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hepatic_encephalopathy

hepatic encephalopathy

factors that contribute to encephalopathy:

  • 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)

features:

  • 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

classification of hepatic encephalopathy

  • 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

severity grades

  • 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)

medical therapy:

  • 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
hepatic_encephalopathy.txt · Last modified: 2018/08/11 17:41 (external edit)