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Paradoxical glucose infusion for hypernatraemia in diabetic hyperglycaemic hyperosmolar syndrome

2000; Wiley; Volume: 248; Issue: 2 Linguagem: Inglês

10.1046/j.1365-2796.2000.00710-2.x

1365-2796

Sho Tanaka, T. Kobayashi, Daiji Kawanami, Amane Hori, Minoru Okubo, K Nakanishi, Hideyuki Katori, Takayo Murase,

Hyperglycemia and glycemic control in critically ill and hospitalized patients

Journal of Internal MedicineVolume 248, Issue 2 p. 166-168 Free Access Paradoxical glucose infusion for hypernatraemia in diabetic hyperglycaemic hyperosmolar syndrome S. Tanaka, S. Tanaka Department of Endocrinology and Metabolism, and Okinaka Memorial Institute for Medical Research, Tokyo, JapanSearch for more papers by this authorT. Kobayashi, T. Kobayashi Department of Endocrinology and Metabolism, and Okinaka Memorial Institute for Medical Research, Tokyo, JapanSearch for more papers by this authorD. Kawanami, D. Kawanami Department of Endocrinology and Metabolism, andSearch for more papers by this authorA. Hori, A. Hori Department of Endocrinology and Metabolism, andSearch for more papers by this authorM. Okubo, M. Okubo Department of Endocrinology and Metabolism, and Okinaka Memorial Institute for Medical Research, Tokyo, JapanSearch for more papers by this authorK. Nakanishi, K. Nakanishi Department of Endocrinology and Metabolism, and Okinaka Memorial Institute for Medical Research, Tokyo, JapanSearch for more papers by this authorH. Katori, H. Katori Department of Nephrology, Toranomon Hospital; andSearch for more papers by this authorT. Murase, T. Murase Department of Endocrinology and Metabolism, and Okinaka Memorial Institute for Medical Research, Tokyo, JapanSearch for more papers by this author S. Tanaka, S. Tanaka Department of Endocrinology and Metabolism, and Okinaka Memorial Institute for Medical Research, Tokyo, JapanSearch for more papers by this authorT. Kobayashi, T. Kobayashi Department of Endocrinology and Metabolism, and Okinaka Memorial Institute for Medical Research, Tokyo, JapanSearch for more papers by this authorD. Kawanami, D. Kawanami Department of Endocrinology and Metabolism, andSearch for more papers by this authorA. Hori, A. Hori Department of Endocrinology and Metabolism, andSearch for more papers by this authorM. Okubo, M. Okubo Department of Endocrinology and Metabolism, and Okinaka Memorial Institute for Medical Research, Tokyo, JapanSearch for more papers by this authorK. Nakanishi, K. Nakanishi Department of Endocrinology and Metabolism, and Okinaka Memorial Institute for Medical Research, Tokyo, JapanSearch for more papers by this authorH. Katori, H. Katori Department of Nephrology, Toranomon Hospital; andSearch for more papers by this authorT. Murase, T. Murase Department of Endocrinology and Metabolism, and Okinaka Memorial Institute for Medical Research, Tokyo, JapanSearch for more papers by this author First published: 25 December 2001 https://doi.org/10.1046/j.1365-2796.2000.00710-2.xCitations: 8 Dr S. Tanaka, Department of Endocrinology and Metabolism, Toranomon Hospital, 2-2-2, Toranomon, Minato-ku, Tokyo 105-8470, Japan (fax: + 81 3-3582 7068; e-mail: [email protected]). AboutSectionsPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Dear Sir, Half (0.45%) or normal (0.9%) saline infusion is usually applied for the treatment of hyperglycaemic hyperosmolar syndrome (HHS) [1–3]. Half saline infusion sometimes induces hypernatraemia with a progressive hyperosmolar state and eventual mortal outcome [2–4]. We have succeeded in treating progressive hypernatraemia by using paradoxical glucose infusion instead of half saline infusion in a type 2 diabetic patient with HHS. A 21-year-old male patient was admitted with mild disorientation complaining of fatigability and with a history of polyuria. Several weeks before admission, he habitually drank 2 L or more of soft drinks. He had lost 12 kg of body weight during this period. On admission, his plasma glucose, sodium and osmolality were 80.6 mmol L–1, 165 mmol L–1 and 441 mmol kg–1, respectively. Half saline at a rate of 500 mL h–1 and continuous regular insulin infusion were started (Fig. 1, upper panel). There was a temporary improvement in his consciousness 2 h after initiation of insulin and half saline infusion. Eleven hours after initiation of infusion therapy, he became comatose again. At this time, his plasma glucose value decreased to 23.4 mmol L–1. However, his serum sodium level increased progressively up to 172 mmol L–1 (Fig. 1, middle panel). Despite his high blood glucose value, we tried to start an infusion of 5% glucose at a rate of 500 mL h–1 in order to improve the hypernatraemia that was estimated to be the cause of his unconsciousness. There was a remarkable improvement in the hypernatraemia, from 172 to 150 mmol L–1, and 3 h after initiation of the glucose infusion, he regained consciousness (Fig. 1, middle panel). Increased plasma renin and serum aldosterone levels improved remarkably after glucose infusion (Fig. 1, lower panel). Two-hour blood glucose values during 75 g oral glucose tolerance test were 12.7 mmol L–1 just before discharge and 9.5 mmol L–1 5 months after discharge. Figure 1Open in figure viewerPowerPoint Treatment and laboratory data after admission in a case with diabetic hyperglycaemic hyperosmolar syndrome. Upper panel: Insulin, fluid, sodium and glucose infusion rate. Middle panel: Changes in plasma glucose (○) and serum sodium (●) levels; Lower panel: Serum osmolality (▴), plasma renin (▪) and serum aldosterone (□) levels. Most patients with diabetic hyperosmolar coma can be treated with normal or half saline infusion [1–3]. However, in some cases, this therapy improves hyperglycaemia but reciprocally exaggerates hypernatraemia which causes disturbed consciousness [2–4]. In such circumstances, hypotonic water infusion through a central venous catheter [5] or water infusion through a nasogastric tube [6] has been proposed. However, hypotonic water infusion is related to haemolysis [5]. Intragastric infusion of water through a nasogastric tube is a potentially dangerous treatment in the comatose state because of the risk of aspiration. Paradoxical isotonic glucose infusion is an effective treatment regimen in HHS cases with exacerbated unconsciousness due to hypernatraemia during half saline infusion. A 5% glucose solution is isotonic so that it is easy and safe to administer through the peripheral venous route. Glucose infusion to HHS patients increased the plasma glucose value temporarily (Fig. 1, middle panel). However, glucose is finally metabolized to water after sufficient insulin infusion. The hypernatraemia that was induced by half saline infusion decreased progressively, and this patient regained consciousness. The mechanisms responsible for hypernatraemia in this case remain speculative. Firstly, high insulin infusion at the initial high dose of 10 U h–1 might have induced the hyperinsulinaemic state, exerting antinatriuretic action at the renal tubule [7]. Second, the exaggerated renin–aldosterone system observed in our case might have enhanced renal reabsorption of sodium and water [8]. Finally, along with a fall in blood glucose, water then escaped into dehydrated cells and the CNS, thereby causing a progressive elevation of extracellular sodium concentration [2–4]. Subsequently, adequate water replacement with isotonic glucose infusion improved intravascular volume depletion, as shown by the remarkable decrease in plasma renin and serum aldosterone levels in our case. References 1 Lorber D. Nonketotic hypertonicity in diabetes mellitus. Med Clin North Am 1995; 79: 39– 52. 2 Marshall SM, Walker M et al. Diabetic ketoacidosis and hyperglycaemic non-ketotic coma. In: KGMM Alberti, RA DeFronzo, H Keen, P Zimmet, eds. International Textbook of Diabetes Mellitus. Chichester: John Wiley & Sons, 1992; 1151– 64. 3 Alberti KGMM. Diabetic acidosis, hyperosmolar coma, and lactic acidosis. In: KL Becker, ed. Principles and Practice of Endocrinology and Metabolism. Philadelphia: J.B. Lippincott, 1995; 1316– 29. 4 To LB, Phillips PJ. Hyperosmolar non-ketotic diabetic coma – less sodium in therapy? Anaesth Intensive Care 1980; 8: 349– 52. 5 Worthley LI. Hyperosmolar coma treated with intravenous sterile water. A study of three cases. Arch Intern Med 1986; 146: 945– 47. 6 Feig PU. Hypernatremia and hypertonic syndromes. Med Clin North Am 1981; 65: 271– 90. 7 Quinones-Galvan A, Ferrannini E. Renal effects of insulin in man. J Nephrol 1997; 10: 188– 91. 8 Guyton AC. Renal and associated mechanisms for controlling extracellular fluid osmolality and sodium concentration. In: MJ Wonsiewicz, ed. Textbook of Medical Physiology. Philadelphia: W.B. Saunders, 1991; 308– 19. Received 18 February 2000; revision received 13 April 2000; accepted 3 May 2000. Citing Literature Volume248, Issue2August 2000Pages 166-168 FiguresReferencesRelatedInformation