see also:

• gastroenterology
• hepatitis
• cirrhosis
• ascites
• assessment of hepatic function
• prescribing drugs in patients with liver impairment
• AFTB lectures - acute liver failure

• elevated levels of gut derived substances due to portosystemic shunting:
  • ammonia
  • false neurotransmitters (eg. octopamine)
  • changes in sensitivity of brain to inhibitory neurotransmitters (eg. GABA)

• changes in intellect, personality & emotions
• sleep disturbances
• disorientation in time & place
• flapping tremor (not specific)
• hepatic fetor due to mercaptans in breath
• impaired ability to draw or construct objects (eg. 5 pointed star)
• elevated arterial ammonia
• EEG changes

• In the World Congress of Gastroenterology 1998 in Vienna, a proposed classification of hepatic encephalopathy was presented to standardize the subclasses. According to this classification, hepatic encephalopathy is subdivided in type A, B and C:
  • Type A (=acute) describes hepatic encephalopathy associated with acute liver failure
  • Type B (=bypass) is caused by portal-systemic shunting without associated intrinsic liver disease
  • Type C (=cirrhosis) occurs in patients with cirrhosis

• Grade 1 - Trivial lack of awareness; Euphoria or anxiety; Shortened attention span; Impaired performance of addition. 67% of cirrhotic patients may have 'minimal hepatic encephalopathy'
• Grade 2 - Lethargy or apathy; Minimal disorientation for time or place; Subtle personality change; Inappropriate behavior; Impaired performance of subtraction
• Grade 3 - Somnolence to semistupor, but responsive to verbal stimuli; Confusion; Gross disorientation
• Grade 4 - Coma (unresponsive to verbal or noxious stimuli)

• recognition & aggressive Rx of precipitating factors:
  • renal impairment
  • GIT bleeding
  • infections
  • electrolyte disturbances eg. hypokalaemia
  • hypoxia
  • hyperthermia
• avoid drugs that aggravate it (eg. sedatives, hypnotics and anxiolytics, opiates and opioids)
• stop dietary protein in acute hepatic failure
  • if recovery occurs, increase by 10g/day every 3rd day as encephalopathy improves
  • in chronic liver disease consider mild protein restriction 40-50g/d but less will exacerbate hypoalbuminaemia
• reduce GIT absorption of toxic amines by decreasing colonic bacteria & lowering colonic pH:
  • in the past, lactulose was used to reduce GIT bacteria but its risk of aspiration appears to outweigh its dubious benefits
    • example regime used: lactulose 30ml o bd then adjust to achieve 2-3 soft stools daily
  • in the past, neomycin was used to further reduce GIT bacteria but appears not to be effective and risks nephrotoxicity & ototoxicity
  • consider intermittent use of enemas for further reduction in bacteria
• correct coagulopathy
• if cerebral oedema likely:
  • IPPV if Grade 3 or 4 coma or respiratory failure
    • early ICP monitoring as clinical signs of cerebral oedema unreliable
    • if ICP < 25mmHg, give 5% dextrose but watch for hyponatraemia
    • if ICP > 25mmHg, give either:
      • mannitol 0.5g/kg, or,
      • 7.5% hypertonic saline 2ml/kg