Case Report 1358 www.thelancet.com Vol 372 October 11, 2008 Can glucose make you faint? Suehana Rahman*, Antonia I Scobie*, Mohamed Elkalaawy, Louise E Bidlake, Alberic G Fiennes, Rachel L Batterham In April, 2008, a 27-year-old woman came to the emergency department of her local hospital, with a 3-week history of dizziness, low appetite, and occasional vomiting. 2 months before, she had undergone an uncomplicated laparo- scopic proximal gastric bypass for obesity; on discharge, she was prescribed multivitamins and lansoprazole. She had sinus tachycardia, and was dehydrated. Doctors provisionally diagnosed gastric outflow obstruction. The patient was transferred to our unit for oesophagogastro- duodenoscopy—which showed nothing of note. Her total weight loss since surgery was 18∙9 kg. Blood tests showed sodium, urea, and creatinine concentrations of 155 mmol/L, 10∙4 mmol/L, and 155 μmol/L respectively, consistent with dehydration. We therefore administered intravenous fluids, including 5% glucose. Additionally, the patient drank high-sugar energy drinks. The next day, she said she felt light-headed; she fell in the shower. We found severe postural hypotension (blood pressure 122/79 mm Hg lying down, 75/35 mm Hg standing), and bilateral ankle oedema. An electrocardiogram (ECG) showed sinus rhythm, and inverted T waves in the lateral leads (figure); the serum concentration of troponin T was 0∙23 μg/L (normal range <0·01 μg/L). The patient rapidly developed nystagmus on lateral gaze, diplopia on central gaze, hyper-reflexia of the arms, weakness of the thighs, and patchy hypoaesthesia. She was not ataxic or confused. We diagnosed thiamine deficiency, and administered intravenous thiamine (500 mg, 8-hourly). Echocardio- graphy showed a left ventricular (LV) ejection fraction of 32%, moderately to severely impaired LV systolic function, diastolic dysfunction, and widespread marked hypokinesia. Within 24 h of thiamine being given, the diplopia, nystagmus, postural hypotension, and inversion of T waves resolved. We continued to administer thiamine intravenously for a further 3 days, before prescribing oral thiamine (100 mg, 8 hourly). In a blood sample taken before treatment began, the concentration of thiamine pyrophosphate (TPP), measured by high-performance liquid chromatography, 1,2 was 41 nmol/L (normal concen- tration 66–200 nmol/L). The patient admitted that she had not taken her multivitamins. We discharged her with a prescription for thiamine and multivitamins. 4 weeks later, echocardiography revealed a normal LV ejection fraction of 63%, with restoration of LV and diastolic function; the thiamine concentration in the blood was 218 nmol/L. When last seen, in August, 2008, the patient was well, with a body-mass index of 25∙2 kg/m². She was taking multivitamins. Thiamine is converted by the liver to TPP, an essential cofactor in carbohydrate metabolism. The CNS requires thiamine to maintain myelin, and synthesise acetyl- choline, γ-aminobutyrate, and glutamate. 3 Total body thiamine stores last 18–60 days; data on stores in obese patients are limited. Thiamine deficiency can cause wet beriberi, characterised by cardiovascular dysfunction; dry beriberi, of which peripheral neuropathy is the main feature; and Wernicke’s encephalopathy, an acute neuro- logical disorder characterised by nystagmus, diplopia, ophthalmoplegia (all three ocular signs are present in only 16% of patients), 2 ataxia, and confusion. 2–4 Worldwide, thiamine-fortification programmes have reduced the incidence of thiamine deficiency; however, outbreaks still occur among refugee populations. 2 In economically developed countries, thiamine deficiency is most com- monly associated with chronic alcoholism, but also occurs in people with habitually restricted diets, hyperemesis gravidarum, gastrointestinal disorders, malignancy, AIDS, severe infection, kidney disease—and after surgery for obesity. 2–4 Wernicke’s encephalopathy most commonly occurs 4–12 weeks after surgery, 4 mainly in people who have lost more than 7 kg per month. 2 Glucose admini- stration can cause thiamine deficiency to manifest acutely, perhaps by using up remaining thiamine stores. 5 If thiamine deficiency is suspected, thiamine should be administered before a patient is given glucose. References 1 Talwar D, Davidson H, Cooney J, O’Reilly DStJ. Vitamin B(1) status assessed by direct measurement of thiamin pyrophosphate in erythrocytes or whole blood by HPLC: comparison with erythrocyte transketolase activation assay. Clin Chem 2000; 46: 704–10. 2 Sechi G, Serra A. Wernicke’s encephalopathy: new clinical settings and recent advances in diagnosis and management. Lancet Neurol 2007; 6: 442–55. 3 Wilson RK, Kuncl RW, Corse AM. Wernicke’s encephalopathy: beyond alcoholism. Nat Clin Pract Neurol 2006; 2: 54–58. 4 Singh S, Kumar A. Wernicke encephalopathy after obesity surgery: a systematic review. Neurology 2007; 68: 807–11. 5 Corcoran TB, O’Hare B, Phelan D. Shoshin beri-beri precipitated by intravenous glucose. Crit Care Resusc 2002; 4: 31–34. Lancet 2008; 372: 1358 * These authors contributed equally Bariatric Unit, Division of Surgery, University College London Hospitals, London, UK (R L Batterham FRCPE, S Rahman MB, A I Scobie MB, M Elkalaawy MB, L E Bidlake RGN, A G Fiennes FRCS) and Centre for Diabetes and Endocrinology, Department of Medicine, University College London, London, UK (R L Batterham) Correspondence to: Dr Rachel L Batterham, Reader in Diabetes, Endocrinology and Obesity, Honorary Consultant, Centre for Diabetes and Endocrinology, Department of Medicine, University College London, Rayne Building, 5 University Street, London WC1E 6JJ, UK r.batterham@ucl.ac.uk A B V4 V5 V6 V4 V5 V6 Figure: Beriberi in the UK (A) Inversion of T waves, which (B) resolved within 24 h of commencing treatment with thiamine.