Hyperglycemic Crises in Adult Patients With Diabetes

A consensus statement from the American Diabetes Association

  1. Abbas E. Kitabchi, PHD, MD1,
  2. Guillermo E. Umpierrez, MD2,
  3. Mary Beth Murphy, RN, MS, CDE, MBA1 and
  4. Robert A. Kreisberg, MD3
  1. 1Division of Endocrinology, Diabetes, and Metabolism, University of Tennessee Health Science Center, Memphis, Tennessee
  2. 2Clinical Research Center and Diabetes Unit, Grady Memorial Hospital/Emory University School of Medicine
  3. 3Teaching Faculty, University of South Alabama, Baptist Health System, Birmingham, Alabama
  1. Address correspondence and reprint requests to Dr. Abbas E. Kitabchi, Director, Division of Endocrinology, Diabetes and Metabolism, University of Tennessee Health Science Center, 956 Court Ave., Suite D334, Memphis, Tennessee 38163. E-mail: akitabchi{at}utmem.edu

Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are the two most serious acute metabolic complications of diabetes. Most patients with DKA have autoimmune type 1 diabetes; however, patients with type 2 diabetes are also at risk during the catabolic stress of acute illness such as trauma, surgery, or infection. Table 1 outlines the diagnostic criteria and electrolyte and fluid deficits for both disorders. The mortality rate in patients with DKA is <5% in experienced centers, whereas the mortality rate of patients with HHS still remains high at ∼11% (1–8). Death in these conditions is rarely due to the metabolic complications of hyperglycemia or ketoacidosis but rather relates to the underlying precipitating illness. The prognosis of both conditions is substantially worsened at the extremes of age and in the presence of coma and hypotension (7,9–11)

This consensus statement will outline precipitating factors and recommendations for the diagnosis, treatment, and prevention of DKA and HHS in adult subjects. It is based on a previous technical review and more recently published peer-reviewed articles since 2001, which should be consulted for further information.


Although the pathogenesis of DKA is better understood than that of HHS, the basic underlying mechanism for both disorders is a reduction in the net effective action of circulating insulin coupled with a concomitant elevation of counterregulatory hormones, such as glucagon, catecholamines, cortisol, and growth hormone (1,3,4,8–13). DKA and HHS can fall anywhere along the disease continuum of diabetic metabolic derangements. At one extreme, pure DKA without significant hyperosmolarity typically indicates the total or relative absence of insulin (seen in type 1 diabetes). At the other extreme, HHS without ketoacidosis typically occurs with lesser degrees of insulin deficiency, as seen in type 2 diabetes. However, …

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