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Ketosis-Prone Type 2 Diabetes Treatment & Management

  • Author: Richard S Krause, MD; Chief Editor: George T Griffing, MD  more...
 
Updated: Jan 06, 2016
 

Approach Considerations

The treatment of patients who present with DKA is fairly standardized and does not differ according to their Aß phenotype. Detailed discussion of DKA treatment can be found in the following Medscape Reference articles: Diabetic Ketoacidosis and Pediatric Diabetic Ketoacidosis.

At the time of initial presentation with new-onset diabetes and DKA, determining what "type" of diabetes is present is not possible or needed; predicting the need for long-term insulin treatment is also impossible. Therefore, after an initial episode of DKA, all patients should be continued on insulin treatment for some period of time (typically weeks to months). Patients who are found to be ß- should be continued on insulin indefinitely.

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Patient Disposition

No generally accepted guidelines are available for disposition of DKA after initial treatment. Clinical experience and practice suggests that patients with mild DKA may be safely discharged with close follow-up after successful initial treatment. One large, multicenter study of US EDs found that 13% of patients were discharged; approximately one fourth were admitted to an ICU.[8] Appropriate initial treatment may decrease length of stay and the need for ICU admission.[9]

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Long-Term Monitoring

Patients who are ß+ need outpatient assessment of the need for long-term insulin treatment. If glucose levels are under control on an insulin regimen, the dose of insulin can be decreased by 50% and the patient reassessed at 1-2 weeks. If glycemic control is maintained, insulin can be discontinued with close monitoring. Other agents can be continued or added as needed. New onset of diabetes, older age at onset and higher levels of ß cell function all are associated with less likelihood of requiring long-term insulin treatment.

For newly diagnosed patients discharged after a first episode of DKA, a typical insulin regimen is a total of 0.6-0.7 units of insulin/kg/d. Typically, two thirds of the total daily dose is given before breakfast, and one third is given before dinner. Two thirds of the dose is given as intermediate-acting insulin (NPH), and one third is given as short-acting (regular insulin).

Long-term management of diabetes is discussed in the following Medscape reference articles: Type 1 Diabetes Mellitus, Type 2 Diabetes Mellitus, Pediatric Type 1 Diabetes Mellitus, and Pediatric Type 2 Diabetes Mellitus.

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Contributor Information and Disclosures
Author

Richard S Krause, MD Senior Clinical Faculty/Clinical Assistant Professor, Department of Emergency Medicine, University of Buffalo State University of New York School of Medicine and Biomedical Sciences

Richard S Krause, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

George T Griffing, MD Professor Emeritus of Medicine, St Louis University School of Medicine

George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science, International Society for Clinical Densitometry, Southern Society for Clinical Investigation, American College of Medical Practice Executives, American Association for Physician Leadership, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical and Translational Research, Endocrine Society

Disclosure: Nothing to disclose.

References
  1. Umpierrez GE, Smiley D, Kitabchi AE. Narrative review: ketosis-prone type 2 diabetes mellitus. Ann Intern Med. Mar 7 2006. 144(5):350-7. [Medline].

  2. Maldonado M, Hampe CS, Gaur LK, et al. Ketosis-prone diabetes: dissection of a heterogeneous syndrome using an immunogenetic and beta-cell functional classification, prospective analysis, and clinical outcomes. J Clin Endocrinol Metab. Nov 2003. 88(11):5090-8. [Medline].

  3. Umpierrez GE, Woo W, Hagopian WA, Isaacs SD, Palmer JP, Gaur LK, et al. Immunogenetic analysis suggests different pathogenesis for obese and lean African-Americans with diabetic ketoacidosis. Diabetes Care. 1999 Sep. 22 (9):1517-23. [Medline].

  4. Hampe CS, Nalini R, Maldonado MR, Hall TR, Garza G, Iyer D, et al. Association of amino-terminal-specific antiglutamate decarboxylase (GAD65) autoantibodies with beta-cell functional reserve and a milder clinical phenotype in patients with GAD65 antibodies and ketosis-prone diabetes mellitus. J Clin Endocrinol Metab. 2007 Feb. 92 (2):462-7. [Medline].

  5. Brooks-Worrell BM, Iyer D, Coraza I, Hampe CS, Nalini R, Ozer K, et al. Islet-specific T-cell responses and proinflammatory monocytes define subtypes of autoantibody-negative ketosis-prone diabetes. Diabetes Care. 2013 Dec. 36 (12):4098-103. [Medline].

  6. Balasubramanyam A, Garza G, Rodriguez L, et al. Accuracy and predictive value of classification schemes for ketosis-prone diabetes. Diabetes Care. Dec 2006. 29(12):2575-9. [Medline].

  7. Mauvais-Jarvis F, Sobngwi E, Porcher R, et al. Ketosis-prone type 2 diabetes in patients of sub-Saharan African origin: clinical pathophysiology and natural history of beta-cell dysfunction and insulin resistance. Diabetes. Mar 2004. 53(3):645-53. [Medline].

  8. Ginde AA, Pelletier AJ, Camargo CA Jr. National study of U.S. emergency department visits with diabetic ketoacidosis, 1993-2003. Diabetes Care. Sep 2006. 29(9):2117-9. [Medline].

  9. Bull SV, Douglas IS, Foster M, Albert RK. Mandatory protocol for treating adult patients with diabetic ketoacidosis decreases intensive care unit and hospital lengths of stay: results of a nonrandomized trial. Crit Care Med. Jan 2007. 35(1):41-6. [Medline].

 
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