A diagnosis of diabetic ketoacidosis requires the patient's plasma glucose concentration to be above 250 mg per dL (although it usually is much higher), the pH level to be less than 7.30, and the bicarbonate
level to be 18 mEq per L or less. Beta-hydroxybutyrate is a better measurement of the degree of ketosis than serum ketones. Intravenous insulin and fluid replacement are the mainstays of therapy, with careful
monitoring of potassium levels. Phosphorous and magnesium also may need to be replaced. Bicarbonate therapy rarely is needed. Infection, insulin omission, and other problems that may have precipitated
ketoacidosis should be treated. Myocardial infarction is a precipitating cause of diabetic ketoacidosis that is especially important to look for in older patients with diabetes. Cerebral edema is a major complication
that occurs primarily in children. Education to prevent recurrence should be offered to all patients, including how to manage sick days and when to call a physician. (Am Fam Physician 2005;71:1705-14,
1721-2. Copyright© 2005 American Academy of Family Physicians.)
Many patients with diabetes die from diabetic ketoacidosis (DKA) every year. DKA is caused by reduced insulin levels, decreased glucose use, and increased gluconeogenesis from elevated counter regulatory hormones, including catecholamines, glucagon, and cortisol. DKA primarily affects patients with type 1 diabetes, but also may
occur in patients with type 2 diabetes, and is most often caused by omission of treatment, infection, or alcohol abuse.1 Use of a standard protocol provides consistent results in treating DKA.2 An evidence-based guideline
for the management of DKA from the American Diabetes Association (ADA) is the basis for much of this article.3
Initial Evaluation:
Initial evaluation of patients with DKA includes diagnosis and treatment of precipitating factors (Table 14-18). The most common precipitating factor is infection, followed by noncompliance with insulin therapy.3 While insulin pump therapy has been implicated as a risk factor for DKA in the past, most recent studies show that with
proper education and practice using the pump, the frequency of DKA is the same for patients on pump and injection therapy.
DIFFERENTIAL DIAGNOSIS
Three key features of diabetic acidosis are hyperglycemia, ketosis, and acidosis. The conditions that cause these metabolic abnormalities overlap. The primary differential diagnosis for hyperglycemia is hyperosmolar hyperglycemic state (Table 23,20), which is discussed in the Stoner article21 on page 1723 of this issue. Common problems that produce ketosis include alcoholism and starvation. Metabolic states in which acidosis is predominant include lactic acidosis and ingestion of drugs such as salicylates and methanol. Abdominal pain may be a symptom of
ketoacidosis or part of the inciting cause of DKA, such as appendicitis or cholecystitis. If surgery is necessary, the timing needs to be individualized for each patient with input from a surgical consultant.
SIGNS AND SYMPTOMS
DKA can develop in less than 24 hours. Metabolic changes occur one and one half towo hours earlier in patients who are managed only with a short-acting insulin such as lispro (Humalog).22 Patients with DKA usually present
with polyuria, polydipsia, polyphagia, weakness, and Kussmaul's respirations. Nausea and vomiting are present
in 50 to 80 percent of patients, and abdominal pain is present in about 30 percent.23 Coffee-ground emesis,
usually from hemorrhagic gastritis, occurs in about 25 percent of vomiting patients.3 Often, the patient's
breath will have a fruity odor. Body temperature usually is normal or low, even with an infection. If the patient's temperature is elevated, infection invariably is present.23 Signs of dehydration, such as dry mucous membranes, tachycardia, and hypotension, often are found. Most patients are about 10 percent dehydrated. Consciousness ranges from alert to confused to a comatose state in less than 20 percent of patients.3
