Objectives: After reviewing this information, the reader should be able to:
Diabetic ketoacidosis (DKA) is a potentially life-threatening metabolic emergency that occurs as a complication of uncontrolled diabetes. Low serum insulin levels in DKA prevent glucose from entering the cells to perform normal metabolic functions, causing the cells to respond as if in a starvation state. DKA occurs mainly in patients with diabetes mellitus, type 1 (DM1), but it can affect patients with diabetes mellitus, type 2 (OM2) or, rarely, patients with gestational diabetes (i.e., pregnancy-induced diabetes). Most patients with DKA are seen in the emergency department and require admission to the ICU for close monitoring and management. Treatment includes insulin and glucose administration, fluid/electrolyte restoration, and resolution of the underlying cause.
Diabetic ketoacidosis (DKA) is a potentially life-threatening metabolic emergency that occurs as a complication of uncontrolled diabetes. Low serum insulin levels in DKA prevent glucose from entering the cells to perform normal metabolic functions, causing the cells to respond as if in a starvation state. The production of counter-regulatory hormones (e.g., catecholamines, cortisol, glucagon, growth hormone) in response to the low insulin levels exacerbates the perceived state of starvation. To compensate, the liver begins to break down stored glycogen and fat to produce glucose, which produces ketone acid byproducts that lead to metabolic acidosis and hyperlipidemia. Hyperventilation with deep, gasping breaths (i.e., Kussmaul respirations) can ensue as a compensatory mechanism to counteract the acidosis. The kidneys initiate osmotic diuresis to excrete the excess glucose that is entering the bloodstream. Unless impaired, the kidneys also excrete water and electrolytes, leading to dehydration and electrolyte imbalances. Blood becomes concentrated due to dehydration. Although electrolyte levels can be elevated according to the laboratory test results, the total body electrolyte stores in the tissues can be low. Electrolyte imbalances and hyperosmolarity (i.e., increased solution concentration expressed as osmoles of solute/kg of serum water) can result in cardiac arrhythmias and even coma. DKA in pregnancy can cause fetal distress, fetal malformation, fetal demise, and maternal mortality.
DKA occurs mainly in patients with diabetes mellitus, type 1 (DM1), but it can affect patients with diabetes mellitus, type 2 (DM2) or, rarely, patients with gestational diabetes (i.e., pregnancy-induced diabetes). Regardless of whether affected by DM1 or DM2, the patient can have impaired beta-cell (i.e., the pancreatic cells that produce insulin) function. Pregnant women have a reduced buffering capacity (i.e., the ability to compensate for pH imbalances), which makes them more susceptible to acidosis; they can be unable to produce enough insulin to meet fetal demands despite normal beta-cell function. The most common precipitating factors for DKA regardless of the type of diabetes are insulin administration errors, infection, and new-onsetdiabetes. Other known precipitating factors include medications (e.g., corticosteroids, thiazides, salicylates, atypical antipsychotics), recreational drug use, alcohol abuse, severe medical illness, starvation, surgery, trauma, pregnancy, and emotional stress. The severity of DKA does not correspond to the blood glucose level; pregnant women with DKA can even have normal blood glucose levels. Most patients with DKA are seen in the emergency department and require admission to the ICU for close monitoring and management. The differential diagnosis includes hyperglycemic hyperosmolar syndrome (i.e., a life-threatening diabetic emergency with similar symptoms but without ketoacidosis) and other types of acidosis. Treatment includes insulin and glucose administration, fluid/
electrolyte restoration, and resolution of the underlying cause. DKA is best prevented via patient education.
Facts and Figures
The reported incidence of DKA in adults with DM1 is 0–56 per 1,000 persons per year (Farsani et al., 2017). DKA incidence is 50% or 2 of every 100 persons with DM1. Approximately 20% of patients with DM1/DM2 initially present with DKA. DKA can occur at any age; 36% of cases occur in patients aged < 30 years, 27% occur in those aged 30–60 years, 23% occur in those aged 51–70 years, and 14% occur in those aged > 70 years (for information on DKA in children, see Quick Lesson About … Diabetic Ketoacidosis in Children ). DKA is the most common cause of death in patients with DM1 who are under the age of 40. The reported mortality rate for DKA is as high as 10%. There are more than 100,000 annual hospital admissions for DKA in the United States, and DKA accounts for 8–29% of all hospital admissions in patients with diabetes mellitus (DM).
Two primary risk factors for DKA include insulin dependence and age < 25 years. Other significant risk factors include Black race, chronic alcohol abuse, recreational drug use, and mental illness, all of which often result in noncompliance with drug regimens and/or drug-induced hyperglycemia. Additional specific medical risk factors include new-onset DM, infection, gastroparesis, pancreatitis, stroke, myocardial infarction, abdominal crisis, and trauma, but any severe medical illness can trigger DKA.
Signs and Symptoms/Clinical Presentation
Common signs and symptoms of DKA include polyuria (i.e., excessive urination), polydipsia (i.e., excessive thirst), nausea, emesis, abdominal pain, change in appetite, weakness, malaise, sudden weight loss, blurred vision, headache, drowsiness, fruity breath odor, dry mucous membranes, tachycardia, hypotension, and hypothermia. As DKA progresses, Kussmaul respirations and coma can develop. Fever can be present in patients with a coexisting infection.
Food for Thought
What Do I Need to Tell the Patient/Patient’s Family?
1. Butalia, S., Johnson, J. A., Ghali, W. A., & Rabi, D. M. (2013). Clinical and socio-demographic factors associated with diabetic ketoacidosis hospitalization in adults with type 1 diabetes. Diabetic Medicine, 30(5), 567-573. doi:10.1111/dme.12127 (R)
2. Canadian Diabetes Association Clinical Practice Guidelines Expert Committee. (2013). Clinical practice guidelines: hyperglycemic emergencies in Adults. Canadian Journal of Diabetes, 37, S72-S76. Retrieved from http://guidelines.diabetes.ca/App_Themes/CDACPG/resources/cpg_2013_full_en.pdf, doi:10.1016/j.jcjd.2013.01.023 (G)
3. Chico, M., Levine, S. N., & Lewis, D. F. (2008). Normoglycemic diabetic ketoacidosis in pregnancy. Journal of Perinatology, 28(4), 310-312. doi:10.1038/sj.jp.7211921 (C)
4. Cooper, H., Tekiteki, A., Khanolkar, M., & Braatvedt, G. (2016). Risk factors for recurrent admissions with diabetic ketoacidosis: A case-control observational study. Diabetic Medicine, 33(4), 523-528. doi:10.1111/dme.13004 (R)
5. Farsani, S. F., Brodovicz, K., Soleymanlou, N., Marquard, J., Wissinger, E., & Maiese, B. A. (2017). Incidence and prevalence of diabetic ketoacidosis (DKA) among adults with type 1 diabetes mellitus (T1D): A systematic literature review. BMJ Open, 7, e016587. doi:10.1136/bmjopen-2017-016587 (SR)
6. Gaillard, T. (2018). Assessment and management of patients with diabetes mellitus. In J. L. Hinkle & K. H. Cheever (Eds.), Brunner & Suddarth's textbook of medical-surgical nursing (14th ed., pp. 1483-1485). Philadelphia, PA: Wolters Kluwer. (GI)
7. Gosmanov, A. R., & Wall, B. M. (2017). Diabetic ketoacidosis. In E. T. Bope & R. D. Kellerman (Eds.), Conn's current therapy 2017 (pp. 257-260). Philadelphia, PA: Elsevier. (GI)
8. Kitabachi, A. E., Umpierrez, G. E., Miles, J. M., & Fisher, J. N. (2009). Consensus statement: Hyperglycemic crises in adult patients with diabetes. Diabetes Care, 32(7), 1335-1343. doi:10.2337/dc09-9032 (RV)
9. Lippman, M. J. (2018). Diabetic ketoacidosis. In F. J. Domino (Ed.), The 5-minute clinical consult standard 2018 (26th ed., pp. 286-287). Philadelphia, PA: Wolters Kluwer. (GI)
10. Mills, L. S., & Stamper, J. E. (2014). Adult diabetic ketoacidosis: Diagnosis, management and the importance of prevention. Journal of Diabetes Nursing, 18(1), 8-12. (R)
11. Palmer, C., & Jessup, A. (2012). Ketoacidosis in patients with type 2 diabetes. The Nurse Practitioner, 37(5), 13-17. doi:10.1097/01.NPR.0000413492.49324.97 (C)
12. Umpierrez, G., & Korytkowski, M. (2016). Diabetic emergencies – ketoacidosis, hyperglycaemic hyperosmolar state and hypoglycaemia. Nature Reviews. Endocrinology, 12(4), 222-232. doi:10.1038/nrendo.2016.15 (RV)
13. Whitlatch, H. B., Gaddam, S., & Ferri, F. F. (2018). Diabetic ketoacidosis. In F. F. Ferri (Ed.), 2018 Ferri's clinical advisor: 5 books in 1 (pp. 386-388). Philadelphia, PA: Elsevier. (GI)
14. Wisse, B. (2015, July 24). Diabetic ketoacidosis. MedlinePlus. Retrieved March 5, 2018, from http://www.nlm.nih.gov/medlineplus/ency/article/000320.htm (GI)