Hepatic encephalopathy: Difference between revisions
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==Clinical Features== | ==Clinical Features== | ||
[[File:Jaundice08.jpg|thumb|Jaundice of the skin]] | |||
[[File:SpiderAngioma.jpg|thumb|Spider angioma]] | |||
[[File:Hepaticfailure.jpg|thumb||Ascites secondary to [[cirrhosis]].]] | |||
===Stages=== | ===Stages=== | ||
*Stage I - General apathy | *Stage I - General apathy | ||
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===Evaluation=== | ===Evaluation=== | ||
*Elevated ammonia level | *Full neuro exam including asterixis | ||
*[[Elevated ammonia]] level. Ammonia is not predictive of severity of disease. | |||
*History of any new medications or toxin ingestion | *History of any new medications or toxin ingestion | ||
*Focus exam on looking for signs of [[GI bleed]] or [[hypovolemia]] | *Focus exam on looking for signs of [[GI bleed]] or [[hypovolemia]] | ||
| Line 59: | Line 63: | ||
**In colon degrades into lactic acid: acidic environment traps ammonia | **In colon degrades into lactic acid: acidic environment traps ammonia | ||
**Also inhibits ammonia production in gut wall | **Also inhibits ammonia production in gut wall | ||
*Rifaximin is second line. | |||
*Some new evidence suggest use of PEG in patients who are not candidates for Lactulose. | |||
==Disposition== | ==Disposition== | ||
*Discharge stage I | *Discharge stage I if good resources. | ||
*Stage II will need admission unless known encephalopathy and who is otherwise well. | |||
*Stage III and IV admission +/- ICU or obs bed. | |||
==Patient Information== | ==Patient Information== | ||
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==See Also== | ==See Also== | ||
*[[Acute hepatic failure]] | |||
==References== | ==References== | ||
<references/> | <references/> | ||
[[Category:GI]] | [[Category:GI]] | ||
Latest revision as of 12:57, 23 October 2021
Background
- Diagnosis of exclusion
- Due to accumulation of nitrogenous waste products normally metabolized by the liver
- Increased metabolism of ammonia to glutamine in CNS
- 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 (e.g. SBP)
- Hypokalemia
- Metabolic Alkalosis
- Constipation
- Dehydration
- Drugs
- Opioids
- Benzodiazepines (including withdrawal)
- ETOH (including withdrawal)
Clinical Features
Ascites secondary to cirrhosis.
Stages
- Stage I - General apathy
- Stage II - Lethargy, drowsiness, variable orientation, asterixis
- Stage III - Stupor with hyperreflexia, marked disorientation, inability to follow commands, extensor plantar reflexes
- Stage IV - Coma
Differential Diagnosis
- Subdural Hematoma
- Hypoglycemia
- Wernicke-Korsakoff Syndrome
- Hyper/hyponatremia
- Benzodiazepine Overdose (decreased hepatic clearance)
- Renal Failure
- Sepsis
Evaluation
Workup
- CBC
- Chemistry
- Ammonia level
- LFTs
- PT/PTT
- Urinalysis
- CXR
- Head CT
- Paracentesis in patient with ascites (rule out SBP)
- Consider LP
Evaluation
- Full neuro exam including asterixis
- Elevated ammonia level. Ammonia is not predictive of severity of disease.
- History of any new medications or toxin ingestion
- Focus exam on looking for signs of GI bleed or hypovolemia
Management
- Lactulose 20g 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
- Rifaximin is second line.
- Some new evidence suggest use of PEG in patients who are not candidates for Lactulose.
Disposition
- Discharge stage I if good resources.
- Stage II will need admission unless known encephalopathy and who is otherwise well.
- Stage III and IV admission +/- ICU or obs bed.
Patient Information
Hepatic Encephalopathy (Medline Plus)