacille Calmette-Guerin (BCG) vaccination1.History of immunosuppression from a known disease or drug therapy 20DIAGNOSIS Symptoms and signs uA gradual onset uFever, headache, alternant of irr

17、itability and drowsiness, vomiting, constipation of unknown originuAltered mental status 21DIAGNOSIS Tuberculin Skin Test Purified protein derivative (PPD)uInjected intradermally on the volar surface of the forearmuReaction peaks at 48 to 72 hoursuA nonreactive result does not exclude M. tuberculosi

18、s infection or disease, the tuberculin skin test is nonreactive in up to 50% of cases 22DIAGNOSIS Spinal Tap Cerebrospinal FluidGross appearanceClear or slightly turbida fine clot resembling a pellicle or cobweb may formCell counts, differential count50-500cells/mm3Lymphocytic predominancebut Polymo

19、rphonuclear cells may predominate early GlucoseHypoglycorrhachiaProteinHigh protein level with 1-3g/L 23DIAGNOSIS Spinal Tap Cerebrospinal FluidChloridate：low Acid-fast stain (+), Gram stain, India inkCulture for M tuberculosis (+) ELISA test for Specific PPD-IgM and PPD-IgG in CSF ELISA test for Sp

20、ecific TB-antigen in CSF is a sensitive and rapid method 24DIAGNOSIS Spinal Tap Cerebrospinal Fluid Total IgG, IgA and IgM10. PCR : specific PCR to detect the gene of M tuberculosis bacilli can provide a rapid and reliable diagnosis of TBM, although false-negative results potentially occur 25DIAGNOS

21、IS Chest X-ray Chest x-ray: Posteroanterior and lateral views may reveal the followinglHilar lymphadenopathylSimple pneumonialInfiltratelPleural effusion/pleural scar 26DIAGNOSIS CT or MRIu CT scan and MRI of the brain reveal hydrocephalus, basilar meningeal thickening, infarcts, edema, and tubercul

22、omas, all these are helpful clues, but nonspecificu MRI and CT scan lack specificity, but help in monitoring complications that require neurosurgery, making the differentiations, and knowing the prognosis 27DIFFERENTIAL DIAGNOSISuViral Meningocephalitisu Pyogenic Meningitisu CNS Cryptococcosis 28DIF

23、FERENTIAL DIAGNOSISViral Meningocephalitis Mumps, polio, enteroviruses, Measles, Herpes viruses, EBV, and Japanese encephalitis virus, etcCSF examination is the most important test CSF examination is the most important test in differentiating the cause of meningitis:in differentiating the cause of m

24、eningitis:lClear appearancelCells: 50 -200 cells/mm3 , Mononuclear cell predominancelProtein: slightly elevated or normal lGlucose and Chloridate : normal 29DIFFERENTIAL DIAGNOSISPyogenic MeningitisClinical manifestationAcute onset of intense headache, fever, nausea, vomiting, photophobia, and stiff

25、 neck Group B streptococci, Neisseria meningitidis,Streptococcus pneumoniae, Haemophilus influenzae, and Staph. aureus, etc.lPyogenic foci located other sites of the hostlTypical rash of meningococcal infectionlExamination of CSF 30DIFFERENTIAL DIAGNOSISPyogenic MeningitisTypical CSF abnormalities i

26、n meningitisinclude the following: Appearance is turbid Pleocytosis of PMN ( WBC counts always above 1000, even to a very high level as 10,000 cells/mm3, predominantly neutrophils) Decreased glucose concentration Increased protein concentration Gram stain and culture of CSF identify the etiological

27、organism 31Brain surface (Pyogenic meningitis ) 32TBM 33DIFFERENTIAL DIAGNOSISCNS CryptococcosisCNS CryptococcosisuCryptococcosis is the most common fungal infection of the central nervous system uIt is the fourth most common cause of opportunistic infections in patients with AIDSuDisease onset is u

28、sually insidious and has a longer latent perioduFever always be absent at beginning of disease uVery notable intracranial hypertension: severe headacheuVisual disturbances and papilledema are common 34DIFFERENTIAL DIAGNOSISCNS CryptococcosisCNS CryptococcosisCSFlAppearance can be clear or turbid.lPr

29、otein levels exceed lGlucose and ChloridatelMononuclear pleocytosis , numbers vary from 50 to 500 mononuclear cells/mm3.lIt is easy to get the positive result for C neoformans of CSFlIndia ink stain is positive CSF or serum cryptococcal antigen tests are positive 35Cryptococcus is a cause of meningi

30、tis, a common complication in AIDS. The organisms are usually easy to demonstrate histologically. In this slide they are the circular-to-ovoid structures with thick capsules. 36TREATMENTu Supportive treatment u Antituberculous drugsu Decreasing intracranial pressureu Corticosteriodsu Symptomatic tre

31、atmentu Follow-up visit 37TREATMENTSupportive treatmentuBed rest and close respiratory contacts uNutritional support are paramount uKeep good hygiene for the coma children to prevent of secondary infections, help them to change position frequently to prevent decubitalu Management of electrolyte abno

32、rmalities uAntipyreticsuControl of seizures: Diazepam (Valium) 38TREATMENTAntituberculous drugsuisoniazid INH, rifampin RIF, pyrazinamide PZA, streptomycin SM, and sometimes ethambutol EMB.uINH and RIF are bactericidal for all M. tuberculosis population in any milieu.uSM is most effective against ra

33、pidly multiplying organisms.uPZA is most effective against organisms found in macrephages.uenter CSF readily in the presence of meningeal inflammation. 39TREATMENTAntituberculous drugsu Any regimen must contain multiple drugsu In addition, the therapy must be taken regularly and continued for a suff

34、icient period. 40TREATMENTAntituberculous drugsu intensification chemotherapy stage: 3-4 monthsu INH (15-25mg/kg) , RFP, PZA, SMu consolidation chemotherapy stage: with total course 1 year at least in order to prevent relapse, permit elimination organisms persistent exist in the host INH, RFP or EMB

35、 (ethambutol) 41TREATMENT Decreasing intracranial pressureuDehydrant: Mannitol (MNT)uDiuretic agent: Acetazolamide Decreasing CSF secretion by the choroid plexus uVentricular tap or Open ventricular drainage uRepeat LPs and intrathecal injectionuShunting: to establish a communication between the CSF

36、 (ventricular or lumbar) and a drainage cavity. Performed only in cases of communicating hydrocephalus. Ventricular shunt to cisterna magna 42TREATMENTCorticosteriodsu Children should be treated for 6-8 weeks u More effective in early stageu Decrease the immflamatory exudates, there fore lower the i

37、ntracranial pressure. Relieve the meningeal irritation. Improve the CSF circulation Reduce the adherence and prevent the hydrocephalus.u Dexamethasoneu pay attention to the side effects of corticosteriods 43Criteria for RecoveryFollow-up visitFollow-up visit u Disappearance of all clinical manifesta

38、tionsu CSF examination is normalu No relapse within 2 years after completion of antituberculosis treatment 44Which symptom should be excluded in the early stage of TBM?uDrowsinessuLow fever, night sweat, poor appetite, loss of weightuPersonality changesuHeadacheuRecurrent convulsion 45A baby who was

39、 definited as TBM when he was 1 years old and began to receive regular treatment with antituberculosis drugs. How old is he when he can be definited as full recovery? u11/2 yu2 yu21/2 yu3 yu4 y 46Which one is the typically cellular characteristics of CSF in TBM? u50-500 cells/mm3, with neutrophils p

40、redominanceu50-500 cells/mm3, with mononuclear predominanceu0-50 cells/mm3,with mononuclear predominanceu1000, sometimes can above 10,000 with neutrophil predominanceu 0-50cells/mm3 with neutrophils predominance结束语当你尽了自己的最大努力时，失败也是伟大的，所以不要放弃，坚持就是正确的。When You Do Your Best, Failure Is Great, So DonT Give Up, Stick To The End感谢聆听不足之处请大家批评指导Please Criticize And Guide The Shortcomings演讲人：XXXXXX 时 间：XX年XX月XX日