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Updates in the Management of Diabetic
Ketoacidosis
Kathryn Evans Kreider, DNP, FNP-BC
ABSTRACT Diabetic ketoacidosis (DKA) is an emergency for people with diabetes characterized by hyperglycemia, metabolic acidosis, and ketosis. DKA onset and recurrence can largely be prevented through patient education. Nurse practitioners are well positioned to promote patient education, self-management, and individualized patient care. This article outlines updates in the clinical management of patients with DKA to optimize care and reduce costs.
Keywords: diabetes, diabetes mellitus, diabetic ketoacidosis, endocrine emergency, hyperglycemia Ó 2018 Elsevier Inc. All rights reserved.
D
iabetic ketoacidosis (DKA) is a metabolic derangement characterized by hyperglyce- mia, metabolic acidosis, and ketosis.^1 DKA occurs in patients with diabetes who have a lack of circulating insulin relative to physiologic requirement, such as in type 2 diabetes mellitus (T2DM), or absolute depletion, such as in type 1 diabetes mellitus (T1DM),^2 in the presence of increased counterregulatory hormones (cortisol, growth hormone, epinephrine, and glucagon). The lack of adequate insulin can occur from medication noncompliance, infection, or a precipitating pathologic event, such as a myocardial infarction, that causes an increased metabolic demand for insulin. The Centers for Disease Control and Prevention (CDC) United States Diabetes Surveillance System recently reported an increase in DKA episodes in the US between 2009 and 2014, with an average annual increase of 6.3%.^3 DKA can occur at any age but primarily occurs in those aged younger than 30 years (36% incidence) and between 30 and 50 years (27% incidence). 2 The highest incidence of DKA is for those aged between 11 and 15 years. 4 In addition, girls and women and the immigrant population are at higher risk. In the past, DKA had a fatality rate of 1% to 5%. Older adults and individuals who have comorbid risk factors are in the highest risk category. 1 In recent years, however, the overall mortality of DKA has
declined due to earlier detection and increased evidence-based management. In fact, the recent CDC US Diabetes Surveillance System report indi- cated that the mortality for DKA has decreased to 0.4%.^3 Episodes of DKA typically require an emergency department visit or hospital admission for the patient to receive insulin, intravenous (IV) fluids, and elec- trolyte correction. Hospital encounters can be costly, with recent reports suggesting that a single hospital encounter for DKA treatment can cost up to $17,500, 5 with an average length of stay of 3.4 days. Further, the annual direct and indirect cost of DKA treatment in the US exceeds $2.3 billion.^1 DKA and recurrent DKA are largely preventable through better outpatient management, patient ed- ucation, and promoting self-care behaviors.^6 Nurse practitioners (NPs) have an opportunity to educate patients about the risks of DKA, promote self- management, and offer patient-centered care. Pre- sented here is a review the management of DKA and updates in clinical care.
DIAGNOSIS The diagnosis of DKA is made based on the meta- bolic triad of high blood glucose (BG) levels (generally > 250 mg/dL), acidosis (pH < 7.2), and the presence of urine or serum ketones (Table).^5 Inpatient providers commonly rely on laboratory data
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to confirm DKA, whereas outpatient providers rely on history, presentation, BG levels, and urine ketones. Common presenting symptoms include abdom- inal pain and the classic triad of hyperglycemia symptoms: polydipsia, polyphagia, and polyuria. Physical examination findings can include any or all of tachycardia, hypotension, Kussmaul respirations, significant dehydration, or a change in mental status. 7 It is important to consider differential diagnoses of metabolic acidosis that may include lactic acidosis or hyperchloremic acidosis. Differential diagnoses for ketosis include starvation ketosis (dietary history, weight trends) or alcoholic ketoacidosis (alcohol consumption history), hyperemesis, isopropyl alcohol, or ketotic hypoglycemia.^1 Euglycemic DKA (euDKA), which occurs when the patient presents with acidosis and ketosis but has a glucose 200 mg/dL, has become an emerging concern. Causes of euDKA can include recent insulin administration, decreased caloric intake, substantial alcohol consumption, chronic liver disease, or rarely, glycogen storage issues. 8 In addition, there have been increasing reports of euDKA caused by a new class of drugs for diabetes, sodium glucose cotransporter 2 (SGLT-2) inhibitors. In May 2015, the US Food and Drug Administration added a warning about the risk of DKA with use of these drugs. One study suggested that the risk of DKA for patients using SGLT-2 inhibitors was twice as high as those prescribed a dipeptidyl peptidase IV inhibitor, after controlling for other risk factors, although the risk of hospitalization was low. 9 The exact cause of this relationship is unknown, but several theories include reduced insulin doses when SGLT-2 is
initiated, an increase in glucagon, or decreased excretion of ketone bodies.^1 Other related factors may be mild infection, increased activity, reduced food intake, or insulin reduction or omission. 10 Case reports of traditional and euDKA occurring while using SGLT-2 inhibitors has been shown in patients with T1DM and in those with T2DM.^11 Many patients with euDKA present with nausea and vomiting but are misdiagnosed due to the lack of clear glucose elevation.
DIAGNOSTIC WORKUP Providers in outpatient settings where laboratory re- sults are not readily available should rely on BG and ketone values for the initial diagnosis. BG values will typically be > 250 mg/dL, although up to 10% of patients in DKA may present with euDKA.^9 For this reason, some experts argue that the cutoff BG value for diagnosing DKA should be decreased to 200 mg/dL.^12 Ketone measurement is an important diagnostic component and severity classification of DKA for patients in the outpatient setting. Urine ketones will test positive, although may be as minimal as “trace” ketones. Urine dipsticks measure acetoacetate (AcAc)
and acetone but not b-hydroxybutyrate (b-OHB).
Given this, the measurement of AcAc in the urine tends to underestimate the severity of DKA, because
the ratio of AcAc to b-OHB can be 1:10 during
ketoacidosis.^13 Other limitations with urine ketone testing include lag time in change in urine ketones, difficulty obtaining urine from dehydrated patients, and subjective measurements by the patient. Many experts agree that measurement of blood or capillary ketones is preferred due to these limitations. 9
Table. Diagnosis of Diabetic Ketoacidosis 7
Variable
Diabetic Ketoacidosis Mild Moderate Severe Arterial pH 7.25-7.3 7- < 7.24 < 7. Serum bicarbonate, mEq/L 15-18 10- < 15 < 10 Urine ketones Positive (trace or higher) Positive Positive Serum ketones Positive Positive Positive Anion gap, mEq/L > 10 > 12 > 12 Mental status Alert Alert/drowsy Stupor/coma
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bradycardia, and lethargy, and other neurologic changes. 2
HYPERGLYCEMIA BG levels are typically > 250 mg/dL unless euDKA is present. Hyperglycemia is precipitated by an increase in catecholamines, such as growth hormone, cortisol, and epinephrine, that are released during periods of imminent physiologic stress. Catecholamines stimu- late the liver to produce more glucose, often making it difficult to reduce BG levels. The treatment of hyperglycemia should be initiated after fluid replacement has begun because the initiation of IV fluids can lower glucose significantly. For many patients with mild DKA, the administration of IV
fluids is enough to restore metabolic balance and clear the ketone bodies. Most patients with moderate to severe DKA require insulin to restore homeostasis. The current guidelines state that the most effective method of glucose reduction is IV insulin. 16 Most DKA algorithms recommend an IV bolus of 0.1 U/kg, followed by a continuous infusion of 0.1 U/kg/h. There is some evidence suggesting that the initial bolus does not improve patient outcomes, but this aspect remains controversial. 5 Recommendations for insulin dosing are found in Box 2. The cost of IV insulin treatment is significant because this requires admission to the intensive care unit in many facilities, substantially increasing the cost of hospitalization. Multiple studies have suggested
Box 2. Overview of Diabetic Ketoacidosis Management 5,
Intravenous fluids 1,000e2,000 mL 0.9% NaCl over 1e2 h. Continue 0.9% NaCl or switch to 0.45% NaCl at 250e500 mL/h depending on serum sodium. When BG level ¼ 200-250 mg/dL, change to 5% dextrose in 0.45% NaCl. Insulin Regular human insulin intravenous bolus of 0.1 U/kg (optional), followed by continuous insulin infusion at 0.1 U/kg/h. When BG 250 mg/dL, reduce insulin rate to 0.05 U/kg/h; thereafter, adjust rate to maintain glucose level at w200 mg/dL. Subcutaneous rapid-acting insulin might be an alternative to intravenous insulin in patients with mild-to-moderate DKA. Potassium Serum potassium (K+) level > 5.0 mEq/L (no supplement required; monitor every 2 hours) K+ level 3.3e5 mEq/L (add 20-40 mEq potassium chloride to replacement fluid) K+ level <3.3 mEq/L (hold insulin; give 20-30 mEq/h until > 3.3) Goal K+ level 4-5 mEq/L Oral potassium may be considered depending on patient status Bicarbonate Not routinely recommended. If pH < 6.9 consider 50 mmol/L in 500 mL of 0.45% normal saline over 1 hour until pH increases to 7. Transition to subcutaneous insulin Continue insulin infusion until resolution of ketoacidosis. To prevent recurrence of ketoacidosis or rebound hyperglycemia, continue intravenous insulin for 2e4 h after subcutaneous insulin (basal) is given. For patients treated with insulin before admission, restart previous insulin regimen and adjust doses as needed. For patients with newly diagnosed diabetes mellitus, start total daily insulin dose at 0.6 U/kg/d. Consider multidose insulin given as basal and prandial regimen.
BG ¼ blood glucose; DKA ¼ diabetic ketoacidosis.
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that rapid-acting subcutaneous (SQ) insulin, such as lispro or aspart, given every 1 to 2 hours, can be effective in the management of mild DKA.^1 SQ insulin can also be administered in lower levels of care, which can assist in the cost reduction of the hospitalization. In fact, using insulin analogs may reduce hospitalization costs by up to 30%.^1 An earlier study evaluating SQ vs IV regular in- sulin used 0.3 U/kg SQ rapid-acting insulin as a loading dose, followed by 0.1 U/kg/h until the BG was < 250 mg/dL. The dose was then reduced to 0.05 U/kg/h until the DKA resolved. Compared with IV insulin, there was no difference in length of stay or total amount of insulin needed.^19 Other more recent studies have supported these findings, including no difference in rates of hypoglycemia when using SQ insulin compared with IV insulin. 20,21^ Recommended doses of rapid-acting SQ insulin analogs are between 0.075 and 0.1 U/kg/h. This is similar to the recommended dose of IV insulin that is initiated in the hospital setting. Alternately, 0. to 0.2 U/kg can be administered every 2 to 3 hours.^22 For patients in DKA, the goal BG at the time of treatment is 150 to 200 mg/dL.^16
METABOLIC ACIDOSIS In the case of DKA, metabolic acidosis occurs when hyperglycemia precipitates an increase in free fatty acid breakdown, which produce ketone bodies when metabolized. These ketone bodies cause a decrease in the alkali reserve causing ketoacidosis. Metabolic acidosis can be determined by calculating the AG, the difference between serum cations and anions. 1 A normal AG level is < 9 mEq/L. Patients who present in DKA typically have an AG > 10 mEq/L. 16 Patients who present with symptomatic metabolic acidosis (Kussmaul respirations, confusion, lethargy) should be managed as high-acuity patients. The calculation of AG is (serum cations [sodium] e anions [chloride þ bicarbonate]). 1
ELECTROLYTE MONITORING Hyponatremia and hyperkalemia are the primary electrolyte abnormalities that occur in DKA. Hypo- natremia is caused when the acidosis precipitates a shift of potassium out of the intracellular space,
causing an influx of sodium into the cell and extra- cellular depletion of sodium. The opposite occurs with potassium: Acidosis causes extracellular shifts of potassium, creating high serum potassium levels but relative cellular depletion. In otherwise healthy pa- tients, hyponatremia and hyperkalemia are both generally resolved with fluid replacement. Patients in DKA may occasionally present with hypokalemia, particularly if they are taking diuretics or were vomiting. In the case of hypokalemia upon presen- tation, fluids and potassium replacement should be given before starting insulin because the insulin administration may cause a further drop in potassium levels. 1 Patients with severe hypokalemia require cardiac monitoring. Resolution of DKA occurs when BG is < 200 mg/dL and 2 of the following have occurred: a serum bicarbonate level 15 mEq/L, a venous pH > 7.3, and a calculated AG 12 mEq/L. 16 Box 2 contains a summary of recommendations regarding the treatment of DKA in adult patients. Comprehensive algorithms detailing the comprehensive management of DKA have been published elsewhere.1,
TREATING THE UNDERLYING PRECIPITANT Successful identification of precipitating factors is paramount to effective DKA management. Common triggers include medication noncompliance, infec- tion, myocardial infarction, pancreatitis, alcohol abuse, cerebrovascular accident, trauma, hyperthy- roidism, or new diagnosis of T1DM.^7 Any stress or inflammatory response in the body could trigger the production of ketones, resulting in DKA. Patients should be thoroughly evaluated for underlying causes based on history, presentation, physical examination, and laboratory findings. Patients with new-onset diabetes represent w20% of those presenting with DKA. 5 Newly diagnosed patients will require a comprehensive care plan, including diabetes education.
PREVENTION DKA commonly reoccurs in the same cohort of patients, and poor adherence to treatment is the number one precipitant of DKA in the US. 5 Discussing medication regimens, feasibility, cost, and patient satisfaction is imperative to encouraging
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- Barski L, Kezerle L, Zeller L, Zektser M, Jotkowitz A. New approaches to the use of insulin in patients with diabetic ketoacidosis. Eur J Intern Med. 2013;24:213-216.
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- AADE Practice Paper. Continuous subcutaneous insulin infusion (CSII) with and without sensor integration. American Association of Diabetes Educators, 2018. https://www.diabeteseducator.org/practice/practice-documents/practice -papers. Accessed May 17, 2018.
- Goldenberg RM, Berard LD, Cheng AY, et al. SGLT2 inhibitoreassociated diabetic ketoacidosis: clinical review and recommendations for prevention and diagnosis. Clin Ther. 2016;38:2654-2664.
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Kathryn Evans Kreider, DNP, FNP-BC, is from the Division of Endocrinology, Metabolism & Nutrition, Duke University Medical Center, and is an assistant professor at Duke University School of Nursing, Durham, NC. She is available at kathryn. evans@duke.edu In compliance with national ethical guidelines, the author reports no relationships with business or industry that would pose a conflict of interest.
1555-4155/18/$ see front matter © 2018 Elsevier Inc. All rights reserved. https://doi.org/10.1016/j.nurpra.2018.06.
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