Diabetic Ketoacidosis

Early prevention, recognition and early management can improve clinical outcomes.

To view the Course Outline and take the test online, click here.

For a printer-friendly version of the exam you can print out, complete and mail in to ADVANCE, click here.

Learning Scope #374
1 contact hour
Expires Dec. 19, 2013

You can earn 1 contact hour of continuing education credit in three ways: 1) For immediate results and certificate; take the test online; grade and certificate are available immediately after taking the test. 2) Mail your completed exam (or a photocopy) along with the $8 fee (check or credit card) to ADVANCE for Nurses, Learning Scope, 2900 Horizon Dr., King of Prussia, PA 19406. 3) Fax the completed exam to 610-278-1426. If faxing or mailing, allow 30 days to receive certificate or notice of failure. A certificate of credit will be awarded to participants who achieve a passing grade of 70 percent or better.

Merion Matters, Inc. is an approved provider of continuing nursing education by the Pennsylvania State Nurses Association (No. 221-3-O-09), an accredited approver by the American Nurses Credentialing Center's Commission on Accreditation. Merion Matters Inc. is also approved as a provider by the California Board of Registered Nursing (No. 13230) and by the Florida Board of Nursing (No. 3298).

The goal of this continuing education offering is to provide nurses with current information on disease and nursing management of diabetic ketoacidosis (DKA) they can apply to their practice. After reading this article, you will be able to:

1. Discuss the physiological mechanisms that contribute to clinical manifestations of DKA.
2. Describe best practices used to treat DKA.
3. Develop an educational plan for patients with diabetes to prevent DKA.

Can you identify a prevalent chronic disease that is also listed as one of the top 10 causes of death? If your responses include diabetes mellitus you are correct. According to the CDC, it affects more than 25 million people in the U.S., and in 2007 it was listed as the seventh leading cause of death.1

However, 7 million of these individuals do not know they have the disease.1 They represent our undiagnosed population and are completely unaware this disease threatens to shorten their life. Many individuals find out they have diabetes after they present to the emergency department with life-threatening complications such as hyperglycemic hyperosmolar states or diabetic ketoacidosis (DKA).

The CDC reports that in 2005, there were more than 100,000 discharges with DKA as the primary diagnosis and more than 2,000 deaths were due to hyperglycemic crises.2 Nurses should be prepared to readily identify and treat DKA and educate patients on how to prevent this extreme hyperglycemic state. This article focuses on early prevention, recognition and initial management of DKA to improve clinical outcomes.

What Is Diabetes?

Diabetes mellitus (DM) is a term that represents a group of four disorders that share one common factor: glucose intolerance.3,4 Why an individual is intolerant to glucose helps determine which type of disorder is present. In type 1 diabetes, the patient develops an absolute insulin deficiency; however, in type 2 there is insulin resistance with a progressive insulin secretory defect. In gestational diabetes, the glucose intolerance occurs during pregnancy and may increase one's risk for developing type 2. The fourth disorder, other specific types, may stem from pancreatic disease, genetic defects or chemically induced dysfunction of beta cells. Despite having different etiologies, prolonged hyperglycemia is characteristic of all four types of DM.

The American Diabetes Association lists criteria for diagnosing diabetes which includes an A1c ≥6.5 percent, a fasting plasma glucose ≥126 mg/dL, a 2-hour plasma glucose level ≥200 mg/dL during an oral glucose tolerance test level or a random glucose levels ≥200 mg/dL in a patient with classic signs of hyperglycemia.3 The ADA says results should be confirmed unless the patient presents with unequivocal hyperglycemia.

Prolonged hyperglycemia in an individual with absolute or relative insulin deficiency has severe implications; this extreme hyperglycemic state is also known as DKA.4,5 While nurses may see DKA occurring more frequently in individuals with type 1 diabetes, they should also be mindful individuals with type 2 could develop DKA as well. When there is a relative deficiency of insulin, hormones that act antagonistically to insulin begin to rise. These counterregulatory hormones include: catecholamines, cortisol, glucagon and growth hormone, and they not only enhance glucose production (gluconeogenesis) but they lead to elevated serum glucose levels as well.

Fat Metabolism

When insulin levels are absent or deficient. the body may falsely assume the individual is in a fasting state. As a result, an emphasis in fat metabolism occurs. Fat metabolism in the absence of insulin can have deleterious effects. When insulin deficiency is profound, less glucose is taken up by cells (e.g., muscle, fat) and counter-regulatory hormones promote the breakdown of triglycerides.4,6 This results in an increase in free fatty acids. Beta-oxidation of free fatty acids will then result in ketone formation and a rise in serum ketone levels (hyperketonemia). Acetone, a type of ketone, has a distinct odor and may be smelled on a person's breath during ketosis.

While this fruity smell could be mistaken as something pleasant, it is a dangerous sign of DKA and warrants the attention of an astute nurse. Nurses should recall that when ketones are produced, bicarbonate is loss. The loss of bicarbonate also contributes to the development of metabolic acidosis.

Don't Miss Warning Signs

The classic signs of hyperglycemia are polyphagia, polydipsia and polyuria.4,6,7 When cells hunger for glucose, they signal the brain to induce eating (polyphagia). However, the cells are unaware there is plenty of glucose in the bloodstream and due to a total or partial lack of insulin, glucose can't enter the cell. As counter-regulatory hormones increase, a further rise in serum glucose levels occur and the individual becomes more and more hyperglycemic. The blood starts to thicken, causing serum osmolality levels to rise as well.

As a result of increased serum osmolality, individuals may start to complain of extreme thirst (polydipsia). The hyperosmolar state also contributes to osmotic dieresis, which causes the individual to void frequently (polyuria). This voided urine consists of large amounts of sodium, potassium, phosphate and magnesium, and patients are at risk for electrolyte imbalances and dehydration.

Although potassium is lost in the renal filtrate, serum potassium levels may appear normal despite a decrease in total body potassium levels. This stems from intracellular potassium shifting into the acidic intravascular compartment causing normal serum potassium levels. However, once acidosis is corrected and potassium is pushed back into the cells, patients may present with signs of hypokalemia. Nurses should be prepared to prevent this potential complication that occurs during DKA treatment.

DKA does not occur in every patient with type 1 diabetes. However, common precipitating factors include concurrent infection and missed insulin treatments.3,5,6 Sometimes DKA presents at the same time as type 1 diagnosis. Some patients with type 1 diabetes who use an insulin pump develop DKA if their pump runs out of or fails to deliver insulin.5 In type 2 diabetes, DKA may be precipitated by medications such as corticosteroids or concurrent illnesses that cause increased stress on the body (e.g., MI and pneumonia). Although not as common, DKA can also occur during pregnancy.

The mortality rate for DKA ranges as high as 10 percent with cerebral edema being a common cause of mortality in children.8 Patients who are not seen in the hospital are at a greater risk for dying. Nurses should be able to quickly identify the classic triad of DKA, which includes hyperglycemia, hyperketonemia and acidosis. Rapid identification is necessary to promote optimal outcomes. Patients who present with serum and urine ketones, a serum pH <7.30, a serum bicarbonate <15 mg/dL and a serum glucose >200 mg/dL meet the biochemical criteria for DKA. The degree of acidosis helps determine the severity of DKA. A venous pH <7.3 or bicarbonate <15 mmol/L is considered mild DKA. A pH <7.2 with a bicarbonate <10 mmol/L is moderate. Patients with a pH <7.1 and a bicarbonate <5 mmol/L are considered to have a severe form of DKA.5

Nurses should assess diabetic patients who are at risk for DKA for polyuria, polydipsia, dehydration, hyperglycemia and ketonuria. Other signs may include vomiting, abdominal pain, a flushed face, fruity breath and a change in mental status. Kussmaul respirations (rapid and deep respirations) may occur as the body attempts to get rid of excess acid. Patients who are dehydrated could also become tachycardic, hypotensive and go into shock. Patients who have abnormal skin turgor, sunken eyes, absent tears, dry mucus membranes or weak pulses may be more severely dehydrated.

Patients who are diagnosed with DKA will need both dehydration and hyperglycemia managed. Airway, level of consciousness, fluid and electrolyte status and blood sugars should be routinely assessed and documented. A baseline electrocardiogram is performed to evaluate potassium status and cardiac monitoring is used to assess for evidence of hyper or hypokalemia.

Nurses should be prepared to give oxygen, use the Glasgow coma scale to determine level of consciousness and watch closely for signs of cerebral edema (headache, bradycardia, increased blood pressure, vomiting and increased restlessness). Vital signs should be taken routinely. Nurses should start intravenous (IV) fluids to restore circulatory volume and correct electrolyte deficits.

During the first 24 hours, patients with severe dehydration may require more than over 6 L of fluid to replace existing and ongoing fluid losses. However, fluid resuscitation is reserved for patients requiring restoration of peripheral circulation and the possibility of over-hydration should be monitored.5,8 Nurses should also monitor for complications related to fluid volume excess. To avoid hypoglycemia and cerebral edema from a rapid drop in osmolality, glucose is added to IV solutions once the blood glucose level decreases to about 250 mg/dL.5 Initially, low-dose insulin is administered intravenously 1-2 hours after initiating fluid replacement. Subcutaneous insulin can be initiated once the patient is able to take oral fluids and ketosis has subsided.

Arterial blood gases and electrolyte levels are monitored closely. The administration of bicarbonate may rapidly reverse acidosis and trigger hypokalemia and fatal cardiac dysrhythmias. Thus, bicarbonate is reserved for select patients with severe acidosis.5,8 During insulin administration and hydration, further ketoacid production stops, bicarbonate levels rise, arterial pH returns to a normal level and potassium shifts back into the intracellular compartment. This could place the patient at risk for hypokalemia and patients may require IV potassium. Nurses must confirm the kidneys are functioning adequately with at least 30 mL of urine output/hour prior to infusing IV potassium.

Diabetic ketoacidosis has occurred less frequently in patients with diabetes who are aware of this extreme hyperglycemic state.6,7,9 Through education, nurses can empower individuals with diabetes to prevent DKA. Patients should be able to discuss how they plan to achieve and maintain target glucose levels, demonstrate the correct procedure for checking their urine for ketones and self-monitoring blood glucose levels, and verbalize when they should seek medical assistance.

Since illness with vomiting and diarrhea can precipitate DKA, nurses should instruct patients to check their urine for ketones and adjust their insulin dose during sick days. Sick-day management includes checking glucose levels every 2 hours and checking urine for ketones every 4 hours when blood glucose levels are greater than 240 mg/dL.7,10 Patients should continue with insulin administration and understand that higher insulin dosages may be needed during sickness. In the absence of vomiting or severe dehydration, patients can be taught to manage hyperglycemia and ketosis at home with provider supervision.

To reduce the risk for dehydration, patients should also be reminded of the importance of maintaining fluid intake during sick days. It should consist of both glucose and electrolytes and may include sports drinks like Gatorade, ice pops, Jello and fruit juices. Patients should continue to take their insulin to decrease their ketone levels. They should also be reminded of the importance of eating to prevent hypoglycemia from insulin administration.

Besides teaching patients about DKA prevention, nurses should help patients recognize the ABCs of DKA. Abdominal pain, breath that is fruity, complaints of nausea/vomiting, dehydration, elevated ketones and glucose levels, and fatigue are a few signs patients should be able to readily recall. Patients should be instructed to contact their healthcare provider immediately if high ketonuria occurs with or without hyperglycemia and vomiting.7 In addition, the importance of not exercising with ketonuria and blood sugar levels greater than 240 mg/dL should be emphasized. Blood sugars can rise to dangerously high levels due to the effects of counter-regulatory hormones and contribute to increased ketone levels in this setting.

Over the past 25 years, the prevalence of type 1 diabetes has doubled.3 What's more, obesity has caused a significant increase in type 2 diabetes as well. Although nurses are likely to care for more patients who have diabetes, the rate of complications does not have to increase. Nurses should have a primary goal of educating patients on glycemic control and how to prevent the extreme state of hyperglycemia: DKA.

To view the Course Outline and take the test online, click here.

For a printer-friendly version of the exam you can print out, complete and mail in to ADVANCE, click here.

References for this article can be accessed here.

Kenya V. Beard, an assistant professor at Hunter College, New York, NY, teaches pathophysiology and advanced health assessment. She also has her own clinical practice where she manages patients with acute and chronic illnesses. The author has completed a disclosure form and reports no relationships relevant to the content of this article.




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