1 Tuberculous Meningitis CHCUMS DIVISION OF INFECTIOUS DISEASE AND GASTROENTEROLOGY November 24th,...
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Transcript of 1 Tuberculous Meningitis CHCUMS DIVISION OF INFECTIOUS DISEASE AND GASTROENTEROLOGY November 24th,...
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Tuberculous Meningitis
CHCUMSCHCUMS
DIVISION OF INFECTIOUS DISEASE AND DIVISION OF INFECTIOUS DISEASE AND GASTROENTEROLOGYGASTROENTEROLOGY
November 24th, 2004
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EPIDEMIOLOGY - 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%
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TBM (Tuberculous meningitis)
TBM is the most 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.
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Tuberculous Bacilli
Primary Complex
Bacteremia
Rich Foci
Subarachnoid Space
Brain or Spinal Cord PerenchymaTuberculom
as
Meningitis
PATHOPHYSIOLOGY
Trauma/Diseases measles, pertussis
Miliary TB
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PATHOLOGICAL EFFECTS
Meninges Diffuse Hyperemia Edema Inflammatory Exudates Conformation of Tubercles
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PATHOLOGICAL EFFECTS
Subarachnoid SpaceA large amount of thick 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.
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PATHOLOGICAL EFFECTS
Cerebral ParenchymaTuberculous meningoencephalitis swelling 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 leads to paraplegina.
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PATHOLOGICAL EFFECTS
Cerebral 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 obliterative vasculitis, which may facilitate the ischemia, encephalomalacia and necrosis of parenchyma.
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Circulation of CSFChoroid plexus
Lateral ventricle
Interventricular foramen
the 3rd ventricle
Cerebral aqueduct
4th ventricle
2 Lateral foramina
1 Medial foramen
Subarachnoid space
Arachnoid granulations
Dural sinus
Venous drainage
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PATHOLOGICAL EFFECTSHydrocephalus
Hyperemia of choroids overproduction of CSF
Inflammatory adherence of
Meninge
defective absorption of CSF
Communicating hydrocephalus
CSF flow is obstructed on the route before the cerebral aqueduct and the
4th ventricle
Noncommunicating hydrocephalus
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In 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.
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CLINICAL MANIFESTIONS
A. Prodrome (1-2 week)
1. Fever, fatigue, malaise, myalgia, drowsiness, headache, vomiting
2. Mental status changes
3. Focal neurologic signs are absent
4. CSF abnormity
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CLINICAL MANIFESTIONS
B. Meningeal Irritation Stage (1-2 week)
1. More serious TB toxic symptoms2. Intracranial hypertension: severe headache, irritation,
projectile vomiting, seizures; 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
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CLINICAL MANIFESTIONS
C. Coma Stage (1-3 week)1. Frequent convulsion, progressive altered
state of consciousness: lethargy, confusion, semicoma, deep coma, decerebrate or decorticate posturing
2. Depletion: extremely maransis, constipation, urinary retention
3. progressive abnormalities of vital signs, and eventual die from cerebral hernia
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Characteristics of TBM in infants and young children
1. A rapid onset with convulsion, abruptly high fever
2. Atypical miningeal irritation3. Intracranial hypertension
manifests as bulging of anterior fontanelle and widening of cranial sutures in infant
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PROGNOSIS
The prognosis of tuberculous 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 regimen
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It 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.
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DIAGNOSIS
History Clinical Symptoms and Signs Auxiliary Examinations
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DIAGNOSIS - History
Elucidate the following:1. Medical and social history, including
recent contact with patients with TB
2. Negative history for Bacille Calmette-Guerin (BCG) vaccination
3. History of immunosuppression from a known disease or drug therapy
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DIAGNOSIS – Symptoms and signs
A gradual onset Fever, headache, alternant of irritability and
drowsiness, vomiting, constipation of
unknown origin Altered mental status
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DIAGNOSIS – Tuberculin Skin Test
Purified protein derivative (PPD)1. Injected intradermally on the volar
surface of the forearm
2. Reaction peaks at 48 to 72 hours
3. A nonreactive result does not exclude M. tuberculosis infection or disease, the tuberculin skin test is nonreactive in up to 50% of cases
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DIAGNOSIS – Spinal Tap
Cerebrospinal Fluid1. Gross appearanceClear or slightly turbida fine clot resembling a pellicle or cobweb may form
2. Cell counts, differential count50-500cells/mm3
Lymphocytic predominancebut Polymorphonuclear cells may predominate early
3. GlucoseHypoglycorrhachia
4. ProteinHigh protein level with 1-3g/L
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DIAGNOSIS – Spinal Tap
Cerebrospinal Fluid5. Chloridate : low
6. Acid-fast stain (+), Gram stain, India ink
7. Culture for M tuberculosis (+)
8. ELISA test for Specific PPD-IgM and PPD-IgG in CSF
9. ELISA test for Specific TB-antigen in CSF is a sensitive and rapid method
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DIAGNOSIS – Spinal Tap
Cerebrospinal Fluid10. Total IgG, IgA and IgM
11. 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
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DIAGNOSIS – Chest X-ray
Chest x-ray: Posteroanterior and lateral views may reveal the followingHilar lymphadenopathySimple pneumoniaInfiltratePleural effusion/pleural scar
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DIAGNOSIS – CT or MRI
CT scan and MRI of the brain reveal hydrocephalus, basilar meningeal thickening, infarcts, edema, and tuberculomas, all these are helpful clues, but nonspecific
MRI and CT scan lack specificity, but help in monitoring complications that require neurosurgery, making the differentiations, and knowing the prognosis
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DIFFERENTIAL DIAGNOSIS
Viral Meningocephalitis Pyogenic Meningitis CNS Cryptococcosis
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DIFFERENTIAL DIAGNOSIS
Viral Meningocephalitis Mumps, polio, enteroviruses, Measles, Herpes
viruses, EBV, and Japanese encephalitis virus, etc
CSF examination is the most important test in differentiating the cause of meningitis:
Clear appearance
Cells: 50 -200 cells/mm3 , Mononuclear cell predominance
Protein: slightly elevated or normal Glucose and Chloridate : normal
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DIFFERENTIAL DIAGNOSIS
Pyogenic 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.
Pyogenic foci located other sites of the hostTypical rash of meningococcal infectionExamination of CSF
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DIFFERENTIAL DIAGNOSIS
Pyogenic MeningitisTypical CSF abnormalities in meningitis
include 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 organism
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Brain surface (Pyogenic meningitis )
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TBM
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DIFFERENTIAL DIAGNOSIS
CNS CryptococcosisCryptococcosis is the most common fungal
infection 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 disturbances and papilledema are
common
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DIFFERENTIAL DIAGNOSIS
CNS CryptococcosisCSF
Appearance 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 ink stain is positive CSF or serum
cryptococcal antigen tests are positive
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Cryptococcus 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.
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TREATMENT
Supportive treatment Antituberculous drugs Decreasing intracranial pressure Corticosteriods Symptomatic treatment Follow-up visit
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TREATMENT
Supportive treatmentBed rest and close respiratory contacts Nutritional support are paramount Keep good hygiene for the coma children to
prevent of secondary infections, help them to change position frequently to prevent decubital
Management of electrolyte abnormalities AntipyreticsControl of seizures: Diazepam (Valium)
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TREATMENT
Antituberculous drugs isoniazid INH, rifampin RIF, pyrazinamide
PZA, streptomycin SM, and sometimes ethambutol EMB.
INH and RIF are 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.
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TREATMENT
Antituberculous drugs Any regimen must contain multiple
drugs In addition, the therapy must be taken
regularly and continued for a sufficient period.
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TREATMENT
Antituberculous drugs1. intensification chemotherapy stage: 3-4
months 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)
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TREATMENT
Decreasing intracranial pressure Dehydrant: Mannitol (MNT) Diuretic agent: Acetazolamide Decreasing CSF secretion by the choroid plexus Ventricular tap or Open ventricular drainage Repeat LPs and intrathecal injection Shunting: 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 magna
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TREATMENT
Corticosteriods 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 Reduce the adherence and prevent the hydrocephalus.
Dexamethasone pay attention to the side effects of corticosteriods
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Criteria for Recovery
Follow-up visit Disappearance of all
clinical manifestations CSF examination is
normal No relapse within 2
years after completion of antituberculosis treatment
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Which symptom should be excluded in the early stage of TBM?
a) Drowsiness
b) Low fever, night sweat, poor appetite, loss of weight
c) Personality changes
d) Headache
e) Recurrent convulsion
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A 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 y
b) 2 y
c) 21/2 y
d) 3 y
e) 4 y
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Which one is the typically cellular characteristics of CSF in TBM?
a) 50-500 cells/mm3, with neutrophils predominance
b) 50-500 cells/mm3, with mononuclear predominance
c) 0-50 cells/mm3,with mononuclear predominance
d) >1000, sometimes can above 10,000 with neutrophil predominance
e) 0-50cells/mm3 with neutrophils predominance
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THNAK YOU !