What you don't know about Wernicke's encephalopathy

Megan Spyres, toxicologist and emergency physician at LA County-USC, gives a primer on diagnosing and treating Wernicke's encephalopathy. The title of this post "What you don't know about Wernicke's encephalopathy" is more from my perspective than a commentary on what you, the listener, may know. After all, you might be a genius when it comes to this disease. For me, this has always been confusing and difficult to diagnose. So let's sharpen our clinical acumen and learn why neglecting thiamine can be a really bad thing. Special thanks to Dr. Anand Swaminathan for his journalistic excellence in putting together this interview.   Pathophysiology secondary to thiamine deficiency (vitamin B1). Thiamine is a cofactor for pyruvate dehydrogenase. This enzyme is needed to take glucose from anaerobic glycolysis into the Krebs cycle (where we make the majority of our ATP) pyruvate dehydrogenase converts pyruvate (the end product of glucose metabolism in glycolysis) to acetyl co-A. Acetyl co-A is the entry point into the Krebs Cycle. if there is no thiamine, there is no Acetyl co-A... no Krebs Cycle... no ATP. The heart and brain get quite upset and function poorly when they don’t have ATP we only have a few weeks of thiamine reserves (best case scenario) Clinical Presentations Cardiac: Wet beriberi high output heart failure. Fatigue SOB, peripheral edema CNS: Wernicke's encephalopathy ophthalmoplegia ataxia altered mental status/confusion/memory problems Extra nuggets It would be nice, in a clinical sense, if patients presented with all elements of this triad, but the overwhelming majority do not (there may be just one or two) Wernicke's encephalopathy can progress to Korsakoff syndrome - an irreversible anterograde amnesia. May also include confabulation, apathy, lack of insight. In addition to the above findings, there may also be absent reflexes on physical exam How common is Wernicke's encephalopathy? estimated to be present in 2% of the US population Who is at risk? insufficient intake insufficient absorption enhanced elimination Specific groups who are at risk for thiamine deficiency Chronic Alcoholics: poor nutrition, poor absorption Bariatric surgery, AIDS, malignancy, hyperemesis gravidarum Insufficient intake: eating disorders, prisoners, institutionalized elderly Enhanced elimination: patients on furosemide Evaluating for Wernicke's encephalopathy It’s an easy disease to overlook. Consider in an alcoholic patients with multiple presentations with confusion Do a good neurologic exam. Don’t blow off persistent ataxia, especially when the intoxication has resolved to the point where the patient can be discharged In 1997, Caine et al suggested that the diagnosis could be made with two or more of the following: dietary deficiencies oculomotor abnormalities cerebellar dysfunction either an altered mental state or mild memory impairment Treatment give thiamine in the presence of ETOH, thiamine absorption is reduced by up to 50%. Don't think you will be able to rapidly correct this disease with PO treatment alone 100mg IV is good for prevention and might protect patients for at least a week. This dose is not, however, considered sufficient for treatment treat with  500mg IV thiamine three times daily  for 2-3 days, then 250mg IV TID for 3-5 days Does thiamine need to be given before glucose? a glucose load will increase thiamine requirements. historically, it has been thought that giving a load of glucose (or dextrose) might ‘push patients over the edge’ into encephalopathy. There’s no evidence that this occurs in patients who aren’t already overtly thiamine deficient. Bottom Line: Wernickes encephalopathy is easy to treat but also easy to miss. When we miss it, our patients can suffer

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