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Hyperosmolar Coma: Cellular Dehydration and the Serum Sodium Concentration

John T. Daugirdas, MD; Nouhad O. Kronfol, MD; Antonios H. Tzamaloukas, MD; and Todd S. Ing, MD
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Requests for Reprints: T.S. Ing, MD, Veterans Administration Hospital, Hines, IL 60141.

Ann Intern Med. 1989;110(11):855-857. doi:10.7326/0003-4819-110-11-855
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Nonketotic hyperosmolar coma is a syndrome found mostly in diabetic patients with marked hyperglycemia; the relative pathogenetic roles of hyperglycemia, hyperosmolality, and cellular (especially brain) dehydration in causing the comatose state have not been fully delineated (1-3). Examination of recent reports of dialysis patients with extreme hyperglycemia who were not comatose (4-6), and re-analysis of descriptions of nondialysis patients with nonketotic hyperosmolar coma (1) can help us better understand the proposed causes for hyperosmolar coma.

Hyperglycemia has an important indirect pathogenetic role (1-3); in patients with adequate renal function, hyperglycemia initiates an osmotic diuresis (7) that continues until stopped by


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