If there’s one area of medicine that suffers from more dogma than any other, it’s toxicology.
I’m not razzing tox, I love tox. But management in toxicology usually = throw kitchen sink at patient, followed by a case report that concludes the last intervention done just prior to the patient improving is a new treatment for that toxicity. One of the biggest researchers I’ve published with once told me, “I don’t do case reports, that’s not real evidence based medicine”.
Over the next few weeks we’re going debunk a few of the best tox myths.
Before we get into myth #1, if you do not know about Leon Gussow’s blog at The Poison Review, you should check it out here.
The other day, a fellow EM resident asked me about one of my favorite toxicology related myths.
Will giving glucose before thiamine cause acute development or worsening of Wernicke’s encephalopathy?
Like most medical dogma, this teaching can be traced back to case reports/series and a few animal studies. This article from Schabelman and Kuo in JEM 2012 reviews the literature on this topic, and concludes that while prolonged (at least >24 hours and usually longer) administration of glucose without thiamine may worsen Wernicke’s, there is no evidence for the near instantaneous development of Wernicke’s that we are taught in medical school.
Reading some of the studies that form the basis of this concept is both enlightening and entertaining. One of the two studies that forms the basis of the Thiamine teaching comes from Drenick et al. in the NEJM, 1966.
In this case report, a morbidly obese man (180 cm, 335 lbs.) was starved for just under two months (Feb.25 to April 20th), on a 500 calorie per day diet with no vitamin supplementation. They measured daily thiamine in the urine and found it to be absent by 30 days. There were 4 others originally in the study who also had absent thiamine by 30 days.
The obese male developed nausea and required withdrawal from the study on April 20th, at which point they re-fed him with only glucose and orange juice for 13 days! Over that period, he developed worsening symptoms of Wernicke’s encephalopathy, and upon administration of thiamine, his symptoms resolve over a period of days.
The study that is most often cited regarding this myth is a 1981 article by Watson et al. This case series looked at 4 patients who were given between 24 hours and 5 days of glucose without thiamine and developed partial/complete Wernicke’s. These resolved either partially or fully with the administration of thiamine.
Finally, you may want to read this 1952 study by Phillips et al, if only to see what a crazy study design and lack of ethics looks like. The study design here could be called random case series, observational study or high school science project. They looked at 9 alcoholic patients with 6th nerve palsies other Wernicke’s symptoms (presumably, as this was pre-CT head era, these patients may have had chronic SDH for all we know) and then fed them glucose only diets for days. After a few days of getting worse, they’d start supplementing various quantities of thiamine, and some patients improved.
Bottom line: Giving glucose prior to thiamine will not precipitate an acute Wernicke’s encephalopathy. Prolonged administration (at least > 24 hours) of glucose only diets may worsen symptoms, but can then be reversed by giving thiamine.
Over the next few weeks, the site will be moving, so please bear with me.
Also, as there is so much great FOAM mythbusting going on out there, you may start to notice more short posts that collate already great FOAM resources.
Finally, there may be some guest bloggers coming on board in the near future, so you can look forward to an increased volume of posts here at SOCMOB.
Drenick et al. N Engl J Med 1966; 274:937-939
Watson AJ, Walker JF, Tomkin GH, Finn MM, Keogh JA. Acute Wernickes encephalopathy precipitated by glucose loading. Ir J Med Sci 1981;150:301–3.
Phillips GB, Victor M, Adams RD, Davidson CS. A study of the nutritional defect in Wernicke’s syndrome; the effect of a purified diet, thiamine, and other vitamins on the clinical manifestations. J Clin Invest 1952;31:859–71.
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