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Wernicke's Encephalopathy - #MEDSHED

Writer's picture: Mark Nguyen, PharmD, BCEMPMark Nguyen, PharmD, BCEMP
Feb 5, 20241 min read
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šŸ”® Wernicke's Encephalopathy - #MEDSHED šŸ‘¹


Pathophysiology

Severe, life-threatening complication from thiamine (Vitamin B1) deficienc Thiamine deficiency results in dysregulation of the Krebā€™s cycle and pentose phosphate pathway Accumulation of toxic intermediate metabolites (lactate, glutamate), leading to cytotoxic edema Vasogenic edema develops from ATP depletion and disruption of blood-brain-barrier (BBB)


šŸ¤” Clinical Presentation

Classical triad of Wernickeā€™s Encephalopathy (WE) altered mental status , ataxia, and oculomotor abnormalities only found in up to 33% of patients Alcoholism contributes to a large portion of WE cases, but can also be caused by malnutrition and digestive disorders WE can manifest into permanent, irreversible neurologic deficits (Korsakof Syndrome)


šŸŒ Thiamine Replacement

The mainstay of therapy for WE is thiamine replacement and should be given with a high degree of clinical suspicion Dosing Thiamine 200 - 500 mg IV piggyback over 30 minutes Varying dosing recommendations Consider high-dose thiamine TID for three days in acute WE treatment


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Not medical advice. Educational purposes only. No relationships to report.


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