Hepatic Encephalopathy – Diagnosis & Management
Neurological
Context
- Hepatic Encephalopathy (HE) defined as disturbances of brain function resulting from (1) advanced liver disease and/or (2) portosystemic shunting.
- Patients with cirrhosis have 30-40% chance of experiencing HC at some time during their clinical course and it is associated with poor prognosis and high risk of recurrence.
- We will focus on HE in the context of chronic liver disease which is the vast majority of cases.
- Less common scenario is HE due to acute liver failure.
Clinical Presenation
- Tends to cause a more hypoactive delirium along a wide spectrum ranging from subtle alterations in level of consciousness to frank coma.
- Hallmark sign on clinical examination is asterixis or “flapping tremor” although it is not specific to hepatic encephalopathy and may disappear in more severe forms of HE.
Diagnostic Process
- Should suspect HE in any patients with cirrhosis or possible liver disease who present with cognitive dysfunction.
- It is a clinical diagnosis not always seen in isolation and clinicians should consider a broad, overlapping differential including subdural hematoma, hypoglycemia, hyponatremia, drug-induced, uremic encephalopathy, CNS infection and Wernicke’s encephalopathy.
- Presence of precipitating factors that would support diagnosis of HE includes bacterial infections, GI bleed, constipation, renal failure, and electrolyte abnormalities.
- Initial investigations should include fingerstick glucose, basic labwork including extended electrolytes and liver enzymes, CXR, urinalysis and blood cultures as indicated.
- Diagnostic paracentesis should be performed in all patients with ascites.
- Low threshold to perform non-contrast CT head.
OTHER INVESTIGATIONS
- Serum ammonia levels rarely change management and are not universally available
- Isolated finding of elevated serum ammonia is not sufficient to diagnose and treat HE, especially if other causes of cognitive dysfunction have not been excluded
- Serial ammonia levels may be more useful in testing efficacy of ammonia-lowering therapies
WESTHAVEN CLASSIFICATION
- Severity grading criteria for HE
- Grade I: Trivial lack of awareness
- Grade II: Disorientation to time, asterixis, lethargy
- Grade III: Gross disorientation, stupor
- Grade IV: Coma
Management
- All patients with HE should be started on serum ammonia-lowering therapies:
- Lactulose 25-30ml q1-2h until frequent BM, then down-titrate to target 2-3 daily bowel movements.
- If Lactulose has proven ineffective within 48h, consulting services may add Rifaximin 550mg PO bid or PEG.
- Initiate thiamine therapy with initial dosing regimen 100-200mg IV q8h.
- Consider high-dose (500mg IV q8h) if concerned about Wernicke’s encephalopathy.
- Correcting precipitating factors (i.e., antimicrobial therapy, correcting electrolyte abnormalities, treating GIB or AKI, thiamine replacement) will resolve symptoms of HE in 90% of patients.
- (Grade I) Select patients may be managed as outpatient or but most require ward admission with frequent neurological assessments.
- (Grade II) These patients will require hospital admission and have high likelihood to progressing to Grade III/IV HE.
- (Grade III/IV) These patients will require airway management and urgent consultation with intensivist for high priority transfer to critical care center.
Quality Of Evidence?
High
We are highly confident that the true effect lies close to that of the estimate of the effect. There is a wide range of studies included in the analyses with no major limitations, there is little variation between studies, and the summary estimate has a narrow confidence interval.
Moderate
We consider that the true effect is likely to be close to the estimate of the effect, but there is a possibility that it is substantially different. There are only a few studies and some have limitations but not major flaws, there are some variations between studies, or the confidence interval of the summary estimate is wide.
Low
When the true effect may be substantially different from the estimate of the effect. The studies have major flaws, there is important variations between studies, of the confidence interval of the summary estimate is very wide.
Justification
- Benefit of lactulose in hepatic encephalopathy: MODERATE. Weak beneficial effect seen in several low-quality trials.
- Rifaximin in hepatic encephalopathy: HIGH. Mortality benefit in treatment of overt HE in combination with lactulose and efficacy in secondary prevention with rifaximin alone in multiple RCTs.
Related Information
OTHER RELEVANT INFORMATION
- Asterixis (video) https://www.youtube.com/watch?v=h5T8rWqLM-U
- West Haven Criteria
- https://www.mdcalc.com/hepatic-encephalopathy-grades-stages#use-cases
- NU EM Blog: Hepatic Encephalopathy in the ED https://www.nuemblog.com/blog/hepatic-encephalopathy
- Patient education: American Liver Foundation
- AASLD: Practice guidelines for management of HE in context of acute liver failure
https://www.aasld.org/publications/practice-guidelines
Related Information
Reference List
- Ong JP, Aggarwal A, Krieger D, et al. Correlation between ammonia levels and the severity of hepatic encephalopathy. Am J Med 2003; 114:188.
- Als-Nielsen B, Gluud OL, Gluud C. Non-absorbable disaccharides for hepatic encephalopathy: systematic review of randomized trials. BMJ 2004;328:1046.
- Kimer N, Krag A, Moller S, et al. Systematic review with meta-analysis: the effects of rifaximin in hepatic encephalopathy. Aliment Pharmacol Ther 2014;40:123.
- Vilstrup H, Amodio P, Bajaj J, et al. Hepatic encephalopathy in chronic liver disease: 2014 Practice Guideline by the American Association of the Study of Liver Diseases and the European Association for the Study of the Liver. Hepatology 2014;60:715.
RESOURCE AUTHOR(S)
DISCLAIMER
The purpose of this document is to provide health care professionals with key facts and recommendations for the diagnosis and treatment of patients in the emergency department. This summary was produced by Emergency Care BC (formerly the BC Emergency Medicine Network) and uses the best available knowledge at the time of publication. However, healthcare professionals should continue to use their own judgment and take into consideration context, resources and other relevant factors. Emergency Care BC is not liable for any damages, claims, liabilities, costs or obligations arising from the use of this document including loss or damages arising from any claims made by a third party. Emergency Care BC also assumes no responsibility or liability for changes made to this document without its consent.
Last Updated Feb 17, 2022
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