Wernicke Encephalopathy

thiamine deficiency · triad often incomplete · treat empirically · thiamine before glucose · Super Compact

  • Sx: classic triad — encephalopathy (confusion/apathy) + oculomotor (nystagmus, lateral rectus/CN VI palsy, gaze palsy) + gait ataxia; full triad in only ~10–30% — any ONE in an at-risk patient is enough to treat; if untreated → Korsakoff (irreversible amnesia, confabulation)

  • Neg: denies fever + meningismus (CNS infection) · denies focal motor deficit (stroke) · denies asterixis + organ failure (hepatic/uremic — can coexist) · denies pure alcohol intoxication picture (will not fix triad) · glucose alone doesn't explain

  • SHx: chronic alcohol use (most common), but also: hyperemesis gravidarum, bariatric surgery, malnutrition/starvation, prolonged vomiting, dialysis, malignancy, refeeding

  • Etiology: thiamine (B1) deficiency → impaired cerebral glucose metabolism in thiamine-dependent regions (mammillary bodies, thalamus, periaqueductal gray); glucose load without thiamine accelerates depletion → precipitates WE

  • RF: modifiable — alcohol, poor nutrition, unsupplemented IV dextrose, post-bariatric noncompliance · non-mod — malabsorption, hyperemesis, malignancy

  • Data: clinical diagnosis — TREAT, don't wait for tests · thiamine level (don't delay tx) · MRI (mammillary bodies, medial thalami, periaqueductal — supportive not required) · glucose, CMP, Mg (Mg is cofactor — replete) · rule out other AMS causes

  • DDx: alcohol intoxication/withdrawal (won't resolve with thiamine) · hepatic encephalopathy (asterixis, ↑NH3) · structural/stroke (focal, imaging) · CNS infection (fever, CSF) · other B-vitamin deficiency · delirium

  • Home Meds: ensure thiamine BEFORE any dextrose-containing fluids; replete Mg; multivitamin/folate

Plan — ward

  • Consults: neurology · nutrition/dietitian · addiction medicine if alcohol · GI/bariatric if post-surgical

  • Thiamine BEFORE glucose — always. A dextrose bolus into a deficient patient can precipitate or worsen Wernicke

  • High-dose IV thiamine (vit B1) 500 mg IV TID ×2–3 days, then 250 mg IV/IM daily ×3–5 days, then oral 100 mg daily — treatment doses, not the token 100 mg

  • Replete magnesium (required cofactor — thiamine won't work if hypomagnesemic); give folate + multivitamin

  • Treat empirically on clinical suspicion — do not await thiamine level or MRI

  • Supportive: manage alcohol withdrawal (benzos), nutrition, fall precautions, aspiration precautions

  • Trend: ophthalmoplegia (resolves first, within hours-days), then ataxia/confusion (slower); watch for Korsakoff

  • → ICU if: depressed consciousness/coma, hemodynamic instability, or severe concurrent withdrawal (DTs)

Wernicke Encephalopathy

complete reference · incomplete triad · empiric high-dose thiamine · thiamine-before-glucose · Korsakoff · Full Card

Symptoms / Associated Sx

  • Classic triad: encephalopathy (global confusion, apathy, inattention, disorientation), oculomotor dysfunction (horizontal nystagmus, bilateral lateral rectus/CN VI palsy, conjugate gaze palsies), and gait ataxia (wide-based, from vermian/vestibular involvement). The complete triad is present in only ~10–30% of cases — relying on it causes missed diagnoses. Any single component in an at-risk patient warrants treatment.

  • If untreated, progresses to Korsakoff syndrome — a largely irreversible anterograde and retrograde amnesia with confabulation. Wernicke is the acute, treatable phase; Korsakoff is the chronic, often permanent sequel.

Neg

  • No fever, meningismus, or photophobia — argues against CNS infection (but a low threshold to investigate if febrile)

  • No focal motor deficit or aphasia — argues against stroke (WE signs are symmetric/global; focal findings → image)

  • Asterixis and hyperammonemia absent (or, if present, coexisting) — argues against hepatic encephalopathy as the sole cause (both occur in alcoholics; treat for both)

  • Picture not explained by intoxication or hypoglycemia alone — those will not resolve the ophthalmoplegia/ataxia, which thiamine does (a therapeutic response supports the diagnosis)

Social History (SHx)

  • Chronic heavy alcohol use is the most common context — but Wernicke is NOT only an alcoholic disease.

  • Non-alcoholic causes: hyperemesis gravidarum, bariatric/GI surgery, prolonged vomiting or starvation, anorexia, malabsorption, dialysis, advanced malignancy/chemotherapy, prolonged unsupplemented parenteral nutrition, and refeeding.

Main Etiology

  • Deficiency of thiamine (vitamin B1), a cofactor for enzymes central to cerebral glucose metabolism (transketolase, pyruvate dehydrogenase, α-ketoglutarate dehydrogenase). Deficiency causes energy failure and injury in highly metabolically active, thiamine-dependent regions — mammillary bodies, medial thalami, periaqueductal gray, and cerebellar vermis. Administering glucose without thiamine consumes remaining stores and can precipitate or worsen the syndrome.

RF

  • Modifiable: ongoing alcohol use, poor nutritional intake, administration of IV dextrose without thiamine, non-adherence with post-bariatric supplementation.

  • Non-modifiable: malabsorptive states, hyperemesis, malignancy, critical illness with high metabolic demand.

Data

  • Wernicke is a clinical diagnosis — treat empirically and do NOT wait for confirmatory testing.

  • Serum thiamine / erythrocyte transketolase activity (supportive; do not delay treatment for results, and normal levels don't exclude it)

  • MRI brain (symmetric T2/FLAIR signal in mammillary bodies, medial thalami, periaqueductal gray, tectal plate; contrast enhancement of mammillary bodies is fairly specific — but sensitivity is limited, so a normal MRI does not rule it out)

  • Glucose, CMP, magnesium (magnesium is a required cofactor for thiamine-dependent enzymes — hypomagnesemia causes refractoriness; replete it)

  • Workup for alternative/coexisting causes of altered mental status as clinically indicated.

DDx

Alcohol intoxication / withdrawal (timing; won't resolve with thiamine) · hepatic encephalopathy (asterixis, hyperammonemia — frequently coexists) · structural lesion / stroke (focal, imaging) · CNS infection (fever, CSF) · other nutritional deficiency (B12, niacin) · delirium from other cause · posterior circulation stroke (can also cause ophthalmoplegia + ataxia)

Home Meds

  • Ensure thiamine is given before any glucose-containing fluids or nutrition — a standing principle for every at-risk patient.

  • Replete magnesium and provide folate and a multivitamin; reconcile and address the precipitating nutritional state.

Plan

Consults

  • Neurology — confirm, assess for Korsakoff, guide treatment.

  • Nutrition / dietitian — repletion plan, refeeding precautions.

  • Addiction medicine — if alcohol use disorder; GI/bariatric or OB if post-surgical or hyperemesis.

Thiamine repletion (do this first)

  • Thiamine (vitamin B1) before glucose, always. If both are needed urgently, give thiamine first or concurrently — never dextrose alone in an at-risk patient.

  • High-dose IV regimen: thiamine 500 mg IV three times daily for 2–3 days; if responding, 250 mg IV/IM once daily for 3–5 more days; then transition to oral thiamine 100 mg daily. The traditional single 100 mg dose is inadequate for established Wernicke — use treatment doses.

  • Replete magnesium (cofactor — thiamine is ineffective if hypomagnesemic); give folate and a multivitamin.

Supportive

  • Manage concurrent alcohol withdrawal with benzodiazepines (see alcohol withdrawal card); nutritional rehabilitation with attention to refeeding syndrome (monitor and replete phosphate, potassium, magnesium); fall and aspiration precautions.

Always

  • PT / OT eval and treat — gait/balance rehabilitation; functional and safety assessment.

  • Trend: the ocular findings respond first (often within hours to days), then ataxia and confusion improve more slowly and may be incomplete; watch for emerging Korsakoff amnesia; monitor magnesium and refeeding electrolytes.

  • Escalation triggers: depressed consciousness/coma → ICU · severe alcohol withdrawal/DTs → ICU · hemodynamic instability or aspiration → higher level of care.

  • Discharge checklist: continue oral thiamine 100 mg daily (often long-term) plus multivitamin/folate · alcohol-use-disorder treatment and referral · nutritional follow-up (and bariatric supplementation reinforcement if applicable) · counsel patient/family that some deficits (memory) may persist · neurology follow-up · document the diagnosis prominently so future dextrose is always thiamine-covered · return precautions.

Red Flags — ICU / Urgent

• Dextrose given before thiamine in an at-risk patient — can precipitate acute Wernicke; give thiamine immediately.
• Depressed consciousness/coma → ICU; consider other/coexisting causes.
• Severe alcohol withdrawal / delirium tremens concurrently → ICU.
• Refeeding syndrome during nutritional repletion (falling phosphate/potassium/magnesium) → monitor closely, replete.
• Evolving Korsakoff (fixed amnesia, confabulation) — signals delayed/inadequate treatment; maximize thiamine.

Senior IM Resident Pearls

• Thiamine before glucose — burn this in. A banana bag is not optional trivia: giving dextrose to a thiamine-deficient brain can trigger Wernicke. If you're reaching for D50, thiamine goes first or with it.
• The full triad is the exception, not the rule. Only a minority have all three findings. Treat on any one (confusion, eye signs, or ataxia) in an at-risk patient — the cost of thiamine is trivial, the cost of missing it is permanent.
• It's not only alcoholics. Hyperemesis gravidarum, bariatric surgery, starvation, and malignancy all cause it — don't anchor on a drinking history.
• Use real treatment doses. 500 mg IV TID for established disease, not a single 100 mg dose. Underdosing is a common and consequential error.
• Replete the magnesium — thiamine-dependent enzymes need it as a cofactor; thiamine "won't take" if the patient is hypomagnesemic.
• Don't wait for the MRI or the level. It's a clinical diagnosis; normal imaging and normal thiamine levels don't exclude it. Treat first.
• The eyes recover first. Resolving ophthalmoplegia within hours-days both confirms the diagnosis and is reassuring; ataxia and memory lag and may not fully recover.
• Common mistake: labeling the confused alcoholic as simply "intoxicated" or "withdrawing" and missing Wernicke — then watching it harden into Korsakoff. Give thiamine to essentially every at-risk altered patient.