结核性脑膜炎英文课件

Tuberculous MeningitisCHCUMSDIVISION OF INFECTIOUS DISEASE AND DIVISION OF INFECTIOUS DISEASE AND GASTROENTEROLOGYGASTROENTEROLOGYNovember 24th,20041Tuberculous MeningitisNovemberEPIDEMIOLOGY-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%2EPIDEMIOLOGY-TBM 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.3TBM(Tuberculous meningitis)TTuberculous BacilliPrimary ComplexBacteremiaRich FociSubarachnoid SpaceBrain or Spinal Cord PerenchymaTuberculomasMeningitisPATHOPHYSIOLOGYTrauma/Diseases measles,pertussis Miliary TB4Tuberculous BacilliPrimary ComPATHOLOGICAL EFFECTSMeningesuDiffuse HyperemiauEdemauInflammatory Exudates uConformation of Tubercles 5PATHOLOGICAL EFFECTSMeninges5PATHOLOGICAL 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 EFFECTSSubarachnoPATHOLOGICAL EFFECTSCerebral ParenchymaTuberculous 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 EFFECTSCerebral PPATHOLOGICAL 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 may facilitate the ischemia,encephalomalacia and necrosis of parenchyma.8PATHOLOGICAL EFFECTSCerebral VCirculation of CSFChoroid plexusLateral ventricleInterventricular foramenthe 3rd ventricleCerebral aqueduct4th ventricle2 Lateral foramina1 Medial foramenSubarachnoid spaceArachnoid granulationsDural sinusVenous drainage9Circulation of CSFChoroid plexPATHOLOGICAL 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 hydrocephalus10PATHOLOGICAL EFFECTSHydrocephaIn 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.11In tuberculous meningitis therCLINICAL MANIFESTIONS A.Prodrome(1-2 week)1.Fever,fatigue,malaise,myalgia,drowsiness,headache,vomiting2.Mental status changes3.Focal neurologic signs are absent4.CSF abnormity 12CLINICAL MANIFESTIONS A.ProdrCLINICAL MANIFESTIONSB.Meningeal Irritation Stage (1-2 week)1.More serious TB toxic symptoms2.Intracranial hypertension:severe headache,irritation,projectile vomiting,seizures;3.Bulging of anterior fontanelle,widening of cranial sutures in infant 3.Meningeal Irritation:nuchal rigidity,hypertonia Kernig sign or Brudzinski sign 4.Cranial nerve abnormalities:3,6,75.Some children have no evidence of meningeal irritation but may have signs of encephalitis:disorientation,abnormal movements and speech impairment 13CLINICAL MANIFESTIONSB.MeningCLINICAL MANIFESTIONSC.Coma Stage(1-3 week)1.Frequent convulsion,progressive altered state of consciousness:lethargy,confusion,semicoma,deep coma,decerebrate or decorticate posturing2.Depletion:extremely maransis,constipation,urinary retention 3.progressive abnormalities of vital signs,and eventual die from cerebral hernia 14CLINICAL MANIFESTIONSC.Coma SCharacteristics of TBM in infants and young children1.A rapid onset with convulsion,abruptly high fever2.Atypical miningeal irritation3.Intracranial hypertension manifests as bulging of anterior fontanelle and widening of cranial sutures in infant 15Characteristics of TBM in infaPROGNOSISu 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 regimen16PROGNOSIS The prognosis of tubIt 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.17It is imperative that antitubeDIAGNOSIS HistoryClinical Symptoms and SignsAuxiliary Examinations18DIAGNOSIS History18DIAGNOSIS-History Elucidate the following:1.Medical and social history,including recent contact with patients with TB2.Negative history for Bacille Calmette-Guerin(BCG)vaccination3.History of immunosuppression from a known disease or drug therapy19DIAGNOSIS-History Elucidate DIAGNOSIS Symptoms and signs uA gradual onset uFever,headache,alternant of irritability and drowsiness,vomiting,constipation of unknown originuAltered mental status20DIAGNOSIS Symptoms and signsDIAGNOSIS Tuberculin Skin Test Purified protein derivative(PPD)1.Injected intradermally on the volar surface of the forearm2.Reaction peaks at 48 to 72 hours3.A nonreactive result does not exclude M.tuberculosis infection or disease,the tuberculin skin test is nonreactive in up to 50%of cases21DIAGNOSIS Tuberculin Skin TeDIAGNOSIS Spinal Tap Cerebrospinal Fluid1.Gross appearance2.Clear or slightly turbid3.a fine clot resembling a pellicle or cobweb may form2.Cell counts,differential count50-500cells/mm3Lymphocytic predominancebut Polymorphonuclear cells may predominate early 3.GlucoseHypoglycorrhachia4.ProteinHigh protein level with 1-3g/L22DIAGNOSIS Spinal Tap CeDIAGNOSIS Spinal Tap Cerebrospinal Fluid5.Chloridate：low 6.Acid-fast stain(+),Gram stain,India ink7.Culture for M tuberculosis(+)8.ELISA test for Specific PPD-IgM and PPD-IgG in CSF9.ELISA test for Specific TB-antigen in CSF is a sensitive and rapid method23DIAGNOSIS Spinal Tap CeDIAGNOSIS Spinal Tap Cerebrospinal Fluid10.Total IgG,IgA and IgM11.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 occur24DIAGNOSIS Spinal Tap CeDIAGNOSIS Chest X-ray Chest x-ray:Posteroanterior and lateral views may reveal the followinglHilar lymphadenopathylSimple pneumonialInfiltratelPleural effusion/pleural scar25DIAGNOSIS Chest X-ray Chest DIAGNOSIS CT or MRIu CT scan and MRI of the brain reveal hydrocephalus,basilar meningeal thickening,infarcts,edema,and tuberculomas,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 prognosis26DIAGNOSIS CT or MRI CT scanDIFFERENTIAL DIAGNOSISuViral Meningocephalitisu Pyogenic Meningitisu CNS Cryptococcosis27DIFFERENTIAL DIAGNOSISViral MeDIFFERENTIAL DIAGNOSISViral Meningocephalitis Mumps,polio,enteroviruses,Measles,Herpes viruses,EBV,and Japanese encephalitis virus,etcCSF examination is the most important test in differentiating the cause of meningitis:lClear appearancelCells:50-200 cells/mm3,Mononuclear cell predominancelProtein:slightly elevated or normal lGlucose and Chloridate:normal 28DIFFERENTIAL DIAGNOSISViral MeDIFFERENTIAL DIAGNOSISPyogenic MeningitisClinical manifestationAcute onset of intense headache,fever,nausea,vomiting,photophobia,and stiff 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 29DIFFERENTIAL DIAGNOSISPyogenicDIFFERENTIAL DIAGNOSISPyogenic MeningitisTypical CSF abnormalities in meningitisinclude the following:Appearance is turbidPleocytosis of PMN(WBC counts always above 1000,even to a very high level as 10,000 cells/mm3,predominantly neutrophils)Decreased glucose concentrationIncreased protein concentration Gram stain and culture of CSF identify the etiological organism30DIFFERENTIAL DIAGNOSISPyogenicBrain surface(Pyogenic meningitis)31Brain surface(Pyogenic meningTBM32TBM32DIFFERENTIAL DIAGNOSISCNS 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 usually insidious and has a longer latent perioduFever always be absent at beginning of disease uVery notable intracranial hypertension:severe headacheuVisual disturbances and papilledema are common33DIFFERENTIAL DIAGNOSISCNS CrypDIFFERENTIAL DIAGNOSISCNS CryptococcosisCSFlAppearance can be clear or turbid.lProtein 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 positive34DIFFERENTIAL DIAGNOSISCNS CrypCryptococcus is a cause of meningitis,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.35Cryptococcus is a cause of menTREATMENTu Supportive treatment u Antituberculous drugsu Decreasing intracranial pressureu Corticosteriodsu Symptomatic treatmentu Follow-up visit 36TREATMENT Supportive treatmentTREATMENTSupportive 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 abnormalities uAntipyreticsuControl of seizures:Diazepam(Valium)37TREATMENTSupportive treatment3TREATMENTAntituberculous 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 rapidly multiplying organisms.uPZA is most effective against organisms found in macrephages.uenter CSF readily in the presence of meningeal inflammation.38TREATMENTAntituberculous drugsTREATMENTAntituberculous drugsu Any regimen must contain multiple drugsu In addition,the therapy must be taken regularly and continued for a sufficient period.39TREATMENTAntituberculous drugsTREATMENTAntituberculous drugs1.intensification chemotherapy stage:3-4 months2.INH(15-25mg/kg),RFP,PZA,SM2.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(ethambutol)40TREATMENTAntituberculous drugsTREATMENT 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(ventricular or lumbar)and a drainage cavity.Performed only in cases of communicating hydrocephalus.Ventricular shunt to cisterna magna41TREATMENT Decreasing intracranTREATMENTCorticosteriodsu Children should be treated for 6-8 weeks u More effective in early stageu Decrease the immflamatory exudates,there fore lower the intracranial 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 corticosteriods42TREATMENTCorticosteriods42Criteria for RecoveryFollow-up visit u Disappearance of all clinical manifestationsu CSF examination is normalu No relapse within 2 years after completion of antituberculosis treatment43Criteria for RecoveryFollow-upWhich symptom should be excluded in the early stage of TBM?a)Drowsinessb)Low fever,night sweat,poor appetite,loss of weightc)Personality changesd)Headachee)Recurrent convulsion 44Which symptom should be excludA baby who was 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?a)11/2 yb)2 yc)21/2 yd)3 ye)4 y 45A baby who was definited as TBWhich one is the typically cellular characteristics of CSF in TBM?a)50-500 cells/mm3,with neutrophils predominanceb)50-500 cells/mm3,with mononuclear predominancec)0-50 cells/mm3,with mononuclear predominanced)1000,sometimes can above 10,000 with neutrophil predominancee)0-50cells/mm3 with neutrophils predominance46Which one is the typically celTHNAK YOU!47THNAK YOU!47