- A life-threatening medical emergency in diabetics, which most commonly occurs in patients with type 1 diabetes
- Characterized by a biochemical triad of hyperglycemia, ketosis, and high anion gap metabolic acidosis
- Rarely, it can occur in the absence of hyperglycemia (i.e., euglycemic diabetic ketoacidosis [DKA]) during pregnancy and in individuals taking sodium-glucose cotransporter-2 (SGLT2) inhibitors (1).
- System(s) affected: endocrine/metabolic, neurologic
Incidence by age group: 1 to 17 years (10.1%), 18 to 44 years (53.3%), 45 to 64 years (27.1%), 65 to 84 years (8.7%), and >85 years (0.8%)
Etiology and Pathophysiology
- Impaired glucose utilization secondary to insulin deficiency leading to the activation of counter regulatory mechanisms (gluconeogenesis, glycogenolysis, proteolysis) which further increase blood glucose level and trigger ketone bodies production. Resulting ketonemia and hyperglycemia lead to osmotic diuresis, dehydration, electrolytes disturbances and acidosis.
- Leading causes include medication noncompliance and infection. Other precipitating factors are:
- First presentation of DM
- Myocardial infarction (MI); cerebrovascular accident (CVA)
- Medications (corticosteroids, sympathomimetics, atypical antipsychotics, SGLT2 inhibitors)
- Alcohol and illicit drugs (cocaine)
- Trauma; surgery
- Emotional stress and psychiatric comorbidities
- Type 1 DM
- Ketosis-prone type 2 DM (Hispanic and African American ethnicity, G6PD deficiency)
- Euglycemic ketoacidosis specially with SGLT2 inhibitor drug use
- Close monitoring of glucose during periods of stress, illness, and trauma with “sick day” management instructions
- Careful insulin control and regular monitoring of blood glucose levels along with education on symptom recognition
Commonly Associated Conditions
>30% of patients have features of both DKA and hyperosmolar hyperglycemic syndrome (HHS).
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