“Resident Reminders”

Practice Guideline Highlights in Gastroenterology 

Hepatic Encephalopathy 

q         A diagnosis of exclusion. Consider:

ü      Intoxication

ü      Withdrawal

ü      CNS trauma (Subdural hematoma)

ü      CNS ischemia

ü      Electrolyte abnormality

ü      Thiamine deficiency

q         Subtle presentation

            Short term memory loss, hypersomnia, insomnia, asterixis, lethargy,    slurred speech, bizarre behavior, or flat out coma 

q         Stages:

West Haven Criteria

Stage 0: Lack of detectable personality changes. No asterixis.

Stage 1: Trivial lack of awareness. Impaired attention span. Altered sleep, euphoria or depression. Mild asterixis may be present.

Stage 2: Lethargy or apathy. Disorientation. Inappropriate behavior. Slurred speech. Asterixis.

Stage 3: Gross disorientation. Bizarre behavior. Semi-stupor. Asterixis absent.

Stage 4: Coma 

q         Causes:

GI bleeding

Infections: not just SBP, pneumonia, urinary sources

Renal/electrolyte disturbances: renal failure, diuretic induced changes, malnutrition

Medications: narcotics, benzodiazepines

Excessive dietary protein

Constipation

Acute deterioration of liver status: portal vein thrombosis, alcoholic hepatitis, post-op cirrhotics, TIPS, superimposed viral hepatitis, drug-induced liver injury 

q         Evaluation

Clinical evaluation with CT, MRI, CSF analysis as indicated 

q         Ammonia

Elevation of serum ammonia correlates poorly with the degree of clinical encephalopathy.  In cases of fulminant liver failure, however, arterial blood ammonia levels greater than 200 mcg/dL have been associated with an increased risk of cerebral herniation.  There is no indication for following serial ammonia levels or making any statements on prognosis on the basis of ammonia levels in patients with chronic liver disease. 

q         Acute Encephalopathy

1. Search for underlying cause

2. Use non-absorbable disaccharide, lactulose (for colon acidification effect) 45ml hourly until colon evacuation, avoid severe diarrhea.

3. Alternatives- Neomycin 3-6g/d for 1-2 weeks. Monitor for renal insufficiency and oto-oxicity. Metronidazole, rifamyxin

4. Nutrition.  Hold feedings for 24-48 hours until encephalopathy improves, use IV glucose.  There is no benefit in using IV or NG hepatic feeding formulas in the early days of hospitalization. 

5. Initiate feedings at 0.5g/kg/d protein and gradually increase to a goal of 1.2-1.5g/kg/d, mostly vegetable and dairy sources of protein. 

q         Chronic Encephalopathy

1. Attention to precipitating factors, sedatives, sleeping aids.

2. Vegetable and dairy sources of protein, goal of 1.2-1.5g/kg/d

3. Lactulose

4. Metronidazole and/or zinc supplementation can be used as an alternative or adjunct. Monitor for toxicity

5.  Reserve specialized hepatic nutritional formulas for the few patients who are unable to tolerate an adequate amount of protein in the diet. 

Selected Citations 

Ferenci P, Lockwood A, Mullen K, et al. Hepatic Encephalopathy---Definition, Nomenclature, Diagnosis, and Quantification: Final Report of the Working Party at the 11^th World Congress of Gastroenterology, Vienna, 1998. Hepatology 2002;35:716-21. 

Blei A, Cordoba J, et al. Hepatic Encephalopathy. Am J Gastroenterol 2001;96:1968-76. 

Ferenci P, Lockwood A, Mullen K, et al.  Hepatic encephalopathy – Definition, nomenclature, diagnosis and quantification:  Final report of the working party at the 11^th World Congresses of Gastroenterology, Vienna, 1998.  Hepatology 2002;35:716-721

 Back to Resident Reminders

Back to Home Page

<- Home

E-mail USA Gastroenterology