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ACUTE LIVER FAILURE
 

Introduction: Acute liver failure (ALF) is an umbrella term covering a spectrum of disease in which liver dysfunction occurs leading to encephalopathy within 6 months of the first clinical evidence of the disease. Three subgroups may be recognized.
1. Hyperacute: jaundice < 7 days before onset of encephalopathy (e.g. paracetamol poisoning)
2. Acute:  jaundice for 8-28 days before onset of encephalopathy
3. Subacute: jaundice for 4-12 weeks before onset of encephalopathy

The development of cerebral edema, intracranial hypertension (ICH), disruption of cerebral autoregulation, coagulopathy, circulatory insufficiency, and poor organ perfusion possibly are the major cause of morbidity and mortality of patients suffering from ALF.

Frequency:
Acetaminophen or paracetamol overdoses are prominent causes of FHF in Europe In the developing world, acute HBV infection dominates as a cause of FHF because of the high prevalence of HBV. Hepatitis delta virus (HDV) superinfection is much more common in developing countries. Hepatitis E virus (HEV) is associated with a high incidence of FHF in women who are pregnant and is of concern in pregnant patients living in or traveling through endemic areas, e.g. Central America, India and the subcontinent, and the Middle East.

Causes:

  1. Viral hepatitis; A,B,D (coinfection, or superinfection with HBV),and E are the principle causes. Others include CMV and HZV.
  2. Infections: P. malaria, leptospirosis
  3. Drugs and toxins: Paracetamol, anti-tubercula drugs, anti-biotics, salicylates (Reye’s syndrome), NSAIDs, statins, glitazones, antiretroviral HIV medications, anti-epileptics, anti-fungal agents, TCA, halothane, mushrooms, herbal hepatotoxicity – notably kava kava, ginseng
  4. Miscellaneous: pregnancy-related syndromes, autoimmune disease, lymphomas, Wilson’s disease, Budd-Chiari syndrome
History
History is valuable for guiding appropriate interventions. If the patient is incapacitated, closely question family members and friends Detail the date of onset of jaundice, alcohol use, medication use (prescription and illicit or recreational), herbal or traditional medicine use, family history of liver disease (Wilson disease), exposure risk factors for viral hepatitis (travel, transfusions, sexual contacts, occupation, body piercing), and toxin ingestion (mushrooms, organic solvents).

Physical
Physical examination includes careful assessment and documentation of mental status and search for stigmata of chronic liver disease (fetor hepaticus, flapping tremor).  Jaundice is often but not always present, especially in rapid inset hyperacute failure. Right upper quadrant tenderness is variably present. Liver span may be small indicative of significant loss of volume due to hepatic necrosis. An enlarged liver may be seen with congestive heart failure, viral hepatitis, or Budd-Chiari syndrome.
  • Development of cerebral edema ultimately may give rise to manifestations of ICP, including papilledema, hypertension, and bradycardia.
  • The rapid development of ascites, especially if observed in a patient with FHF accompanied by abdominal pain, suggests the possibility of hepatic vein thrombosis (Budd-Chiari syndrome).
  • Coagulopathy: bleeding from puncture sites, hematemesis or melena may complicate the presentation of FHF as a result of upper gastrointestinal bleeding.
  • CVS: Typically, patients are hypotensive and tachycardic as a result of the reduced systemic vascular resistance that accompanies FHF.
  • As the disease progresses features of shock and multiorgan failure develop, including ARDS, renal failure, and superinfection with bacteria and fungi. Hypotension and hypoxia lead to a worsening cycle as further damage to the injured liver occurs.
 

TABLE: Grading of hepatic encephalopathy

Grade

Level of consciousness

Intellectual function

Neurological findings

EEG

1

Lack of awareness
Personality change
Day/night reversal

Short attention

Incoordination
Mild asterixis

Slowing
(5-6 cps)
Triphasic

2

Lethargic
Inappropriate behavior

Disoriented

Asterixis
Abnormal reflexes

Slowing
Triphasic

3

Asleep
Reusable

Loss of meaningful communication

Asterixis
Abnormal reflex

Slowing Triphasic

4

Unarousable

Absent

Decerebrate

Very slow (2-3 cps), delta