Diabetic Ketoacidosis (DKA): Etiology, Clinical features & Treatment

In insulin-dependent patients, diabetic ketoacidosis is characterized by hyperglycemia, ketonemia, and acidosis.

ETIOLOGY

Diabetic ketoacidosis is caused by a relative or absolute deficiency of insulin and increased levels of stress hormones (e.g., catecholamines, cortisol, growth hormone). Insulin deficiency leads to lipolysis, which in turn leads to the production of ketone bodies, resulting in acidosis.

PRECIPITATING FACTORS include lack of insulin, infection, injuries, emotional stress, alcohol use, myocardial infarction, and cerebrovascular accident.

CLINICAL FEATURES

1. Symptoms: Nausea, vomiting, abdominal pain, polyuria and polydipsia, and altered mental status.

2. Physical examination findings

a) Kussmaul respirations (i.e., rapid, deep breathing) may be noted, and the breath often smells like acetone.

b) Dehydration may be reflected by hypotension, reflex tachycardia, dry skin, and dry mucous membranes.

DIFFERENTIAL DIAGNOSES

Hypoglycemia, nonketotic hyperosmolar coma, isopropyl alcohol ingestion, alcoholic ketoacidosis, lactic acidosis, uremia, toxin ingestion, and starvation ketosis must be ruled out.

EVALUATION

Laboratory studies:

1. A provisional diagnosis can be obtained via blood gas and bedside glucose determinations.

a) There will be signs of hyperglycemia, which is indicated by a blood glucose level of at least 300 mg/dL.

b) Metabolic acidosis is demonstrated by a serum bicarbonate concentration of less than 15 mEq/L and a pH of less than 7.3.

2. A serum biochemical profile (including electrolytes, blood urea nitrogen [BUN], and creatinine levels), urinalysis, and ketone levels confirm the diagnosis.

a) Ketonemia results from -hydroxybutyrate and acetoacetate. Qualitative tests (e.g., the nitroprusside test) detect acetoacetate but not β-hydroxybutyrate.

b) Depending on the patient's level of hydration, electrolyte imbalances may exist.

3. Other studies, such as a complete blood count (CBC), a chest radiograph, or an electrocardiogram (ECG), may be indicated to identify precipitating causes.

THERAPY

1. Normal saline should be administered at an initial rate of 1 L/hour for the first 2 to 3 hours. The average fluid deficit is 5 to 10 L. Clinical response and urine output are the best indicators of fluid status.

2. Insulin is administered intravenously as a continuous infusion using a low-dose technique (i.e., 5 to 10 U/hour) until the ketonemia and acidosis have resolved.

3. Potassium (20 mEq/L) should be added to the intravenous fluids during early therapy to correct the profound potassium deficiency associated with diabetic ketoacidosis. During the first day of treatment, the patient usually requires 100 to 200 mEq of potassium.

4. Phosphate: Whether phosphate replenishment is required is debatable. Phosphate is given either orally or intravenously if the patient’s serum phosphate level decreases to below 1 mg/dL.

DISPOSITION

Most patients with diabetic ketoacidosis need to be admitted, often to an intensive care unit (ICU). In patients with mild diabetic ketoacidosis, the ketoacidosis may resolve in the emergency department. These patients should be placed under observation until any underlying precipitating causes can be ruled out.