The American journal of emergency medicine · 2021
Euglycemic diabetic ketoacidosis: Etiologies, evaluation, and management.
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Long Brit, Lentz Skyler, Koyfman Alex, Gottlieb Michael
Аннотация
INTRODUCTION: Diabetic ketoacidosis is an endocrine emergency. A subset of diabetic patients may present with relative euglycemia with acidosis, known as euglycemic diabetic ketoacidosis (EDKA), which is often misdiagnosed due to a serum glucose <250 mg/dL.
OBJECTIVE: This narrative review evaluates the pathogenesis, diagnosis, and management of EDKA for emergency clinicians.
DISCUSSION: EDKA is comprised of serum glucose <250 mg/dL with an anion gap metabolic acidosis and ketosis. It most commonly occurs in patients with a history of low glucose states such as starvation, chronic liver disease, pregnancy, infection, and alcohol use. Sodium-glucose cotransporter-2 (SGLT2) inhibitors, which result in increased urinary glucose excretion, are also associated with EDKA. The underlying pathophysiology involves insulin deficiency or resistance with glucagon release, poor glucose availability, ketone body production, and urinary glucose excretion. Patients typically present with nausea, vomiting, malaise, or fatigue. The physician must determine and treat the underlying etiology of EDKA. Laboratory assessment includes venous blood gas for serum pH, bicarbonate, and ketones. Management includes resuscitation with intravenous fluids, insulin, and glucose, with treatment of the underlying etiology.
CONCLUSIONS: Clinician knowledge of this condition can improve the evaluation and management of patients with EDKA.
OBJECTIVE: This narrative review evaluates the pathogenesis, diagnosis, and management of EDKA for emergency clinicians.
DISCUSSION: EDKA is comprised of serum glucose <250 mg/dL with an anion gap metabolic acidosis and ketosis. It most commonly occurs in patients with a history of low glucose states such as starvation, chronic liver disease, pregnancy, infection, and alcohol use. Sodium-glucose cotransporter-2 (SGLT2) inhibitors, which result in increased urinary glucose excretion, are also associated with EDKA. The underlying pathophysiology involves insulin deficiency or resistance with glucagon release, poor glucose availability, ketone body production, and urinary glucose excretion. Patients typically present with nausea, vomiting, malaise, or fatigue. The physician must determine and treat the underlying etiology of EDKA. Laboratory assessment includes venous blood gas for serum pH, bicarbonate, and ketones. Management includes resuscitation with intravenous fluids, insulin, and glucose, with treatment of the underlying etiology.
CONCLUSIONS: Clinician knowledge of this condition can improve the evaluation and management of patients with EDKA.