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Clinical syndrome developing as a result of massive necrosis of liver cells or following any other cause of sudden and severe impairment of hepatic function, occuring in patients without pre-existing liver disease. | SUY GAN SÉT ĐÁNH Fulminant hepatic failure 1. Definition Clinical syndrome developing as a result of massive necrosis of liver cells or following any other cause of sudden and severe impairment of hepatic function occuring in patients without pre-existing liver disease. 2. Etiology Table 1. Etiologies of F HF A. Viral HAV HBV HDV HEV HSV CMV EBV HVZ adenovirus hemorrhagic fever viruses B. Drugs and toxins Dose-dependent acetaminophen ccl4 yellow phosphorus Amanita phalloidcs Bacillus cereus toxin sulfonamides tetracycline Ecstasy methyldioxymethamphetamine herbal remedies Idiosyncratic halothane INH rifampicin valproic acid NSAIDs dislufiram c. Vascular Right heart failure Budd-Chiari syndrome venoocclusive disease shock liver ischemic hepatitis heat stroke D. Metabolic Acute fatty liver of pregnancy Wilson s disease Reye s syndrome galactosemia hereditarv fructose intolerance tyrosinemia E. Miscellaneous Malignant infiltration liver metastases lymphoma autoimmune hepatitis sepsis F. Indeterminate Includes primary graft non-function in liver transplanted patients Abbreviations HAV hepatitis A virus HBV hepatitis B virus HDV hepatitis D virus HEV hepatitis E virus HSV herpes simplex virus CMV cytomegalovirus EBV Epstein Barr virus HVZ herpes varicella zoster virus cclj carbon tetrachloride INH isoniazid NSAIDs non-steroidal antiinflammatory drugs. 3. Pathophysiology Wide variety of agents including ammonia free fatty acids mercaptans phenols bile acids and aromatic amino acids combine to produce hepatic encephalopathy by several different mechanisms direct cellular effect indirect cause metabolic derangement conversion to false neurotransmitters alteration of permeability of BBB allows entry of toxic metabolites into the brain and thus contributes to cerebral oedema - major cause of death present in 32 of patients at PM. Ammonia currently thought to be the main pathophysiological agent Other possible aetiological mechanisms include the presence of benzodiazepine .
