TUBERCULOUS MENINGITIS

Dr Shreedhar PaudelApril, 2009

TUBERCULOUS MENINGITIS……• Infection of meninges by

Mycobacterrium• Serious complication of childhood

tuberculosis• Common between 6 months to 24

months age• May lead to serious disabling

neurological sequale

TUBERCULOUS MENINGITIS……

• PATHOGENESIS– Usually reaches the meninges through

hematogenous route– May occur as a part of miliary tuberculosis

TUBERCULOUS MENINGITIS……

• PATHOLOGY– The meningeal surface is covered with yellow

grayish exudates and tubercles– The subarachnoid space and arachnoid villi are

obliterated leading to poor absorption of CSF– The thick exudates may block the CSF pathway

causing hydrocephalus– There might be thrombophlebitis and tuberculous

encephalopathy

Clinical Features • Prodromal stage ( stage of invasion)– Insidious onset with vauge symptoms– Fever, anorexia, disturbed sleep– Frequent vomiting, headache, photophobia

• Stage of meningitis– Features of meningitis with focal neuroligical

deficits

• Stage of coma– Fever, loss of consciousness and altered

respiratory pattern

Diagnosis…..• LP and evaluation of CSF– Raised CSF pressure: 30-40 CM of water ( normal

3-4 CM of water)– CSF may be clear with formation of cobweb

coagulum on standing ( like suspended pellicle )– Protein: >40 mg/dl– Sugar: < 2/3rd of blood sugar level– Cell count: 100-400/μL, predomonance of

lymphocytes– AFB stain and C/S

Diagnosis…..

• CT Head– May identify • Basal exudates• Inflammatory granuloma• Infarct lesions• Hydrocephalus

• PCR for Mycobacterium• Other tests: Chest X- Ray, HIV ELISA

TUBERCULOUS MENINGITIS• Differential Diagnosis– PURULENT MENINGITIS, – PARTIALLY TREATED MENINGITIS– ENCEPHALITIS, – TYPHOID ENCEPHALOPATHY, – BRAIN ABSCESS, – BRAIN TUMOR, – CHRONIC SUBDURAL HEMATOMA, – AMEBIC MENINGOENCEPHALITIS.

TREATMENT OF TUBERCULOSIS MENINGITIS

• Antitubercular treatment for 12 weeks• INITIAL PHASE-- 2 MTHS: HRZE• CONTINUATION PHASE--10 MTHS: HRE– DOSE OF DRUGS• ISONIAZID: 5mg/kg/day• RIFAMPICIN: 10mg/kg/day• ETHAMBUTOL: 15-20mg/kg/day• PYRAZINAMIDE: 30-40mg/kg/day

TREATMENT OF TUBERCULOSIS MENINGITIS……

• STEROID THERAPY– DEXAMETHASONE IV- 1-2 WEEKS– ORAL PREDNISONE FOR 6 WEEKS – TAPER SLOWLY OVER 2 WEEKS• REDUCE THE INTENSITY OF CEREBRAL EDEMA• REDUCE THE DEVELOPMENT OF ARACHNOIDITIS• REDUCE FIBROSIS AND SPINAL BLOCK

SUPPORTIVE AND SYMPTOMATIC THERAPY

Prognosis• Depends on– Age of the patient– Stage of the disease at diagnosis– Adequacy of treatment– Presence of complications

• Untreated cases die within 4-8 weeks• 20-25% mortality and 25% of survivors would

have neurological deficits in stage 2 • 50% mortality and 100% neurological deficits

among survivors in stage 3

ENCEPHALITIS

An inflammatory process of the central nervous system with

dysfunction of the brain

ENCEPHALITIS…

• Encephalopathy is the cerebral dysfunction due to other causes than inflammatory response– Due to circulating toxins– Poisions– Abnormal metabolites– Intrinsic biochemical disorders

ENCEPHALITIS…• ETIOLOGY– VIRAL: Measles, Mumps, Rubella, Enterovirus,

HSV, CMV, EBV, Japanese B, WEST NILE, RABIES, DENGUE, HIV

• OTHER: RICKETTSIA,• Cryptococcus• TOXOPLASMA, MALARIA • BACTERIAL: Mycobacterium, Salmonella,

Shigella, Leptospirosis• REYE’S SYNDROME

Clinical Features • ONSET: SUDDEN • SIGNS AND SYMPTOMS: FEVER, HEADACHE, VOMITING,

ALTERED MENTAL STATUS, IRRITABILITY, APATHY , COMA

• Typical features– Increased ICP

Papilloedema Evidence of brain stem dysfunctions

• Focal neurological deficits, • Respiratory/ Cardiac arrest due to Herniation

of cerebellum

Clinical Features …

• DECEREBRATION, • DECORTICATION, • EXTRAPYRAMIDAL SYMPTOMS: JAPANEASE B• TEMPORAL OR FRONTAL LOBE FEATURES: HSV

ENCEPHALITIS

• DIAGNOSIS– HISTORY OF EXPOSURE– LP– CSF EVALUATION– PCR– SEROLOGICAL TESTS– TOXICOLOGICAL SCREENING– CT/ MRI

MANAGEMENT OF ENCEPHALITIS

• MANAGEMENT OF ABC• SYMPTOMATIC: ICT, FEVER, SHOCK, SEIZURES• SPECIFIC TREATMENT– HSV: ACYCLOVIR 30 MG/KG/DAY IN 3 DIVIDED

DOSE FOR 10 DAYS– Focal neurological deficits, RBCs in CSF and focal

involvement of temporal lobe on CT are important diagnostic clues for herpes simplex encephalitis

REYE’S SYNDROME

• Acute self limiting metabolic insult resulting in generalised mitochondrial dysfunction due to inhibition of fatty acid beta-oxidation.

• Precipitated by use of aspirin in viral acute respiratory infections

REYE’S SYNDROME

• PATHOGENESIS – DYSFUNCTION OF LIVER, KIDNEY , CNS– GENERALISED MYOCARDIAL DYSFUNCTION– INHIBITION OF B-OXIDATION OF FATTY ACIDS– HYPERAMMONEMIA, NEUROHYPOGLYCAEMIA– COMMON AGE IS 2MTHS – 15 YEARS– RAPID PROGRESSION

CLINICAL FEATURES

• STAGE I - MILD CONFUSION, VOMITING, ANOREXIA

• STAGE II – DELIRIUM, IRRITATION, DISORIENTATION

• STAGE III – COMA• STAGE IV – APNEA, NON REACTING PUPIL,

SHOCK

DIAGNOSIS

• HYPERAMMONEMIA, • ABNORMAL LFT,• INCREASED PROTHROMBIN TIME• GENERALISED SLOW WAVES IN EEG• HYPOGLYCEMIA• LIVER BIOPSY SHOWS FATTY CHANGES AND

GLYCOGEN DEPLETION BUT NO NECROSIS

TREATMENT

• LOW PROTEIN DIET WITH ADEQUATE CALORY• TREATMENT OF HEPATIC FAILURE• TREATMENT OF RAISED ICT• TREATMENT OF HYPOGLYCAEMIA• SUPPLEMENTATION OF VITAMIN K , FFP• TREATMENT OF ACIDOSIS, HYPOXIA AND

DYSELECTROLYTEMIA

PROGNOSIS

• POOR PROGNOSIS• 25-70% MORTALITY• SURVIVORS MAY HAVE NEUROLOGICAL

SEQUALE