Background/Purpose: Wernicke’s encephalopathy (WE) was first characterized by Carl Wernicke in 1881 where he saw a constellation of symptoms: ataxia, nystagmus or ophthalmoplegia, and changes in mentation that was later termed “Wernicke’s Encephalopathy.” Mental status changes are associated with midline thalamic nuclei misconnections, ocular dysfunction result from lesions of the pontine tegmentum, and gait is caused from connections between the vestibular abnormalities and cerebellar vermis. Each of these parts require thiamine in several of its enzymatic reactions, emphasizing thiamine’s vitality in daily living. Several reports exist where all three symptoms of the classic triad of WE are not often seen. In fact, only 16-33% of patients show the triad on initial examination. Other ways WE manifests include appetite loss persisting for several weeks or hyperemesis gravidarum. These non-classical symptoms complicate diagnosis, increase the chance of developing Wernicke Korsakoff syndrome, and provide reasoning for its prevalence even after its original identification over two centuries ago. WE still exists today with a prevalence in the general population estimated from 0.4 – 2.8%. Stronger identification of risk factors and prevention methods are key to reducing prevalence and would serve as progress in the scientific community. Goals: The creation of risk awareness and establishment of practical considerations of predisposing factors outside of the classic triad to consciously observe for to administer thiamine preemptively. Methods/Design: The Cerner EMR from Regional One Hospital in Memphis, Tennessee was examined to identify individuals diagnosed with Wernicke’s Encephalopathy. In data collection for these patients, risk factors, existing diagnoses, and symptoms were recorded to have a complete understanding of the patients’ reasons for developing WE. Results/Findings: 35 unique patient cases were identified, and a variety of causes and linkages were explored in data collection. Linked causes to the development of WE include alcoholism, pancreatitis, cachexia from malignancy, hyperemesis gravidarum, hepatitis C, and GI disease causing malabsorption, among others. Conclusions/Implication: In the conclusion of this retrospective case review, we plan to have recommendations based off the main risk factors established at hand. This will create practical considerations for the monitoring of thiamine levels alongside the adequate and timely administration of thiamine to preserve brain function.

 

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