Treatment of fulminant hepatic failure

The management of fulminant hepatic failure resulting from acetaminophen overdose is based on good intensive care. Optimum management should be directed towards resuscitation and preparation for urgent and safe transfer. Control and protection of the airway is fundamental, particularly as these patients can rapidly become deeply encephalopathic. Sedatives are contraindicated, and patients who cannot be managed safely should be ventilated. Intravenous fluid resuscitation is always necessary and is best directed by either central venous or pulmonary artery pressures. Hypotension may require intravenous vasopressors as well as intravenous fluid. Volume expansion can often correct a mild metabolic acidosis, but bicarbonate infusions should be avoided as the trend in serum bicarbonate is crucial with respect to prognosis (Table2). These patients often experience profound metabolic disturbances, particularly hypoglycemia and hypophosphatemia, which need to be corrected with infusions of 10 per cent glucose and potassium phosphate. The development of coagulopathy and thrombocytopenia can make insertion of venous catheters difficult; however, fresh frozen plasma should be avoided. The prothrombin time is the main prognostic factor with regard to transplantation (Tab[e_2) (O'GradyetaL 1989).

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Table 2 King's College transplantation criteria

All patients should be treated with NAC, which should be restarted with the initial loading regimen if there is doubt as to the dose received and then continued at 150 mg/kg/day until the INR has returned to less than 2. Patients should also be given a replacement dose of vitamin K as well as prophylactic broad-spectrum antibiotics and antifungals (oral fluconazole 50 mg once daily) as sepsis in this group of patients is common and is associated with a particularly poor outcome. If the patient achieves transplant criteria (Tabje„2.) or develops renal failure or grade III/IV encephalopathy, intravenous amphotericin B should be started. Renal failure should be treated with continuous hemofiltration since intermittent dialysis can precipitate cerebral edema.

Forty-five per cent of patients with acetaminophen-induced fulminant hepatic failure and grade III/IV encephalopathy develop cerebral edema ( Makin efa/ 1995). The main aim in the management of these patients is to prevent further surges in intracranial pressure. They should be deeply sedated and paralysed with neuromuscular blocking agents. Stimulation, movement, and physiotherapy should be kept to a minimum. Seizures can be difficult to assess, and so prophylactic anticonvulsants should be started. Cerebral perfusion can be assessed from jugular venous bulb oximetry and intracranial pressure monitoring. Traditionally, a cerebral perfusion pressure of 50 mmHg should be obtained. Hyperventilation should be avoided and a close control on plasma osmolality maintained. Surges in intracranial pressure should be treated with intravenous mannitol (0.5-1.0 mg/kg) but the serum osmolality should not be allowed to exceed 320 mosmol/l.

Patients who develop the transplantation criteria should be offered an orthotopic liver transplant. With a transplant these patients have a survival rate of over 80 per cent, whereas patients developing these criteria but not receiving a transplant have a survival rate of only 40 per cent. Patients who do not develop the transplant criteria have a survival of 90 per cent.

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