From the Guidelines
Diabetic ketoacidosis (DKA) presents with several characteristic clinical manifestations, including polyuria, polydipsia, polyphagia, Kussmaul respirations, fruity breath odor, signs of dehydration, abdominal pain, and mental status changes, as reported in the most recent study 1.
Clinical Manifestations
The clinical manifestations of DKA can vary, but common symptoms include:
- Polyuria, polydipsia, and polyphagia due to hyperglycemia
- Kussmaul respirations (deep, rapid breathing)
- Fruity breath odor from acetone
- Signs of dehydration, including dry mucous membranes and poor skin turgor
- Abdominal pain that can mimic an acute abdomen
- Mental status changes, ranging from mild confusion to lethargy and coma, as acidosis worsens
Laboratory Findings
Laboratory findings in DKA typically include:
- Hyperglycemia (blood glucose typically >250 mg/dL)
- Metabolic acidosis with low pH (<7.3) and low bicarbonate (<18 mEq/L)
- Elevated anion gap
- Positive serum and urine ketones
- Electrolyte abnormalities, particularly potassium depletion
- Patients may also present with tachycardia, hypotension, and hypothermia in severe cases
Importance of Early Recognition
Early recognition of these signs and symptoms is crucial for prompt diagnosis and treatment to prevent life-threatening complications, as emphasized in the study 1. The hyperglycemia creates an osmotic diuresis leading to dehydration and electrolyte imbalances, and the insulin deficiency leads to increased lipolysis and ketone body production, causing metabolic acidosis.
Management Goals
Management goals for DKA include restoration of circulatory volume and tissue perfusion, resolution of hyperglycemia, and correction of electrolyte imbalance and acidosis, as stated in the study 1. It is also essential to treat any correctable underlying cause of DKA, such as sepsis, myocardial infarction, or stroke.
Treatment Approach
In critically ill and mentally obtunded patients with DKA or hyperosmolar hyperglycemia, continuous intravenous insulin is the standard of care, as recommended in the study 1. Successful transition of patients from intravenous to subcutaneous insulin requires administration of basal insulin 2–4 h before the intravenous insulin is stopped to prevent recurrence of ketoacidosis and rebound hyperglycemia.
From the Research
Clinical Manifestations of DKA
- Polyuria and polydipsia are the most common symptoms of DKA, followed by nausea, vomiting, abdominal pain, weight loss, severe fatigue, dyspnea, and preceding febrile illness 2
- Hyperglycemia, ketone body formation, and metabolic acidosis are the characteristic features of DKA 3
- The clinical presentation of DKA can include weight loss, caused by hyperglycemia and acidosis 4
- A fruity odor of acetone on the patient's breath may suggest the presence of ketoacidosis 5
- Classical triad of symptoms associated with hyperglycemia are polyuria, polydipsia, and weight loss 5
Precipitating Causes and Complications
- Precipitating causes of DKA are usually infection or insulin omission 3
- DKA can be the initial presentation of diabetes mellitus or precipitated in known patients with diabetes mellitus by many factors, most commonly infection 6
- Complications of DKA can include cerebral edema, which is the most dreaded, albeit with low incidence 4
- Circulatory insufficiency with hypotension is not uncommon due to the marked fluid loss and acidemia 5
- Neurologic abnormalities may be seen, including lethargy, seizures, or coma 5
Diagnosis and Treatment
- DKA is diagnosed by the triad of hyperglycemia, metabolic acidosis, and elevated serum or urine ketones 2
- However, hyperglycemia has been de-emphasized in recent guidelines because of the increasing incidence of euglycemic DKA 2
- Treatment involves fluid and electrolyte replacement, insulin, treatment of precipitating causes, and close monitoring to adjust therapy and identify complications 2
- Mainstays of therapy are intravenous insulin and fluid replacement, as well as the concomitant treatment of the precipitating factors 3
- Therapy must be directed toward each of the metabolic disturbances: hyperosmolality, ketoacidosis, hypovolemia, and potassium and phosphate depletion 5