Abstract
Diabetic ketoacidosis (DKA) is an acute metabolic disorder that occurs in those with Type 1 diabetes mellitus (T1DM) and Type 2 diabetes mellitus (T2DM) which presents with persistent hyperglycemia (≥250 mg/ dL) leading to a high anion gap metabolic acidosis with ketosis in the setting of either a relative or absolute insulin deficiency. Evaluation for the precipitating cause of DKA, such as trauma, infection, pump malfunction or medication noncompliance is essential. While DKA can be life-threatening, and hospitalizations for DKA are on the rise, adverse outcomes are minimal if promptly treated with aggressive fluid resuscitation, adequate insulin therapy and close monitoring of electrolytes. Prevention of future episodes of DKA is reliant upon adequate patient and caregiver education with a focus on treatment strategies in acute illness or with travel. The aim of this article is to provide a comprehensive overview of the epidemiology, clinical presentation, pathophysiology, treatment and prevention of DKA.
Highlights
Diabetic ketoacidosis (DKA) is an acute metabolic disorder that occurs in those with Type 1 diabetes mellitus (T1DM) and Type 2 diabetes mellitus (T2DM) which presents with persistent hyperglycemia (≥250 mg/ dL) leading to a high anion gap metabolic acidosis with ketosis in the setting of either a relative or absolute insulin deficiency
Diabetic ketoacidosis (DKA) is an acute metabolic disorder which occurs in the presence of prolonged hyperglycemia due to the absence of insulin which leads to a significant increase in the amount of circulating ketone bodies, leading to ketoacidosis
DKA can develop in patients with Type 2 diabetes mellitus (T2DM) in the setting of relative insulin deficiency as well as in Type 1 diabetes mellitus (T1DM) due to relative or absolute insulin deficiency
Summary
Diabetic ketoacidosis (DKA) is an acute metabolic disorder which occurs in the presence of prolonged hyperglycemia due to the absence of insulin which leads to a significant increase in the amount of circulating ketone bodies, leading to ketoacidosis. DKA can develop in patients with Type 2 diabetes mellitus (T2DM) in the setting of relative insulin deficiency as well as in Type 1 diabetes mellitus (T1DM) due to relative or absolute insulin deficiency. In T1DM, DKA tends to occur at the onset of disease but may occur because of lack of insulin either from withdrawal or omission due to a variety of factors not limited to but including pump malfunction or misuse, increased insulin requirements during. Common triggers for the development of DKA and relative insulin deficiency in T2DM include infections, trauma, myocardial infarction, stroke, congestive heart failure, use of steroids as well as lack of adjustment of regimen in pregnancy and other conditions [1]. Use of sodium/glucose co-transporter 2 (SGLT2) inhibitors in patients with T2DM has been associated with increased incidence of DKA and a subsequent FDA issued advisory regarding their use [16]
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