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Schweizerische medizinische Wochenschrift 1986-Apr

Management of acute liver failure.

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Veza se sprema u međuspremnik
J G O'Grady
R Williams

Ključne riječi

Sažetak

We describe our experience in the treatment of acute liver failure in 620 patients who developed grade 3 or 4 encephalopathy between 1973 and June 1985. The principal aetiologies were paracetamol-induced hepatic necrosis, viral hepatitis, halothane hepatitis and idiosyncratic drug reactions. Cerebral oedema is a major cause of death in these patients and is most effectively treated with mannitol (20%). Renal failure occurs in between 30% and 75% of cases, depending on aetiology, and is most effectively managed by haemodialysis. Electrolyte and acid-base abnormalities are common. Haemodynamic abnormalities encountered include a high cardiac output, low peripheral vascular resistance, hypotension and venodilatation. Assisted mechanical ventilation is frequently required to treat hypoxia caused by pneumonia, atelectasis, haemorrhage and oedema. A coagulopathy is always present but coagulation factors and platelets are given only when the patient is clinically bleeding. These patients are prone to sepsis and this is a significant cause of death. Hypoglycaemia is common and must be actively and frequently sought. The use of charcoal haemoperfusion has been associated with improved survival, especially when it is started during the grade 3 phase of encephalopathy. Recently survival figures of between 47% and 60% have been achieved for patients with paracetamol-induced liver failure and hepatitis A and B. However the figure for non A non B hepatitis and halothane- and drug-induced liver failure are disappointing at around 15% and liver transplantation is being explored as a treatment option in these patients.

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