結核性腦膜炎(英文)PPT課件

1、Tuberculous MeningitisCHCUMSDIVISION OF INFECTIOUS DISEASE AND GASTROENTEROLOGYNovember 24th, 20041EPIDEMIOLOGY - TBM Tuberculous Meningitis (TBM) The younger the children, the more readily to develop TBM. 60% in Children aged 1-3 years Death rate: 15-30%2TBM (Tuberculous meningitis) TBM is the most

2、 serious complication of tuberculosis in children and is usually fatal without treatment. TBM always be a part of systemic disseminated tuberculosis. TBM often occurs within 1 year of initial infection, especially in the first 2 to 6 months of infection.3Tuberculous BacilliPrimary ComplexBacteremiaR

3、ich FociSubarachnoid SpaceBrain or Spinal Cord PerenchymaTuberculomasMeningitisPATHOPHYSIOLOGYTrauma/Diseases measles, pertussis Miliary TB4PATHOLOGICAL EFFECTSMeningesDiffuse HyperemiaEdemaInflammatory Exudates Conformation of Tubercles 5PATHOLOGICAL EFFECTSSubarachnoid SpaceA large amount of thick

4、 gelatinous exudates concentrate to the pavimentum cerebri, optic chiasma, bridge of varolius, bulbus rhachidicus and Sylvian fissure. Basal meningitis accounts for the frequent dysfunction of cranial nerves III, VI, and VII.6PATHOLOGICAL EFFECTSCerebral ParenchymaTuberculous meningoencephalitisswel

5、ling 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. Meninges, spinal, and spinal nerve root also involvement. The later always

6、 leads to paraplegina.7PATHOLOGICAL EFFECTSCerebral VesselsThe bacteria invade the adventitia directly in the early stage and initiate the process of acute vasculitis. Progressive destruction of adventitia, disruption of elastic fibers, and finally intimal destruction (endoarteritis), lead to the ob

7、literative vasculitis, which may facilitate the ischemia, encephalomalacia and necrosis of parenchyma. 8Circulation of CSFChoroid plexusLateral ventricleInterventricular foramenthe 3rd ventricleCerebral aqueduct4th ventricle2 Lateral foramina1 Medial foramenSubarachnoid spaceArachnoid granulationsDu

8、ral sinusVenous drainage9PATHOLOGICAL 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 hydroc

9、ephalus10In 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 MANIFESTIONS A. Prodrome (1-2 week)Fever, fatigue, malaise, myalgia, drowsiness, headache, vomitingMen

10、tal status changesFocal neurologic signs are absentCSF abnormity 12CLINICAL MANIFESTIONSB. Meningeal Irritation Stage (1-2 week) More serious TB toxic symptomsIntracranial hypertension: severe headache, irritation, projectile vomiting, seizures; Bulging of anterior fontanelle, widening of cranial su

11、tures in infant Meningeal Irritation : nuchal rigidity, hypertonia Kernig sign or Brudzinski sign Cranial nerve abnormalities: 3, 6, 7Some children have no evidence of meningeal irritation but may have signs of encephalitis: disorientation, abnormal movements and speech impairment 13CLINICAL MANIFES

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

13、erebral hernia 14Characteristics of TBM in infants and young childrenA rapid onset with convulsion, abruptly high feverAtypical miningeal irritationIntracranial hypertension manifests as bulging of anterior fontanelle and widening of cranial sutures in infant 15PROGNOSIS The prognosis of tuberculous

14、 meningitis correlates most closely with the clinical stage of diagnosis and treatment. Age: infants or younger children are generally worse than that of older children Drug resistant strain Variation of host immunity Appropriate therapeutic regimen Completion of the antituberculor agent regimen16It

15、 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 HistoryClinical Symptoms and SignsAuxiliary Examinations18DIAGNOSIS - History Elucidate the followi

16、ng:Medical and social history, including recent contact with patients with TBNegative history for Bacille Calmette-Guerin (BCG) vaccinationHistory of immunosuppression from a known disease or drug therapy19DIAGNOSIS Symptoms and signs A gradual onset Fever, headache, alternant of irritability and dr

17、owsiness, vomiting, constipation of unknown originAltered mental status20DIAGNOSIS Tuberculin Skin Test Purified protein derivative (PPD)Injected intradermally on the volar surface of the forearmReaction peaks at 48 to 72 hoursA nonreactive result does not exclude M. tuberculosis infection or diseas

18、e, the tuberculin skin test is nonreactive in up to 50% of cases21DIAGNOSIS Spinal Tap Cerebrospinal FluidGross appearanceClear or slightly turbida fine clot resembling a pellicle or cobweb may formCell counts, differential count50-500cells/mm3Lymphocytic predominancebut Polymorphonuclear cells may

19、predominate early GlucoseHypoglycorrhachiaProteinHigh protein level with 1-3g/L22DIAGNOSIS 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 Specific TB-antigen in CS

20、F is a sensitive and rapid method23DIAGNOSIS Spinal Tap Cerebrospinal Fluid Total IgG, IgA and IgM 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 Chest X-ray Chest x-ray:

21、Posteroanterior and lateral views may reveal the followingHilar lymphadenopathySimple pneumoniaInfiltratePleural effusion/pleural scar25DIAGNOSIS CT or MRI CT scan and MRI of the brain reveal hydrocephalus, basilar meningeal thickening, infarcts, edema, and tuberculomas, all these are helpful clues,

22、 but nonspecific MRI and CT scan lack specificity, but help in monitoring complications that require neurosurgery, making the differentiations, and knowing the prognosis26DIFFERENTIAL DIAGNOSISViral Meningocephalitis Pyogenic Meningitis CNS Cryptococcosis27DIFFERENTIAL DIAGNOSISViral Meningocephalit

23、is Mumps, polio, enteroviruses, Measles, Herpes viruses, EBV, and Japanese encephalitis virus, etcCSF examination is the most important test in differentiating the cause of meningitis:Clear appearanceCells: 50 -200 cells/mm3 , Mononuclear cell predominanceProtein: slightly elevated or normal Glucose

24、 and Chloridate : normal 28DIFFERENTIAL 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.Pyogen

25、ic foci located other sites of the hostTypical rash of meningococcal infectionExamination of CSF 29DIFFERENTIAL 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

26、 10,000 cells/mm3, predominantly neutrophils)Decreased glucose concentrationIncreased protein concentration Gram stain and culture of CSF identify the etiological organism30Brain surface (Pyogenic meningitis )31TBM32DIFFERENTIAL DIAGNOSISCNS CryptococcosisCryptococcosis is the most common fungal inf

27、ection of the central nervous system It is the fourth most common cause of opportunistic infections in patients with AIDSDisease onset is usually insidious and has a longer latent periodFever always be absent at beginning of disease Very notable intracranial hypertension: severe headacheVisual distu

28、rbances and papilledema are common33DIFFERENTIAL DIAGNOSISCNS CryptococcosisCSFAppearance can be clear or turbid.Protein levels exceed Glucose and ChloridateMononuclear pleocytosis , numbers vary from 50 to 500 mononuclear cells/mm3.It is easy to get the positive result for C neoformans of CSFIndia

29、ink stain is positive CSF or serum cryptococcal antigen tests are positive34Cryptococcus 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. 35TREATMENT Sup

30、portive treatment Antituberculous drugs Decreasing intracranial pressure Corticosteriods Symptomatic treatment Follow-up visit 36TREATMENTSupportive treatmentBed rest and close respiratory contacts Nutritional support are paramount Keep good hygiene for the coma children to prevent of secondary infe

31、ctions, help them to change position frequently to prevent decubital Management of electrolyte abnormalities AntipyreticsControl of seizures: Diazepam (Valium) 37TREATMENTAntituberculous drugsisoniazid INH, rifampin RIF, pyrazinamide PZA, streptomycin SM, and sometimes ethambutol EMB.INH and RIF are

32、 bactericidal for all M. tuberculosis population in any milieu.SM is most effective against rapidly multiplying organisms.PZA is most effective against organisms found in macrephages.enter CSF readily in the presence of meningeal inflammation. 38TREATMENTAntituberculous drugs Any regimen must contai

33、n multiple drugs In addition, the therapy must be taken regularly and continued for a sufficient period. 39TREATMENTAntituberculous drugsintensification chemotherapy stage: 3-4 months INH (15-25mg/kg) , RFP, PZA, SMconsolidation chemotherapy stage: with total course 1 year at least in order to preve

34、nt relapse, permit elimination organisms persistent exist in the host INH, RFP or EMB (ethambutol)40TREATMENT Decreasing intracranial pressureDehydrant: Mannitol (MNT)Diuretic agent: Acetazolamide Decreasing CSF secretion by the choroid plexus Ventricular tap or Open ventricular drainage Repeat LPs

35、and intrathecal injectionShunting: 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 magna41TREATMENTCorticosteriods Children should be treated for 6-8 weeks More effective in early stage Decrease the immflamatory exudates, there fore lower the intracranial pressure. Relieve the meningeal irritation. Improve the CSF circulation Reduc