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West Haven Criteria for Hepatic Encephalopathy

Grades severity of hepatic encephalopathy (HE) from covert to coma based on clinical neuropsychiatric findings

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Why use it

Hepatic encephalopathy occurs in 30–45% of patients with cirrhosis and is the most common cause of acute neurological dysfunction in liver disease. Accurate grading directs clinical management: Grade 1 warrants close monitoring and lactulose therapy; Grade 3–4 requires ICU-level care, airway protection consideration, and urgent liver transplant evaluation. The WHC provides the universal language for describing HE severity across clinical, research, and transplant settings, and is required by most clinical HE trials.

About

The West Haven Criteria (WHC) is the most widely used clinical grading system for hepatic encephalopathy (HE), originally described by Conn and colleagues in 1977 and subsequently modified by Ferenci and colleagues at a 2002 consensus meeting of the International Society for Hepatic Encephalopathy and Nitrogen Metabolism (ISHEN). The criteria classify HE into five grades (0 through 4) based on observable changes in consciousness, intellectual function, behavior, and neurological examination findings. The 2014 AASLD/EASL HE Practice Guideline further divided the spectrum into Covert HE (Grades 0–1, detectable only by psychometric or neurophysiological testing) and Overt HE (Grades 2–4, with clinically apparent neuropsychiatric dysfunction). HE is a complication of acute or chronic liver disease — most commonly cirrhosis — resulting from accumulation of neurotoxic substances (primarily ammonia and inflammatory mediators) that impair astrocyte and neuronal function. Accurate grading guides management intensity, level of care decisions, and prognostic discussions including liver transplant eligibility.

When to use

  • Clinical assessment of any patient with known or suspected liver disease presenting with acute neurological or behavioral change
  • Serial monitoring of HE severity during hospitalization to assess treatment response (lactulose, rifaximin)
  • Prognostication and liver transplant listing discussions in patients with recurrent or persistent HE
  • Grading HE in clinical research and trials of HE therapy
  • Differentiating HE from other causes of encephalopathy (uremia, septic encephalopathy, intracranial pathology, metabolic disorders)
  • Deciding level of care: Grade 3–4 HE typically requires ICU admission with airway assessment

Formula

West Haven Criteria — Grade Definitions: Grade 0 (Covert HE — Minimal): Normal consciousness, personality, neurological exam Deficits detectable ONLY by psychometric or neurophysiological testing (PHES, CFF, NCT) Asterixis absent Grade 1 (Covert HE — Mild): Trivial lack of awareness, shortened attention span Euphoria or anxiety; sleep disturbance (inverted sleep-wake cycle) Impaired performance of mental arithmetic (e.g., serial subtractions) Asterixis may be present on careful examination Grade 2 (Overt HE — Moderate): Lethargy or apathy Disorientation to TIME (cannot state correct date/day) Subtle personality change; inappropriate behavior; slurred speech Asterixis clearly present Grade 3 (Overt HE — Severe): Somnolence to semi-stupor; responds to verbal stimuli Gross disorientation to TIME and PLACE Bizarre behavior; muscular rigidity; hyperreflexia Asterixis may be absent Grade 4 (Overt HE — Coma): No response to verbal or noxious stimuli Decorticate or decerebrate posturing may be present No asterixis (unresponsive)

Pearls & pitfalls

  • Asterixis (hepatic flap — rhythmic flapping tremor of outstretched hands and wrists) is the hallmark finding in Grades 1–2 HE but is absent in Grade 4 (too encephalopathic to maintain posture) and often in Grade 3.
  • West Haven Grade alone cannot distinguish the etiology of encephalopathy — always rule out concurrent intracranial pathology (subdural hematoma), metabolic causes (hypoglycemia, uremia), and septic encephalopathy.
  • Covert HE (Grades 0–1) is detectable ONLY with psychometric testing (PHES, Number Connection Test, Critical Flicker Frequency) — clinically it may appear completely normal.
  • Common precipitating factors of HE: GI bleeding, infection (especially SBP), renal impairment, electrolyte disturbance (hyponatremia, hypokalemia), constipation, excess dietary protein, dehydration, and psychoactive medications (benzodiazepines, opioids).
  • Serum ammonia correlates poorly with HE severity and should NOT be used alone for grading — diagnosis is clinical. A normal ammonia level makes HE less likely.
  • Rifaximin 550 mg BID is the recommended secondary prophylaxis after a first episode of overt HE — it reduces recurrence risk by approximately 50%.
  • Grade 3–4 HE with compromised airway reflexes requires immediate assessment for orotracheal intubation — aspiration pneumonia is a leading cause of death in severe HE.
  • MELD score and Child-Pugh score should be calculated in all patients with overt HE to assess transplant urgency and prognosis.
  • Avoid benzodiazepines and opioids in patients with HE — they worsen encephalopathy. If sedation is required in ICU, use propofol.

Next steps

Covert HE (Grade 0–1): Identify and treat precipitating factors (infection, GI bleeding, dehydration, constipation, hypokalemia, hepatotoxic medications). Lactulose therapy. Rifaximin for secondary prophylaxis if prior overt episode. Outpatient or short-stay management. Overt HE (Grade 2): Hospital admission. Lactulose dosed to 2–3 soft stools/day. Identify and treat precipitants aggressively. Rifaximin add-on therapy. Close monitoring for progression. Overt HE (Grade 3): ICU or high-dependency unit. Airway assessment — Grade 3 HE may require intubation to protect the airway. Lactulose via NGT. Evaluate for liver transplant urgency. Overt HE (Grade 4 — Coma): ICU. Immediate intubation. Urgent liver transplant evaluation. Bowel decontamination. Aggressive treatment of all precipitants. Consider liver support device as bridge to transplant.

Evidence

Conn HO et al. Comparison of lactulose and neomycin in the treatment of chronic portal-systemic encephalopathy. Gastroenterology. 1977;72(4 Pt 1):573-583. Ferenci P et al. Hepatic encephalopathy — definition, nomenclature, diagnosis, and quantification: final report of the working party at the 11th World Congresses of Gastroenterology, Vienna, 1998. Hepatology. 2002;35(3):716-721. PMID:11870389. Vilstrup H et al. Hepatic encephalopathy in chronic liver disease: 2014 Practice Guideline by the AASLD and EASL. Hepatology. 2014;60(2):715-735. PMID:25042402.

References

  1. Ferenci P et al. Hepatic encephalopathy — definition, nomenclature, diagnosis, and quantification: final report of the working party. Hepatology. 2002;35(3):716-721. — link
  2. Vilstrup H et al. Hepatic encephalopathy in chronic liver disease: 2014 Practice Guideline by the AASLD and EASL. Hepatology. 2014;60(2):715-735. — link
  3. Conn HO et al. Comparison of lactulose and neomycin in the treatment of chronic portal-systemic encephalopathy. Gastroenterology. 1977;72(4 Pt 1):573-583. — link