الفهرس 
ANATOMY OF LIVEROnly 14 pages are availabe for public view
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Abstract
A
cute liver cell failure is the appearance of severe complications rapidly after the first signs of liver disease (such as jaundice) and indicates that the liver has sustained damage, this complications include hepatic encephalopathy and impaired protein synthesis.
Common causes of acute liver failure are paracetamol overdose, excessive alcohol intake (sever alcoholic hepatitis), viral hepatitis and Wilson disease, which is important to be identified in order to asses patients with acute liver failure as certain causes demand immediate and specific treatment.
There is widespread hepatocellular necrosis beginning in centrizonal distibution and progressing towards portal tracts.
In acute liver failure, cerebral edema leads to hepatic encephalopathy, coma, brain herniation, and eventually death. Detection of encephalopathy is central to diagnosis of acute liver failure. It varies from subtle dificit in higher brain function e.g. mood, concentration in grade I to deep coma in grade IV.
Hepatocellular necrosis leads to impaired synthesis of many coagulation factors and their inhibitors leading to Coagulopathy, which produces prolongation of prothrombin time. There is also progressive platelet dysfunction with quantitative and qualitative platelet defect.
Renal failure is common present in more than 50% of acute liver failure patients either due to the original insult such as paracetamol resulting in acute tubular necrosis or from hyperdynamic circulation leading to hepatorenal syndrome.
About 60% of all acute liver failure patients fulfill the criteria of systemic inflammatory response syndrome irrespective of presence or absence of infection. Bacterial sepsis mostly due to gram positive organisms and fungal sepsis are observed 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. With 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 to high mortality. Most cases of sever lung injury is due to adult respiratory distress syndrome with or without sepsis. Pulmonary haemorrhage, pleural effusion, atelectasis contribute to respiratory difficulty.
The most important aspects of treatment is to provide good intensive care support with adequate nutrition, optimization of the fluid balance, mechanical ventilation, intracranial pressure monitoring, prompt recognition of gastrointestinal bleeding and removing the underlying cause (such as acetylcysteine for paracetamol poisoning), also 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 related to etiology, degree of encephalopathy and complications that can be assessed with different scoring systems such as Child’s-turcotte-pugh score, Model for end stage liver disease and Acute physiology and chronic health evaluation score.
Historically mortality has been unacceptably high, being in excess of 80%. In recent years the advent of liver transplantation and multidisciplinary intensive care support have improved survival significantly to approximately 60%.