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Centre for Anaesthesia; g.ackland{at}medsch.ucl.ac.uk (Ackland) Department of Anesthesia; University College Hospital; London, UK (Smith, McGlennan)
To the Editor:
Hypoglycemia during general anesthesia is rarely reported in the nonpediatric, nondiabetic population. Here we report the unexpected development of intraoperative hypoglycemia in a 26-year-old Uzbekhastani male management consultant who presented emergently for maxillofacial surgery. He had no medical problems, allergies, significant family history, or previous problems during general anesthesia. Preoperative laboratory studies including liver function tests were normal. He was not intoxicated on admission and had not taken any other prohibited substances. A routine blood glucose level of 84 mg/dL had been recorded on the same morning of hospital admission. Because of other operating room emergencies, the patient arrived in the operating room having been NPO for 14 h; he last ate at midnight after the consumption of approximately two bottles of wine accompanying a meal during the course of the same evening. Five minutes after IV induction [fentanyl (100 µg), propofol (200 mg), and vecuronium (8 mg)] and maintenance of anesthesia (sevoflurane/air/oxygen:MAC 1.3), marked diaphoresis suddenly appeared. No change in blood pressure or heart rate was noted. No skin pallor or neurological, including pupillary abnormalities were noted. Both ETCO2 and esophageal temperature were within normal limits. Blood glucose was 35 mg/dL (Bayer Ascensia Elite glucometer, Bayer AG, Leverkusen, Germany). Exactly 30 mL of 50% glucose was administered IV where upon the profuse diaphoresis stopped. Blood glucose returned to, and remained within, normal limits thereafter. Emergence from anesthesia, extubation, and postoperative recovery were unremarkable. The patient had no neurological sequelae and was discharged home the next day.
Alcoholic hypoglycemia occurs in people who ingest alcohol after fasting long enough to make hepatic glucose production dependent on gluconeogenesis (1). In the absence of both gluconeogenesis and intestinal absorption of glucose, the liver contains enough glycogen to maintain normoglycemia for 8–10 hours. Hepatic alcohol oxidation increases the cytosolic ratio of reduced to oxidized nicotinamide adenine dinucleotide (NAD). Consequently, this reversed NAD ratio inhibits hepatic glucose release by inhibiting major plasma gluconeogenic substrates (lactate, alanine) for glucose synthesis. The incidence of ethanol-induced profound hypoglycemia is very low (2), with approximately 1% of patients with ethanol levels greater than 0.10% sustaining severe hypoglycemia (serum glucose <50 mg/dL). Recent studies confirm that cognitive dysfunction is the most sensitive marker of severe hypoglycemia (3). However, blood glucose levels may be close to, or within, the hypoglycemic range but not necessarily severe enough to elicit clinically obvious cognitive dysfunction (2,3). Because anesthesia masks cognitive dysfunction, the most sensitive clinical marker of hypoglycemia, anesthesiologists should have a low threshold for measuring blood glucose levels in starved patients with a history of significant alcohol intake.
REFERENCES
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