الفهرس 
PATHOPHYSIOLOGY OF FULMINANT HEPATIC FAILUREOnly 14 pages are availabe for public view
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Abstract
Acute liver cell failure is appearance of sever complications rapidly after the first signs of liver disease (such as jaundice) and indicates that the liver has sustained damage, the complications are hepatic encephalopathy and impaired proten synthesis, common causes of Acute liver Failure are paracetamol overdose, excessive alcohol intake (sever alcoholic hepatitis), viral hepatitis, Wilson disease.
There is widespread hepatocellular necrosis beginning in centrizonal distibution and progressing towards portal tracts.
Cerebral oedema hepatic encephalopathy, in ALF cerebral oedema leads to hepatic encephalopathy, coma,brain herniation, and eventually death.detection of encephalopathy is central to diagnosis of ALF. It varies from subtle dificit in higher brain function (e.g. mood, concentration in grade 1)to deep coma in grade 5.
Coagulapathy,hepato cellular necrosis leads to impaired synthesis of many coagulation factors and their inhibitors.the former produces prolongation of prothrombin time. There is progressive platelet dysfunction with quantitative and qualitative platelet dysfunction.
Renal failure is common present in more than 50% of alf patients. Either due to original original insult such as paracetamol resulting acute tubular necrosis or from hyperdynamic circulation leading to hepatorenal syndrome.
About 60% of all ALF patients fulfill the criteria for systemic inflammatory syndrome irrespective of presence or absence of infection. bacterial sepsis mostly due to gram positive organisms and fungal sepsis are obseved in up to 80% and 30% patients respectively.
Hyponatremia is almost universal finding due to water retension and shift in intracellular sodium transport from inhibition of Na/k ATPase.
Hypoglycemia, hypokalemia, hypophosphatemia and metabolic alkalosis are often present. Lactic acidosis occures predominently in paracetamol toxicity.
Hyperdynamic circulation with peripheral vasodilatation from low systemic vascular resistance leads to hypotension.there is compensatory increase in cardiac output.
There is also abnormal oxygen transport and utilization. Although delivery of oxygen to tissues is adequate, there is decrease in tissue oxygen uptake, resulting in tissue hypoxia and lactic acidosis. Pulmonary complications occur in up to 50% patients.
Sever lung injury and hypoxemia result in high mortality.most cases of sever lung injury is due to ARDS with or without sepsis. Pulmonary haemorrhage, pleural effusion, atelectasis contribute to respiratory difficulty.
Treatment involves admission in ICU, often intensive care unit admision.supportive treatment is with adequate nutrition, optimalisation of the fluid balance, mechanical ventilation and intracranial pressure monitoring and treatment aimed at removing the under lying cause(such as acetylcysteine for paracetamol poisoning), other supportive measures such as drainage of ascites.
While many people who develop acute liver failure recover with supportive treatment, liver transplantation is often required in people who continue to deteriorate or have adverse prognostic factors.
Historically mortality has been unacceptably high, being in exess of 80%. In recent years the advent of liver transplantation and multidisciplinary intensive care support have improved survival significantly