Diabetic Ketoacidosis: What Goes Up Must Eventually Come Down

Diabetes is one of the most common and chronic illnesses in the United States, affecting about 30 million people. Among this group, about two-thirds of the individuals know they have diabetes and the remaining one-third are unaware.¹Type 2 diabetes (T2D) accounts for more than 95% of all cases of diabetes and type 1 diabetes (T1D), just 5%. The most recent available international data from between 2000 and 2008 indicate that T1D rose by an average 3.5% compared with more than 20% in the United States.²

Both types of diabetes can cause problems, but the most life-threatening complications of T1D are from diabetic ketoacidosis (DKA). DKA is the most frequent cause of death in people with T1D who are younger than 40 years,^1,3,4-6but it is uncommon in people with T2D. This condition costs nearly $2 billion annually⁶and is a recurrent reason for hospitalizations. The overall rise in T1D coincided with a slight decline in hospitalizations for DKA from 2000 to 2008. However, between 2009 and 2014, hospitalizations for DKA again rose.^1,7Further consequences for patients admitted to the hospital with DKA include one-third requiring readmission and a risk of death that is 3 times greater in the subsequent 2 years than others with diabetes. Improved outpatient treatment and self-care could result in half of hospital DKA admissions being avoided.³

RISK FACTORS

DKA is characterized by ongoing high blood glucose levels caused by an insulin deficiency. The body tries to accommodate by increasing blood glucose production in the liver and converting tissues for energy use instead of glucose. Waste products of this metabolism include high amounts of ketones, metabolic acidosis, and uncontrolled hyperglycemia. The ketones build up and become toxic.^1,3,5Known risk factors for DKA include being young, mental health comorbidities, eating disorders,^2-4socioeconomic depravation,⁴and medication noncompliance.^5,7Certain illnesses that could cause infection are thought to predispose people to DKA, including the common cold, gastroenteritis, influenza, injury, and urinary tract infections.^3,6,7Medications that can contribute to the development of DKA include beta-blockers, glucocorticoids, thiazide diuretics, and some chemotherapeutics.⁷Insulin pump therapy also may increase the risk of DKA if the pump fails.⁸The results of one study found that the risk of DKA increased in December, potentially correlating with the rise in rich food and drinks during the holidays.⁷

CLINICAL PRESENTATION

A thorough and complete history is important to diagnose DKA, initiate treatment, and minimize potential consequences. The history should focus on possible precipitating factors. Patients with DKA often have a history of T1D, but it also can occur in those prone to ketosis with T2D.⁹In fact, DKA is the presenting complaint for nearly one-third of patients with T1D.

Frequent symptoms include the classic ones of diabetes: polydipsia, polyphagia, and polyuria, in addition to abdominal pain, diaphoresis, dry mouth, headache, nausea, tachycardia, and vomiting.^3,4,9,10Gastrointestinal complaints are found in about half of patients,⁷and fever can be seen in those with infection. In extreme cases, Kussmaul respirations⁴and the classic fruity breath odor are present.⁷A diagnosis of DKA is made with the following: pH <7.3, a serum bicarbonate level <18 mEq/L, hyperglycemia (typically >250 mg/dL), and presence of ketones in the blood or urine. Metabolic acidosis is often present with the preceding findings.^2,3,8,9

TREATMENT

Treatment should focus on identifying the trigger, replacing electrolytes and fluids, and insulin therapy.^4,5,7,10Recommended intravenous (IV) fluids should be isotonic, such as 0.9% normal saline or lactated ringers. Insulin should not be administered until at least an hour after fluid replacement has started and should be given by IV infusion. Lab work often includes a complete blood count, comprehensive metabolic pain, an arterial blood, serum ketones, hemoglobin A1C, fasting blood sugar,10 and serum osmolality.9 Blood and urine cultures and a chest x-ray should be considered, to rule out infection.⁴Potassium supplementation is often required,⁹and the routine use of sodium bicarbonate is not recommended.^2,5

COMPLICATIONS

Even with proper treatment, complications can occur. As insulin is usually needed, rebound hypoglycemia may occur.^7,11And cerebral edema is a serious consequence of DKA, killing up to a quarter of patients who develop it. In children, a quarter may have permanent nervous system damage.²Diabetes also is known to cause hypercoagulability and is a risk factor for thrombosis of the cerebral, coronary, mesenteric, and peripheral systems. Rare thrombotic complications may include a heart attack or stroke.¹²

CONCLUSIONS

DKA is a common and well-known diabetes complication. Because half of DKA hospital admissions can be prevented, it is important to have a collaborative relationship with patients’ endocrinologists or primary care providers for ongoing management of their diabetes.⁴

REFERENCES

1. Benoit SR, Zhang Y, Geiss LS, Gregg EW, Albright A. Trends in diabetic ketoacidosis hospitalizations and in-hospital mortality - United States 2000-2014.MMWR Morb Mortality Wkly Rep. 2018;67(12):362-365. doi: 10.15585/ mmwr.mm6712a3.
2. Zee-Cheng JE, Webber EC, Abu-Sultaneh S. Adherence to pediatric diabetic ketoacidosis guidelines by community emergency departments’ providers.Int J Emerg Med. 2017;10(1):11. doi: 10.1186/s12245-017-0137-8.
3. Mills LS, Stamper, JE. Adult diabetic ketoacidosis: diagnosis management and the importance of prevention.J Diabetes Nursing. 2014;18(1):8-12.
4. Mills LS. Garrett CJ. Preventing diabetic ketoacidosis: Bridging the gap between primary and secondary care.Diabetes & Primary Care. 2016;18(4):179-183.
5. Hamelin AL, Yan JW, Steill IG. Emergency department management of diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: national survey of attitudes and practice.Can J Diabetes. 2018;42(3):229-236. doi: 10.1016/j.jcjd.2017.05.005.
6. Bunn S, Halm M. Long-acting insulin on the road to recovery with diabetic ketoacidosis.Am J Crit Care. 2016;25(3):280. doi: 10.4037/ajcc2016681.
7. Fayfman M, Pasquel FJ, Umpierrez GE. Management of hyperglycemic crises diabetic ketoacidosis and hyperglycemia hyperosmolar state.Med Clin North Am. 2017:101(3):587-606. doi: 10.1016/j.mcna.2016.12.011.
8. Marvicsin DM, Jennings P, Ziegler-Bezaire D. What is new in diabetes technology?J Nurs Pract. 2017;13(3):205- 209. doi: 10.1016/j.nurpra.2016.12.025.
9. Elsevier Point of Care. Diabetic ketoacidosis: clinical overview. ClinicalKey website. clinicalkey.com/#!/content/ clinical_overview/67-s2.0-c416092c-b6d9-4626-818d-395e20544802. Published March 18, 2018. Accessed August 24, 2018.
10. Evans MM, Miller A, Favuzza A, Stombaugh N, Harrison G, Shaffer A. Diabetic ketoacidosis- A case study describing standards of care.Med Surg Nursing. 2016;25(3):8-10. 1
11. Butalia S, Johnson JA, Ghali WA, Southern DA, Rabi DM. Temporal variation of diabetic ketoacidosis and hypoglycemia in adults with type 1 diabetes: a nationwide cohort study.J Diabetes. 2016;8(4):552-558. doi: 10.1111/1753- 0407.12336.
12. DeMeulenaere S. Critical hospital event caused by uncontrolled diabetes.J Nurse Pract. 2014;10(3):205-206, 215- 218. doi: 10.1016/j.nurpra.2013.12.009.

Jenna Herman, DNP, APRN, FNP-BC, is the family nurse practitioner program coordinator and an assistant professor at the University of Mary in Bismarck, North Dakota. Her clinical practice includes the emergency department of a level II trauma center, correctional medicine, and locum tenens in primary care clinics, nursing homes, and hospitals across rural North Dakota.