hepatic_encephalopathy
Table of Contents
hepatic encephalopathy
see also:
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 07:41 by 127.0.0.1