A 48-year-old man with chronic alcohol dependence is brought to the hospital by his family after they found him confused and ataxic 3 days after stopping alcohol. On examination, he is disoriented to time and place, has bilateral ophthalmoplegia (inability to abduct eyes), and nystagmus. His gait is wide-based and unsteady. What is the most appropriate immediate next step in management?

Explanation

## Wernicke Encephalopathy: A Medical Emergency The patient presents with the **classic triad of Wernicke encephalopathy**: 1. **Ophthalmoplegia** (bilateral inability to abduct eyes = CN VI palsy) 2. **Ataxia** (wide-based gait, unsteady) 3. **Confusion/disorientation** (acute encephalopathy) This is a **thiamine (vitamin B₁) deficiency syndrome** caused by chronic alcohol use and malnutrition. ### Pathophysiology ```mermaid flowchart TD A[Chronic alcohol use + malnutrition]:::outcome --> B[Thiamine depletion]:::outcome B --> C[Impaired pyruvate dehydrogenase]:::outcome C --> D[Reduced acetyl-CoA production]:::outcome D --> E[Decreased energy in brainstem/midbrain]:::outcome E --> F[Lesions in mammillary bodies, medial thalamus, periaqueductal gray]:::outcome F --> G[Ophthalmoplegia + Ataxia + Confusion]:::outcome ``` **Key Point:** **Wernicke encephalopathy is a medical emergency.** Mortality is 10–20% if untreated; permanent cognitive damage (Korsakoff syndrome) occurs in 80% of survivors if thiamine is delayed. **High-Yield:** **Immediate management:** - **IV thiamine 500 mg stat**, then 100 mg daily for 3–5 days - **Do NOT delay for imaging.** Clinical diagnosis is sufficient; thiamine is safe and must be given immediately - **Always give thiamine BEFORE glucose** in malnourished patients (glucose without thiamine can precipitate Wernicke) - Supportive care: ICU monitoring, correction of electrolytes (Mg²⁺, K⁺, PO₄³⁻) **Clinical Pearl:** Ophthalmoplegia is the **most reversible sign** if thiamine is given early (within hours to days). Ataxia and confusion improve more slowly. If thiamine is delayed > 1 week, permanent cognitive deficits (Korsakoff syndrome) are likely. **Mnemonic: WKS (Wernicke-Korsakoff Syndrome)** - **W**ernicke: acute, reversible (ophthalmoplegia, ataxia, confusion) - **K**orsakoff: chronic, often irreversible (anterograde/retrograde amnesia, confabulation) **Warning:** ~~MRI is not necessary~~ for diagnosis and **delays critical treatment.** Wernicke encephalopathy is a clinical diagnosis. MRI may show mammillary body atrophy or T2 hyperintensity in the medial thalamus, but these findings are not required to initiate thiamine. ~~Oral thiamine~~ is inadequate for acute Wernicke; **IV is mandatory** for rapid CNS penetration. ~~Lorazepam~~ addresses seizure risk, not the underlying thiamine deficiency. While supportive, it is not the primary intervention.