Update on acute liver failure

Here is a recent NEJM review.

There is a paucity of high level evidence to guide clinicians due to the rarity of the condition. However advances in critical care and transplantation have improved the outlook. The authors' recommendations are based largely on expert opinion and lower level evidence.


Definition

The designation acute liver failure (ALF) has largely replaced the old phrase fulminant hepatic failure. The general definition remains the same:

..defined as “a severe liver injury, potentially reversible in nature and with onset of hepatic encephalopathy within 8 weeks of the first symptoms in the absence of pre-existing liver disease..

Subcategories have been proposed, listed in the article, based on time from symptom onset to fully developed ALF. These time intervals provide clues as to etiology.


Etiology

Viral---mainly hep A and E. In addition hep B can be a sleeping giant awakened by immunosuppressive drugs.

Drugs---account for about half of cases in the U.S. Acetaminophen is the most common of these and indeed the most common cause of ALF overall in the U.S. For acetaminophen it's dose related toxicity (subacute worse than a single overdose) but for the other drugs it's idiosyncratic (rare).

Other---ischemic, Budd-Chiari, pregnancy related, miscellaneous, unknown.


Management aspects

Acetylcysteine may be helpful even in patients with non-acetaminophen induced ALF.

Avoidance of hypoglycemia.

Avoidance of hyponatremia (the article recommends maintaining Na on the high side and specifies an optimal range).

Aggressive indications for intubation and mechanical ventilation in patients with encephalopathy (the article specifies an optimal PCO2 range). This is mainly for neuro and airway management though aspiration and ARDS are known complications of ALF.

Preemptive antibiotics (the patients are at high infection risk, and manifestations of ALF often mimic, mask or overlap those of sepsis).


A different profile of encephalopathy compared to that of end stage chronic liver disease

---in which cerebral edema dominates the picture to a greater extent. This is due in large part to the rapidity of ammonia rise in ALF as compared to end stage chronic liver disease. This outpaces the brain's ability to marshal its defenses against swelling.


Dialysis for the liver???

For now extracorporeal treatment modalities are restricted to the setting of clinical trials.