Hepatic encephalopathy: Difference between revisions
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**[[GI Bleed]] | **[[GI Bleed]] | ||
**Excess dietary intake of protein | **Excess dietary intake of protein | ||
**Infection | **[[Infection]] (e.g. [[SBP]]) | ||
**[[Hypokalemia]] | **[[Hypokalemia]] | ||
**[[Metabolic Alkalosis]] | **[[Metabolic Alkalosis]] | ||
**Constipation | **[[Constipation]] | ||
*Dehydration | *[[Dehydration]] | ||
**[[Vomiting]] | **[[Vomiting]] | ||
**Diuretics | **[[Diuretics]] | ||
*Drugs | *Drugs | ||
**Opioids | **[[Opioids]] | ||
**Benzodiazepines (including withdrawal) | **[[Benzodiazepines]] (including [[benzodiazepine withdrawal|withdrawal]]) | ||
**[[ETOH]] (including withdrawal) | **[[ETOH]] (including withdrawal) | ||
==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 | ||
*Stage II - Lethargy, drowsiness, variable orientation, asterixis | *Stage II - Lethargy, drowsiness, variable orientation, asterixis | ||
*Stage III - Stupor with hyperreflexia, extensor plantar reflexes | *Stage III - Stupor with hyperreflexia, marked disorientation, inability to follow commands, extensor plantar reflexes | ||
*Stage IV - Coma | *Stage IV - Coma | ||
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*[[Hypoglycemia]] | *[[Hypoglycemia]] | ||
*[[Wernicke-Korsakoff Syndrome]] | *[[Wernicke-Korsakoff Syndrome]] | ||
*Hyper/[[hyponatremia]] | *[[hypernatremia|Hyper]]/[[hyponatremia]] | ||
*[[Benzodiazepine Overdose]] (decreased hepatic clearance) | *[[Benzodiazepine Overdose]] (decreased hepatic clearance) | ||
*[[Renal Failure]] | *[[Renal Failure]] | ||
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*Chemistry | *Chemistry | ||
*Ammonia level | *Ammonia level | ||
*LFTs | *[[LFTs]] | ||
*PT/PTT | *PT/PTT | ||
* | *[[Urinalysis]] | ||
*[[CXR]] | *[[CXR]] | ||
*Head CT | *[[Head CT]] | ||
*Paracentesis in patient with ascites (rule out [[SBP]]) | *[[Paracentesis]] in patient with ascites (rule out [[SBP]]) | ||
*Consider [[LP]] | *Consider [[LP]] | ||
===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]] | ||
==Management== | ==Management== | ||
*[[Lactulose]] | *[[Lactulose]] 20g PO or (300mL in 700cc H2O retention enema x30min) | ||
**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/> | |||
[[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)