end-expiratory pressure can worsen cerebral edema. coagulopathy and gastrointestinal bleeding impaired liver synthesis of clotting factors, low-grade fibrinolysis, and intravascular coagulation are typical of alf. thrombocytopenia is common and may also be dysfunctional. replacement therapy is recommended only in the setting of bleeding or prior to an invasive procedure. vitamin k can be given to treat an abnormal prothrombin time, regardless of whether there is poor nutritional status. administration of recombinant factor viia has shown promise; however, this treatment approach requires further study. the use of gastrointestinal hemorrhage prophylaxis with a histamine-2 (h2) blocker, proton pump inhibitor, or sucralfate is recommended. nutrition, electrolytes, and metabolic derangements in patients with grade i or ii encephalopathy, enteral feeding should be initiated early. parenteral nutrition should be used only if enteral feeding is contraindicated as it increases the risk of infection. severe restriction of protein is not beneficial; 60 g/day of protein is generally reasonable. fluid replacement with colloid (e.g. albumin) is preferred rather than crystalloid (e.g. saline); all solutions should contain dextrose to maintain euglycemia. multiple electrolyte abnormalities are common in alf. correction of hypokalemia is essential as hypokalemia increases the kidneys' ammonia production, potentially exacerbating encephalopathy. hypophosphatemia is especially common in patients with acetaminophen-induced alf and in those with intact renal function. hypoglycemia occurs in many patients with alf and is often due to depletion of hepatic glycogen stores and impaired gluconeogenesis. plasma glucose concentration should be monitored and hypertonic glucose administered as needed. infection bacterial and fungal infections are common in alf, with one study demonstrating culture-proven infection in 80% of alf patients. defective cellular and humoral immunity as well as presence of indwelling catheters, coma, broad-spectrum antibiotics, and medications that suppress immunity all predispose to infection. localizing symptoms of infection such as fever and sputum production are frequently absent and the only clues to an underlying infectious process may be worsening of encephalopathy or renal function. there must be a low threshold for obtaining frequent cultures (blood, urine, and sputum), chest radiographs, and paracentesis. bacteria that enter through the skin, such as streptococci and staphylococci, tend to predominate. aggressive surveillance is essential as prophylactic antibiotics have shown little benefit. fungal infections, particularly in the setting of broad-spectrum antibiotics, are also common, and disseminated fungemia is a poor prognostic sign. liver transplantation the advent of transplantation has changed survival from as low as 15% in the pretransplant era to more than 60% today. liver transplantation is indicated for many patients with alf, and survival rates of 56–90% can be achieved. in addition to transplantation, better critical care and the trend toward more benign causes, such as acetaminophen, all contribute to improved survival rates. spontaneous survival is now around 40%. the application of transplantation among patients with alf remains low, suggesting that the full potential of this modality may not be realized. timely availability of an allograft is one of the major factors determining transplant outcomes. in the largest u.s. study, only 29% of patients received a liver graft, while 10% of the overall group (one fourth of patients listed for transplantation) died on the waiting list. other series have reported death rates of those listed for transplant as high as 40%. in the alfsg, the transplantation rate was higher in the groups with lower short-term spontaneous survival, making overall survival similar in all groups: acetaminophen, 73%; drug induced, 70%; indeterminate group, 64%; and other causes, 61%. causes of death for the 101 patients who died within the 3-week period included cerebral edema, multiorgan failure, sepsis, cardiac arrhythmia or arrest and respiratory failure. the median time to death after admission was 5 days. acetylcysteine intravenous n-acetylcysteine has been found to be beneficial in acetaminophen toxicity but not in non-acetaminophen-related acute liver failure. prognosis historically mortality has been high, being in excess of 80%. in recent years the advent of liver transplantation and multidisciplinary intensive care support have improved survival significantly. at present overall short-term survival with transplant is more than 65%. several prognostic scoring systems have been devised to predict mortality and to identify who will require an early liver transplant. these include king's college hospital criteria, meld score, and clichy criteria. terminology to date, no universally accepted nomenclature has been adopted. trey and davidson introduced the phrase fulminant hepatic failure in 1970, which they described as a "... potentially reversible condition, the consequence of severe liver injury, with an onset of encephalopathy within 8 weeks of the appearance of the first symptoms and in the absence of pre-existing liver disease". later, it was suggested that the term fulminant should be confined to patients who develop jaundice to encephalopathy within 2 weeks. phrases subfulminant hepatic failure and late onset hepatic failure were coined for onset between 2 weeks to 3 months and for 8 weeks to 24 weeks, respectively. the umbrella phrase of acute liver failure was proposed by king's college group, which has been adopted in this article. paradoxically, in this classification, the best prognosis is in the hyperacute group.