Hepatic Encephalopathy Grade Calculator
Grade hepatic encephalopathy severity using the West Haven Criteria. Assess symptoms, identify precipitants, and determine appropriate treatment.
Select Hepatic Encephalopathy Grade
Clinical Features:
No clinical symptoms apparent. Abnormalities only detected on psychometric or neurophysiological testing. Impaired quality of life.
Treatment Approach:
Usually no treatment needed. Consider lactulose if significantly impacting quality of life or driving ability. Monitor for progression.
Precipitant Checklist
Identify and treat underlying precipitants. Most episodes of hepatic encephalopathy are triggered by identifiable factors:
West Haven Criteria Summary
| Grade | Consciousness | Mental Status | Asterixis |
|---|---|---|---|
| 0 | Normal | Subclinical alterations | Absent |
| I | Mild lack of awareness | Shortened attention, impaired calculation | Rare/absent |
| II | Lethargy, apathy | Disoriented to time, personality change | Present |
| III | Somnolence, semi-stupor | Disoriented to place, confused | Present (if testable) |
| IV | Coma | Unresponsive | Absent |
Treatment Medications
Lactulose (First-Line)
- •Dose: 15-30mL (10-20g) PO 2-3 times daily
- •Goal: Titrate to 2-3 soft, non-diarrheic bowel movements per day
- •Mechanism: Non-absorbable disaccharide that acidifies colon, reduces ammonia absorption
- •For acute/severe HE: Can give via NG tube or as enema if patient cannot take PO
Rifaximin (Second-Line)
- •Dose: 550mg PO twice daily
- •Indication: Add to lactulose for recurrent episodes or inadequate response to lactulose alone
- •Mechanism: Non-absorbable antibiotic that reduces ammonia-producing gut bacteria
- •Evidence: Reduces HE episodes and hospitalizations when added to lactulose
Alternative Therapies
- •L-ornithine L-aspartate (LOLA): Promotes ammonia metabolism (not FDA-approved in US)
- •Zinc supplementation: For zinc-deficient patients (urea cycle cofactor)
- •Branched-chain amino acids: May help in refractory cases
- •Liver transplant: Definitive treatment for recurrent/chronic HE in appropriate candidates
Understanding Hepatic Encephalopathy
What is Hepatic Encephalopathy?
Hepatic encephalopathy (HE) is a spectrum of neuropsychiatric abnormalities seen in patients with liver dysfunction, after exclusion of brain disease. It results from the accumulation of neurotoxins (primarily ammonia) that cross the blood-brain barrier and cause astrocyte swelling and cerebral edema.
Pathophysiology
- Ammonia produced by gut bacteria and protein metabolism is normally detoxified by the liver
- In cirrhosis, portosystemic shunting and impaired hepatic function allow ammonia to reach the brain
- Ammonia causes astrocyte swelling, alters neurotransmission (GABA, glutamate), and leads to oxidative stress
- Other factors include inflammation, zinc deficiency, and gut dysbiosis
Epidemiology
- Occurs in 30-45% of patients with cirrhosis
- Minimal HE present in up to 80% of cirrhotic patients on testing
- Associated with increased mortality and poor quality of life
- Recurrence rate is approximately 40% within 1 year after first episode
Diagnosis
Diagnosis is clinical, based on West Haven Criteria. No single diagnostic test exists. Workup includes:
- Exclude other causes: infection, stroke, intracranial bleeding, metabolic disturbances
- Venous ammonia level (elevated in most cases but not required for diagnosis)
- Identify precipitants: CBC, CMP, blood cultures, urinalysis, imaging as needed
- For minimal HE: psychometric testing (Number Connection Test, others)
Prognosis
The presence of hepatic encephalopathy significantly worsens prognosis. One-year survival after first episode of overt HE is approximately 40%. Recurrent HE is associated with poor quality of life and should prompt liver transplant evaluation in appropriate candidates.
Frequently Asked Questions
What causes hepatic encephalopathy?
HE is caused by liver dysfunction and/or portosystemic shunting, leading to accumulation of neurotoxins (especially ammonia) in the bloodstream. These toxins affect brain function, causing symptoms ranging from subtle cognitive changes to coma.
What is the difference between overt and minimal HE?
Overt HE (Grades I-IV) has clinically apparent symptoms. Minimal (covert) HE has no obvious clinical signs but shows abnormalities on specialized testing. Both impact quality of life and driving ability.
How long does it take for lactulose to work?
Lactulose typically begins working within 24-48 hours. In acute severe HE, higher doses and more frequent administration may be needed. The goal is 2-3 soft bowel movements per day. Over-treatment causing diarrhea should be avoided as it can worsen dehydration and electrolyte imbalances.
Should dietary protein be restricted?
No. Protein restriction is no longer recommended and can worsen malnutrition. Patients should maintain adequate protein intake (1.2-1.5 g/kg/day), preferably from vegetable sources. Only during acute severe episodes might protein be temporarily reduced, but this should be brief.
What is asterixis?
Asterixis (flapping tremor) is a characteristic sign of HE seen in Grades II-III. To elicit: have patient extend arms with hands dorsiflexed (like stopping traffic). Involuntary brief lapses in hand position cause a flapping motion. It's absent in minimal HE and Grade IV (too encephalopathic to cooperate).
Is ammonia level necessary for diagnosis?
No. Diagnosis is clinical. While most patients with HE have elevated ammonia, levels don't correlate well with severity. A normal ammonia doesn't exclude HE, and elevated ammonia without symptoms doesn't warrant treatment. Ammonia can help support diagnosis but shouldn't be used to monitor treatment.
Can patients with HE drive?
Patients with any grade of overt HE should not drive until symptoms resolve. Even minimal HE can impair driving ability (reaction time, attention). After recovery, driving ability should be assessed before resuming. Many states require physician reporting of conditions that impair driving.
What is the role of liver transplantation in HE?
Recurrent or chronic HE is an indication for liver transplant evaluation. Transplantation cures HE by restoring normal liver function. Patients with frequent episodes despite medical therapy, or those with minimal HE significantly affecting quality of life, should be referred to transplant centers.
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