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SUY GAN SÉT ĐÁNH (Fulminant hepatic failure)

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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.

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Nội dung Text: SUY GAN SÉT ĐÁNH (Fulminant hepatic failure)

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:
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 agonists (hepatic coma can be reversed temporarily by flumazenil) and altered GABA status 4. Cerebral oedema * common but onset difficult to determine. Related to acuteness of presentation (24% in hyperacute cases and 9% in subacute). Papilloedema seldom present and bradycardia with pyrexia and hypotension common in fulminant hepatic failure. Often respiratory arrest and brain death due to tentorial herniation is first sign * keys to recognition are: o hypertension (bursts of systolic pressure > 200 mmHg, or a sustained systolic pressure > 150 mmHg)
o rarely bradycardia o any pupillary changes including sluggishness, and cerebral "posturing". o hypotension is a late complication * early diagnosis requires excellent nursing. Pupillary responses may need to be checked as frequently as every 10 mins. * may be associated with or shortly followed by respiratory arrest if not recognised promptly and treated * major cause of death * in contra-distinction cerebral oedema only rarely occurs in patients with decompensated chronic liver disease, regardless of the depth of coma 5. Diagnosis: * in jaundiced patient diagnosis is usually obvious * consider diagnosis in sick patients in whom an underlying diagnosis i s lacking, particularly when coma or metabolic acidosis are present. Best screening test for hepatic aetiology is PT or INR
* consider occult paracetamol poisoning in patients with unexplained metabolic acidosis and marked oliguria with a normal or near normal urea (creatinine will be raised).