Quantitative analysis of glucose loss during acute therapy for hyperglycemic hyperosmolar syndrome.
Four patients with severe hyperglycemia and hyperosmolality were studied to quantitate the major mechanisms responsible for the fall in blood glucose concentration. Insulin was not administered to any of these patients during the first 15 h of therapy. In each case, there was a fall in glucose concentration due to dilution; this was quantitated by chloride space analysis and accounted for 24-34% of the fall in concentration. The size of the glucose pool decreased for two reasons. Glucosuria accounted for the majority of the reduction in the size of the glucose pool in the patients with the smallest decrease in extracellular fluid (ECF) volume [and hence the best preserved glomerular filtration rate (GFR)]. In contrast, glucosuria was a less important factor in causing glucose loss in the patients with very low GFR values. The size of the glucose pool also decreased due to glucose metabolism that did not require exogenous insulin. Thus the fall in glucose concentration in the initial therapy in patients with the hyperglycemic hyperosmolar syndrome is multifactorial and is not absolutely dependent on exogenous insulin. Furthermore, the patients grouped in this diagnostic category represent a heterogeneous population with the common features of severe hyperglycemia, hyperosmolality, and a negative or weakly reactive test for serum ketones.
D000328:Adult; D000368:Aged; D001786:Blood Glucose / Q000378:metabolism; D003926:Diabetic Coma / Q000628:therapy*; D005260:Female; D005440:Fluid Therapy; D005943:Gluconeogenesis; D005947:Glucose / Q000378:metabolism*; D006029:Glycosuria; D006801:Humans; D006944:Hyperglycemic Hyperosmolar Nonketotic Coma / Q000378:metabolism / Q000628:therapy*; D009584:Nitrogen / Q000378:metabolism
D001786:Blood Glucose; D005947:Glucose; D009584:Nitrogen