Assessment of Wernicke's Encephalopathy
Wernicke's encephalopathy (WE) is a clinical diagnosis that should be suspected and treated immediately in any at-risk patient, even when the classic triad is absent, as waiting for diagnostic confirmation risks permanent neurological damage or death. 1, 2
Clinical Diagnosis: Key Features to Assess
The diagnosis is primarily clinical, based on recognizing the following features (though the complete triad is present in only 10% of cases): 3
Mental Status Changes
- Assess for confusion, disorientation, altered consciousness ranging from mild cognitive impairment to coma 1
- Look for impaired cognitive function that cannot be fully explained by other conditions like hepatic encephalopathy 1
- Note that mental status changes are variably present and may be the only presenting feature 3, 4
Ocular Abnormalities
- Examine for nystagmus, ophthalmoplegia, and conjugate gaze palsy 1
- These ocular findings are common but not universally present 1, 3
Gait and Cerebellar Dysfunction
Additional Clinical Red Flags
- Hypothermia, hypotension, and coma should raise immediate suspicion for WE 3
- Unexplained metabolic lactic acidosis may be present 1
Identify High-Risk Populations
Immediately suspect WE in patients with any of these risk factors: 1, 2
- Chronic alcohol use disorder 1, 6
- Post-bariatric surgery 7, 1
- Prolonged vomiting or dysphagia 1
- Hyperemesis gravidarum 1
- Malnutrition or poor oral intake 1
- Gastric carcinoma or pyloric obstruction 1
- Prolonged intravenous feeding without thiamine supplementation 1
- Chronic diuretic therapy or continuous renal replacement therapy 1
- Gastrointestinal surgical procedures 8, 9
Laboratory and Imaging Assessment
Laboratory Testing
- Order routine labs including blood glucose, electrolytes (especially potassium, magnesium, calcium), CBC, and liver function tests 1
- Measurement of thiamine diphosphate (ThDP) in whole blood or red blood cells can be useful, but never delay treatment while awaiting results 1
- Check lactate, pyruvate levels if available 1
Neuroimaging
- Brain MRI is the preferred imaging modality, showing T2 and FLAIR hyperintensities in characteristic locations 1, 8:
- MRI plays an important role especially in non-alcoholic WE with atypical presentations 9
- However, imaging should never delay treatment—treat first, image later 1
- CT is positive only in exceptional cases and is not reliable 4
Critical Differential Diagnoses to Exclude
Rule out these conditions that can mimic or coexist with WE: 1
- Hepatic encephalopathy (frequently coexists with WE and complicates diagnosis) 1
- Hypoglycemia 1
- Hyponatremia, hypokalaemia, hypomagnesaemia 1
- Uraemic encephalopathy 1
- Hypercapnia 1
- Korsakoff syndrome (characterized by anterograde amnesia and confabulation, often follows untreated WE) 1
Common Diagnostic Pitfalls to Avoid
- Failing to consider WE in non-alcoholic patients 1
- Waiting for laboratory confirmation before initiating treatment 1
- Assuming altered mental status is solely due to hepatic encephalopathy or alcohol withdrawal without ruling out WE first 1
- Missing the diagnosis because the classic triad is absent (present in only 10% of cases) 3
- Administering glucose-containing solutions before thiamine, which can precipitate or worsen WE 1, 2, 6
Immediate Treatment Protocol
When WE is suspected, administer thiamine immediately—overdiagnosis and overtreatment are preferred given thiamine's excellent safety profile: 3
- Give 500 mg thiamine IV three times daily for 3-5 days, followed by 250 mg IV daily for at least 3-5 additional days 1, 2
- Always administer thiamine BEFORE any glucose-containing IV solutions 1, 2, 6
- In patients about to undergo emergent general anesthesia with severe vomiting, test and treat for potassium deficiency 7
- Treat magnesium deficiency simultaneously, as it is required for thiamine utilization 5
- After parenteral treatment, transition to oral thiamine 50-100 mg daily 1