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ENCEPHALITIS,CEREBRAL EDEMA. Encephalitis means inflammation of brain parenchyma Cause: usually viral Brain inflammation also develops in bacterial and fungal meningitis Not an isolated entity Usually associated with meningeal inflammation together Also term as “Meningoencephalitis”
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ENCEPHALITIS,CEREBRAL EDEMA Dr. Alka Stoelinga
Encephalitis means inflammation of brain parenchyma • Cause: usually viral • Brain inflammation also develops in bacterial and fungal meningitis • Not an isolated entity • Usually associated with meningeal inflammation together • Also term as “Meningoencephalitis” • Commonest virus is Herpes simplex which reaches brain via the Olfactory nerve • Meningism is the triad of • Nuchal rigidity (neck stiffness) • Photophobia (intolerance of bright light) • Headache. Dr. Alka Stoelinga
Etiology: • Arbo virus • Japanese B encephalitis • Herpes simplex • Coxsackie • Epstein-Barr viruses • Adenovirus • Varicella zoster • Influenza • Measles • Entero virus • Mumps (Aseptic meningitis) • HIV • Rabies Dr. Alka Stoelinga
Clinical features: • Acute onset of Fever, Headache, Meningism and Drowsiness in mild cases. • In severe illness: focal signs(e.g Aphasia, hemiplegia or cranial nerve palsies), siezures and coma may develop • Coma: Rapid deterioration in sensorium • Altered consciousness, focal signs and seizure are more common in encephalitis as compared to meningitis • Patient may agitate(while in meningitis patients is usually calm, conscious, drowsy and non-agitated) Dr. Alka Stoelinga
Examination: • Coma/Altered level of consciousness • Meningeal signs may be present • Focal neurological deficits • Hypertonia/Brisk reflexes/Extensor plantar • Opthalmoscopic examination: Look for papilloedema Dr. Alka Stoelinga
Investigation: • CT scan head :Shows area of edema • In Herpes simplex encephalitis CT scan show low density lesions in the temporal lobes • MRI head • EEG : Shows slow wave changes • CSF analysis • Cell: 10-2000 • Mainly Lymphocytes • Glucose usually normal • Protein normal or Slightly raised 5. Viral serology of blood and CSF 6. PCR: Herpes simplex virus DNA can be detected by PCR Dr. Alka Stoelinga
Management: • Supportive • Fluid balance • Control of seizure • Treatment of raised ICP:Dexamethasone 4mg QID for raised intracranial pressure • Herpes simplex encephalitis: Acyclovir • Dose: 10mg/kg/dose IV 10 hourly • Acyclovir should be given to all suspected cases of viral encephalitis • Anticonvulsants if presence of Epilepsy Dr. Alka Stoelinga
Prognosis: • Mortality is 10-30% when antiviral drugs are used, without antiviral mortality is 70% • Survivors may have cognitive impairment or developed epilepsy Complications: • Focal Neurological deficit • Loss of cognitive function • Seizure Dr. Alka Stoelinga
CEREBRAL MALARIA • Severe form of falciparum malaria • Common in tropical area • Treatable condition Pathogenesis : • Sequestration of parasitized RBC into blood vessels of internal organs: Brain • Rouleax formation • Cerebral anoxia • Hemolysis Dr. Alka Stoelinga
Clinical features: • Chills, Persistent high fever, headache, orthostatic hypotension, myalgia • Red blood cell (RBC) sludging that leads to capillary blockage at several sites • The three initial stages of Cerebral Malaria are: • Cold Stage: It ranges from chills to extreme shaking for 1-2 hours • Hot Stage: It is characterized by a high fever up to 107°F (41.7°C) for 3-4 hours • Wet Stage: It is characterized by profuse sweating for 2-4 hours • There are three primary symptoms of cerebral malaria which are common in both adults and children: • Impaired consciousness with non-specific fever, • Generalized convulsions and neurological abnormalities, and • Coma that lasts for 24-72 hours, initially rousable and then unrousable Dr. Alka Stoelinga
It also manifests with • signs of increased intracranial pressure • Hemiplegia • Encephalopathy • Delirium • seizures and • Coma • If not treated on time, it can lead to complications like • Jaundice • Hemoglobinuria • a tender and enlarged spleen • acute renal failure • Uremia Dr. Alka Stoelinga
Examination: • Altered consciousness • Pallor • Icterus • Bleeding manifestation • No focal neurological deficit • Splenomegaly Dr. Alka Stoelinga
Investigation: • Peripheral blood smear: • Thick and Thin smear • CSF analysis • Blood Sugar, electrolytes, ABG, urea, creatinine Dr. Alka Stoelinga
INTRACRANIAL SPACE OCCUPYING LESION(ICSOL) Dr. Alka Stoelinga
TUBERCULOMA (TBM) • Non-neoplastic mass • Tumor like growth of Tuberculous tissue in the central nervous system, characterized by symptoms of an expanding cerebral, Cerebellar, or spinal mass • Presents as ring enhancing lesion • Seizure: Partial seizure • Focal neurological deficit • Headache Dr. Alka Stoelinga
Investigation: • CT scan head: Ring enhancing lesion • AFB smear • Mantoux • CXR Treatment: • Similar to that of tubercular meningitis Dr. Alka Stoelinga
NEUROCYSTICERCOSIS (NCC) • Cysticercosis, is an infection which results from the ingestion of the eggs of the pork tapeworm (uncooked/undercooked pork meat), Taenia solium • Neurocysticercosis, is when the brain or spinal cord (CNS) is affected by the larval stage of T. solium • Neurocysticercosis is the most common helminthic (tapeworm) infestation to affect the CNS worldwide • Is the prime cause of acquired epilepsy. Dr. Alka Stoelinga
Clinical features: • Seizures: Partial/ Generalised • Hydrocephalus • Features of raised ICP • Stroke, focal neurological deficits • Meningitis Dr. Alka Stoelinga
Investigations: • Neuroimaging: • MRI(early stage)/CT head(late phase) • Ring enhancing lesion • Scolex • Calcification • Perilesional edema 2. Fundoscopy 3. Soft tissue X-ray 4. Serologic test: ELISA Dr. Alka Stoelinga
Treatment: • Treatment of seizure Antiepileptics • Treatment of Hydrocephalus if present • Cysticidal therapy • Indicated for active lesions • Albendazole 15mg/kg/d for 8-28 days • Praziquantel • In immature cyst stage High dosage of corticosteroids • In the colloid cyst stage Surgical removal of the cyst, along with albendazole is indicated • In calcified dead cysts No treatment Dr. Alka Stoelinga
TBM NCC Due to ingestion of T.solium egg Small size <10mm and are multiple in number Usually situated in the periphery with well defined margins Less perilesional edema Calcification Hydrocephalus is uncommon • Secondary to primary or post primary TB • Bigger size than NCC • Situated in the midline and margins are thick and irregular • More perilesional edema seen • Calcification • Midline shift and hydrocephalus Dr. Alka Stoelinga
BRAIN ABSCESS Predisposing factors: • Hematogenous spread: Can occur from any site of primary infection but is commonly associated with: • Infection of chest, including lung abscess, bronchiectasis and empyema • Infection of heart such as infective endocarditis • Infection of bone or dental abscess can be primary site of infection • Direct/Local spread: Penetrating injury of skull, PNS, Middle ear • Mostly involve Frontal and temporal lobes Dr. Alka Stoelinga
Causative organisms: • Mixed aerobic and anaerobic organisms are involved • Staph aureus • Streptococcus milleri • Enterobacteriae Dr. Alka Stoelinga
Clinical feature: • Illness develops more gradually than acute bacterial meningitis. • Fever, headache, drowsiness, altered sensorium • Partial seizure • Focal neurological deficit • Features of meningitis • Septicemia Dr. Alka Stoelinga
Investigations: • Neuroimaging: CT scan head • Single or multiple ring enhancing lesion with perilesional edema(central low density and surrounding edema) • CSF analysis usually not helpful and C/I if there is evidence of raised ICP • Blood : TC,DC,ESR,C/S Dr. Alka Stoelinga
Treatment: • Emperic antibiotic therapy must be started • Inj Benzyl penicillin 2 million units IV hourly +Inj Chloramphenicol 1-2 gm IV 6 hourly + Inj Metronidazole 500mg IV 6 hourly • Steroid: Inj Dexamethasone 4-25 mg 6 hourly followed by tappering of dose to reduce cerebral edema • Along with drainage of Pus • 3rd generation Cephalosporin+Metronidazole+Cloxacillin/Vancomycin • Antibiotics should be continued for 6-8 weeks. Dr. Alka Stoelinga