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  • Diabetic ketoacidosis (DKA), hyperglycemic hyperosmolar nonketotic coma (HHNC), and hypoglycemia are life-threatening disorders of glucose metabolism.
  • Altered glucose metabolism should be considered in the differential diagnosis of all patients with mental status changes, neurologic deficits, and severe illness.
  • Therapy of DKA and HHNC requires replacement of deficits of fluids, electrolytes, and insulin.
  • Mixed-anion-gap acidosis and hyperosmolarity are encountered often in the same patient.
  • Continuous insulin therapy is essential in DKA.
  • In DKA and HHNC, careful physical examination and laboratory follow-up with a flow sheet make it possible to prevent the disastrous consequences of aggressive therapy—cerebral edema, pulmonary edema, hypoglycemia, hypokalemia, and hyperchloremic metabolic acidosis.
  • A search for the underlying cause of metabolic decompensation is required.
  • Therapy of hypoglycemia requires immediate establishment and maintenance of modest hyperglycemia (glucose concentration above 100 mg/dL or 5.5 mmol/L).


Diabetes mellitus and its major life-threatening complications—diabetic ketoacidosis (DKA), hyperglycemic hyperosmolar nonketotic coma (HHNC), and hypoglycemia—may precipitate or complicate critical illness. This chapter will focus on the management of DKA because it has been studied more exhaustively and because the same principles are applicable to HHNC. A brief review of the physiology and therapy of hypoglycemia will follow. These conditions have been the subject of other reviews.ch78ref1–9a,9b,9c


Currently, most patients with diabetes can be classified as having either type 1 diabetes (previously known as juvenile-onset, ketosis-prone, insulin-dependent, or brittle diabetes) or type 2 diabetes (previously, adult-onset, non-ketosis-prone, non-insulin-dependent, or obesity-related diabetes). Type 1 diabetes results from the autoimmune destruction of the insulin-secreting β cells in the pancreas, with consequent insulin deficiency. Most persons with type 1 diabetes present in childhood or early adulthood, although well-documented cases also have been described in the geriatric population. Hyperglycemia is usually not present until approximately 90% of insulin secretory capacity is lost. In times of stress (either physiologic or emotional), however, insulin requirements increase and often precipitate metabolic decompensation because of inadequate insulin secretory reserve. Patients with insulin deficiency require insulin therapy for survival. The half-life of insulin in the circulation is 7 minutes, and therapy for insulin deficiency requires continuous delivery of insulin to the circulation by infusion or by diffusion of insulin from depot injections.


The pathophysiology of type 2 diabetes is more heterogeneous. At presentation, persons with type 2 diabetes exhibit both tissue resistance to the action of insulin and a relative deficiency of insulin secretion. Insulin resistance can be overcome only by (1) increasing circulating insulin concentrations, with insulin (often at high doses) or sulfonylureas, (2) imposing calorie restriction, (3) instituting exercise, (4) administering certain antidiabetic medications (metformin and thiazolidine diones), or (5) treating reversible causes of the disease (e.g., obesity; hyperglycemia; sepsis; uremia; catecholamine; excess levels of glucocorticoids, growth hormone, or thyroxine; and antibodies to insulin or to the insulin receptor). Most persons with type 2 diabetes present in middle age and are overweight and sedentary. There is a growing prevalence of the disorder in ...

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