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GERICLINICS

GeriQBank · Paper II · Q27

Wernicke Encephalopathy

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Chapter
Neurological Emergencies, Encephalopathies and Toxidromes
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Answer

Textbook Core – 6 Points

1.

Definition. An acute, potentially reversible neuropsychiatric emergency caused by thiamine (vitamin B1) deficiency, with lesions in the mammillary bodies, medial thalami, periaqueductal grey matter and the floor of the fourth ventricle. If untreated, it progresses to the largely irreversible Korsakoff syndrome — together, the Wernicke–Korsakoff syndrome.

2.

Causes in the elderly. Chronic alcoholism is the classical cause, but in older adults the non-alcoholic causes dominate and are routinely overlooked: malnutrition and starvation, prolonged vomiting, bariatric surgery and gastrectomy, malignancy and chemotherapy, dialysis, prolonged parenteral nutrition without vitamin supplementation, severe systemic illness and sepsis, thyrotoxicosis, and critically — administration of glucose to a thiamine-deplete patient.

3.

Classical triad. Confusion, ophthalmoplegia and ataxia. However, the complete triad is present in only about 10–16% of cases, so waiting for it is a diagnostic error. Ocular signs: horizontal nystagmus, bilateral lateral rectus palsy and conjugate gaze palsy; the ataxia is predominantly truncal and affects gait. In older adults it frequently presents simply as unexplained delirium, apathy or “failure to thrive”.

4.

Caine criteria — the practical bedside rule. Diagnose (and treat) if any TWO of the following four are present: (i) dietary deficiency, (ii) oculomotor abnormality, (iii) cerebellar dysfunction, (iv) either altered mental state or mild memory impairment. This substantially increases sensitivity over the classical triad and should be quoted in the answer.

5.

Investigations. The diagnosis is clinical and treatment must never await results. Serum thiamine or erythrocyte transketolase activity may be sent, but take the sample before giving thiamine. MRI (about 53% sensitive, 93% specific) shows symmetrical T2/FLAIR hyperintensity of the medial thalami, periaqueductal grey, mammillary bodies and tectal plate. Also check magnesium (an essential cofactor — thiamine will not work while hypomagnesaemia persists), sodium, glucose, liver function and vitamin B12.

6.

Treatment. Give parenteral thiamine BEFORE any glucose load. Standard regimen: thiamine 500 mg IV three times daily for 2–3 days, then 250 mg IV/IM daily for 3–5 days, then oral 100 mg daily long term. Correct magnesium, give the remaining B-complex vitamins, treat the underlying cause and provide nutritional rehabilitation. Ocular signs improve within hours to days and ataxia over weeks, but confusion and memory often do not recover — about 80% of survivors develop Korsakoff syndrome with anterograde amnesia and confabulation.

Latest Update – 1 Point

7.

Reviews and practice guidance published 2023–2025 converge on three messages. First, the low-dose oral or 100 mg intramuscular thiamine still given in many hospitals is inadequate for suspected Wernicke encephalopathy — high-dose parenteral thiamine (500 mg IV three times daily) is the standard, and prophylactic parenteral thiamine (200–300 mg daily) should be given to any at-risk patient before glucose or refeeding. Second, there is growing emphasis on non-alcoholic Wernicke encephalopathy in older patients — after bariatric surgery, prolonged vomiting, chemotherapy and prolonged ICU stay — which is where most missed cases now occur. Third, magnesium must be corrected concurrently, or thiamine replacement fails.

Examiner’s Tip — Verbatim Mark-Earning Lines

“Never give glucose before thiamine in a malnourished or alcoholic patient — it can precipitate Wernicke encephalopathy.”

“The complete triad occurs in only 10–16% — use the Caine criteria (any two of four) and treat on suspicion.” “Wernicke encephalopathy is a clinical diagnosis and a therapeutic emergency; a normal MRI does not exclude it.” “Correct magnesium — thiamine cannot work without it.”

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