Case Presentation: A 61-year-old male with a past medical history of type 2 diabetes mellitus (T2DM), hypertension, hyperlipidemia, coronary artery disease (CAD) with multiple previous PCIs and status post CABG 6 days prior, presented to the ED with a 1 day history of nausea, vomiting, upper abdominal discomfort and chest pain. He was maintained on empagliflozin, liraglutide, ezetimibe, aspirin, ticagrelor and metoprolol. He expressed non-compliance with an insulin glargine regimen started on his most recent hospitalization. On presentation vitals were unremarkable. Physical examination was solely significant for epigastric tenderness. Biochemical investigations revealed a troponin of 0.4 ng/dL (decreased from 10.7 ng/dL post CABG 6 days prior), CK of 87 U/L, serum glucose of 146mg/dL with positive 40mg/dl of ketones on urinalysis, betahydroxybutyrate >4 mmol/l, ABG with pH 7.43, anion gap (AG) of 21, and serum osmolality of 298 mosm/kg. He was diagnosed with euglycemic DKA (EDKA) and commenced on an intravenous infusion of insulin and dextrose in the ICU. Closure of AG was achieved within 24 hours and, after intensive diabetes self-management education, he was restarted on glargine and discharged. Empagliflozin was discontinued.
Discussion: The benefits of certain SGLT2i in patients with T2DM have been well established in recent literature. Empagliflozin and canagliflozin appear to decrease cardiovascular mortality, are reno-protective and, in addition to dapagliflozin, appear to reduce heart failure re-admissions. Unfortunately, an association with EDKA has also been reported. In the absence of polyuria, polydipsia and weight loss, the typical manifestations of hyperglycemia, EDKA symptoms may be vague and nonspecific. Prompt recognition and treatment can improve morbidity, mortality and reduce length of hospital stay. Although a prevailing initial theory in this case was that of a repeat cardiac event in this patient with significant history of CAD and recent CABG, his medication history and vague symptoms prompted further workup, with biochemical results revealing EDKA. Prompt initiation of appropriate therapy resulted in early discharge by day 3 of admission. As such, clinicians must maintain a high index of suspicion for EDKA in patients on SGLT2i, especially in the acutely ill patient with a complex medical or surgical history which may further compound diagnostic uncertainty.
Conclusions: Sodium-glucose cotransporter 2 inhibitors (SGLT2i) are novel agents used in the treatment of T2DM. Recent literature has demonstrated an association with EDKA. In a medically complex patient in EDKA, the presence of non-specific DKA symptoms, and concurrent absence of typical hyperglycemia may cause diagnostic delay, contributing to morbidity and mortality. As SGLTi use becomes more prevalent in the outpatient treatment of T2DM, further literature review and research is needed in the pathophysiologic mechanism of SGLT2i induced EDKA, preventative methods and management guidelines on diagnosis.