Fulminant hepatic failure

Recognition

This is a syndrome characterised by the development of encephalopathy, reduced hepatic synthetic function (coagulopathy and low albumin) and raised enzymes suggestive of hepatocellular damage. Prevention, or early treatment of reversible causes, is desirable, as once established, prognosis is very poor in the absence of liver transplantation. Reversible causes include medications (stop them), paracetamol poisoning (give the antidote), acute fatty liver of pregnancy (deliver the baby) and rarely, Wilson’s disease (check serum copper and then discuss management with an expert).

Management of liver failure

• Adequate nutrition (avoid excess protein) usually via NGT
• Careful monitoring for hypoglycaemia – hourly checks may be needed. Low threshold for considering infection and treating possible gram negative septicaemia with an appropriate third generation cephalosporin.
• Because of risks of hypercapnia and hypoxia, early intubation and ventilation should be considered for markedly confused or comatose patients.
• Watch out for and manage hyponatraemia.
• If the coagulopathy leads to overt bleeding, give 10ml/kg of FFP.
• Intracranial hypertension manifesting with hypertonicity and decerebrate posturing, pupillary changes, and systemic hypertension, is already advanced. Consider giving mannitol 0.5 – 1 mg/kg IV (about 100 ml of the 20% solution.) Do not use it if the patient is anuric or profoundly oliguric, and wait several hours before repeating each dose – timing is best deduced from the clinical response (improved consciousness, reversal of neurological signs) with a further dose being considered once the improvement starts to wear off.
• If the patient seems an appropriate potential candidate for liver transplantation, seek advice early.
• Stop beta-blocker therapy in the acute phase if being used to reduce variceal bleeding risk.

Perspective – mannitol in acute liver failure

Despite most guidelines on ALF advocating the use of mannitol,¹,² the evidence for its efficacy is surprisingly weak, with most authorities referring back to a 1982 report on 34 patients.³ The trial was unblinded with the control group having worse mean enzyme rise at baseline. Nine of the mannitol patients (53%) had invasive intracranial pressure monitoring compared with only 5 controls (29%). Eight of 17 patients given mannitol survived versus only one of the 17 controls. (ARR an impressive 41%, 95% CI 0.17 – 0.61, NNT 3.) In the absence of newer high quality RCTs, the interpretation of this study is, however, problematic.

1. Richardson D, Bellamy M. Intracranial hypertension in acute liver failure. Nephrol Dial Transplant. 2002;17:23-7 ↩

2. Marrero J, Martinez FJ, Hyzy R. Advances in critical care hepatology. Am J Resp Crit Care Med. 2003;168:1421-6 ↩

3. Canalese J, Gimsone AE, Davis C, et al. Controlled trial of dexamethasone and mannitol for the cerebral oedema of fulminant hepatic failure. Gut. 1982;23:625-9 ↩