Esteban Schabelman1, Dick Kuo. 1. Department of Emergency Medicine, Howard County General Hospital, Johns Hopkins School of Medicine, Baltimore, MD, USA.
Abstract
BACKGROUND: The prevailing teaching in medical school curricula and in medical textbooks is that if thiamine deficiency is suspected, thiamine supplementation should be given before administering glucose. OBJECTIVE: We sought to evaluate the published evidence describing the commonly held belief that thiamine supplementation must be given before glucose in hypoglycemic patients to prevent Wernicke encephalopathy. METHODS: Articles were identified through computerized searches of MEDLINE and other online sources. Pertinent references were traced back to their sources and also included in the literature review. The quality and content of each article was evaluated by the authors using the American Academy of Emergency Medicine literature review guidelines. RESULTS: Nineteen papers were ultimately identified and evaluated. No evidence rose above the level of case report/series. There were 13 case reports/series, 4 animal studies, and 2 expert opinion articles. True clinical research about the question of whether or not a glucose load can precipitate acute onset of Wernicke encephalopathy is lacking. CONCLUSIONS: Mounting case report evidence suggests that prolonged glucose supplementation without the addition of thiamine can be a risk factor for the development of Wernicke encephalopathy. Based on our findings, a delay in giving glucose to hypoglycemic patients cannot be recommended at this time, although prompt thiamine supplementation after or concurrent with a return to normoglycemia is recommended.
BACKGROUND: The prevailing teaching in medical school curricula and in medical textbooks is that if thiamine deficiency is suspected, thiamine supplementation should be given before administering glucose. OBJECTIVE: We sought to evaluate the published evidence describing the commonly held belief that thiamine supplementation must be given before glucose in hypoglycemic patients to prevent Wernicke encephalopathy. METHODS: Articles were identified through computerized searches of MEDLINE and other online sources. Pertinent references were traced back to their sources and also included in the literature review. The quality and content of each article was evaluated by the authors using the American Academy of Emergency Medicine literature review guidelines. RESULTS: Nineteen papers were ultimately identified and evaluated. No evidence rose above the level of case report/series. There were 13 case reports/series, 4 animal studies, and 2 expert opinion articles. True clinical research about the question of whether or not a glucose load can precipitate acute onset of Wernicke encephalopathy is lacking. CONCLUSIONS: Mounting case report evidence suggests that prolonged glucose supplementation without the addition of thiamine can be a risk factor for the development of Wernicke encephalopathy. Based on our findings, a delay in giving glucose to hypoglycemicpatients cannot be recommended at this time, although prompt thiamine supplementation after or concurrent with a return to normoglycemia is recommended.