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…
• 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