Wernicke's encephalopathy (WE) is a neurological disorder caused by thiamine (vitamin B1) deficiency.
Clinical presentation typically includes ocular abnormalities, ataxia, and disturbances of consciousness.
Observation:
This report details three patients with Wernicke's encephalopathy.
Two patients received insufficient thiamine substitution, with one experiencing symptom resolution after adequate treatment.
The second patient's acute WE was a terminal event amidst other critical conditions.
Findings:
One patient developed WE despite adequate thiamine substitution, possibly due to hereditary factors.
WE can be a critical complication in patients with alcoholism, malnutrition, malabsorption, cancer, inflammatory conditions, severe illnesses, and those receiving parenteral hyperalimentation.
Implications:
Prompt thiamine substitution (at least 100 mg/day IV or IM) is crucial for preventing and treating Wernicke's encephalopathy.
Clinicians should maintain a high index of suspicion for thiamine deficiency in at-risk populations.
Understanding potential hereditary influences on WE development may inform personalized treatment strategies.