Hepatic encephalopathy
Revision as of 12:37, 26 August 2015 by Rossdonaldson1 (talk | contribs)
Background
- Diagnosis of exclusion
- Due to accumulation of nitrogenous waste products normally metabolized by the liver
- Spectrum of illness ranges from chronic fatigue to acute lethargy
Precipitants
- Increased ammonia production, absorption or entry into brain:
- GI Bleed
- Excess dietary intake of protein
- Infection
- Hypokalemia
- Metabolic Alkalosis
- Constipation
- Dehydration
- Vomiting
- Diuretics
- Drugs
- Opioids
- Benzodiazepines (including withdrawal)
- ETOH (including withdrawal)
Clinical Features
Stages
- Stage I - General apathy
- Stage II - Lethargy, drowsiness, variable orientation, asterixis
- Stage III - Stupor with hyperreflexia, extensor plantar reflexes
- Stage IV - Coma
Differential Diagnosis
- Subdural Hematoma
- Hypoglycemia
- Wernicke-Korsakoff Syndrome
- Hyper/hyponatremia
- Benzodiazepine Overdose (decreased hepatic clearance)
- Renal Failure
- Sepsis
Diagnosis
- Ammonia level
- History of any new medications or toxin ingestion
- Focus exam on looking for signs of GI bleed or hypovolemia
- Chemistry (look for metabolic and electrolyte derrangements)
- Search for source of infection:
- CBC, UA, CXR, paracentesis in patient with ascites (r/o SBP)
- LP if indicated
- Head CT
Treatment
- Lactulose 20mg PO or (300mL in 700cc H2O retention enema x30min)
- In colon degrades into lactic acid: acidic environment traps ammonia
- Also inhibits ammonia production in gut wall
Disposition
- Discharge stage I or II with known ecephalopathy and who is otherwise well
Patient Information
Hepatic Encephalopathy (Medline Plus)