“Impila” poisoning Callilepsis laureola in herbal medicines Causes hypoglycaemia, renal damage, centrilobular necrosis of the liver Sudden onset coma, convulsions, vomiting,diarrhoea Acidotic, not jaundiced, floppy Biochemical evidence of liver failure, hypoglycaemia, renal damage High mortality and residual morbidity
Reye syndrome Preceding viral infection treated with salicylates Rapidly progressive anicteric hepatic encephalopathy with microvesicular fatty infiltration of the viscera High mortality and morbidity in survivors
Management of liver failure Limit further toxic accumulation: enema, gastric lavage, oral neomycin Maintain energy and reduce protein intake Maintain metabolic and hydration state: IV fluids, glucose, vitamin K Identify cause if possible to ascertain possibility of treatment Poor prognostic factors: Progressive shrinkage of liver, failure to respond to vitamin K, progressive rise in bilirubin level
Veno-occlusive disease of the liver Obstruction to hepatic venous outflow Central vein of lobule and branches Endothelial oedema, fibroblastic proliferation, obstruction by fibrosis and thrombosis Caused by drugs/ plant alkaloids: Senecio Massive congestive hepatomegaly and ascites Not usually jaundiced Centrilobular necrosis leads to cirrhosis Symptomatic treatment only Potential danger of herbal medicines!
Hepatic Schistosomiasis Schistosoma mansoni eggs in portal tract Portal fibrosis, not cirrhosis Presinusoidal portal hypertension Liver may be of normal size or firm to hard hepatomegaly, often left lobe Large firm spleen often an incidental finding Features of portal hypertension Liver decompensation is rare, most improve with time
Storage diseases involving the liver Metabolic defects resulting in liver accumulation and damage including progression to cirrhosis Glycogen storage disease Inability to mobilise glycogen Stunting Spleen not involved Fasting hypoglycaemia and lactic acidosis Lipid storage disorders Gaucher’s, Niemann Pick, Tay-Sachs Usually CNS involvement Spleen enlarged
Wilsons disease Defect in copper metabolism results in copper accumulation in liver, brain and other tissues Presents with Hepatic damage: Acute hepatitis Chronic active hepatitis Cirrhosis Fulminant hepatic failure CNS: extrapyramidal and basal ganglia signs Ophthalmological: Kayser-Fleischer ring Other: cardiac, renal, skeletal, endocrine