Hyperglycemic Crisis in Adults: Pathophysiology, Presentation, Pitfalls, and Prevention
Michael Fowler



Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are acute and potentially life-threatening complications of diabetes. Although they have important differences, they both occur because of lack of insulin effect and can be considered two manifestations of the same underlying mechanism: insulin deficiency. Typically, patients with type 1 diabetes are more likely to exhibit DKA because of their absolute insulin deficiency, and patients with type 2 diabetes are more likely to experience HHS because of the presence of some insulin secretion. However, a significant number of patients stray from these patterns.2-4

Both of these conditions carry significant likelihood of morbidity and mortality, including cerebral edema, permanent neurological injury, and death. In large centers, the mortality rate for DKA is < 5%. However, the mortality rate for HHS is ~ 11%.4 With the potential for mortality and an incidence of ~ 100,000 cases of DKA per year, general physicians and physicians in training will be treating patients with these acute complications of diabetes not infrequently. It is important to be familiar with the pathophysiology, presentation, treatment, complications, and—perhaps most importantly—prevention of DKA and HHS.

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