Case Presentation: A 46-year-old male with Type 2 DM presented with 2 weeks of malaise, 3 days of cough, dyspnea, and fatigue. His wife noted his breath smelt different over the last 2 weeks. He had a thyroidectomy for multinodular goiter 2 weeks prior and started a ketogenic, intermittent fasting diet after. Medications include empagliflozin 10 mg/day. On exam, he appeared dyspneic and acutely ill. Vitals included: BP 136/85, HR 128, Temperature 97.8 F, RR 22/min, and SpO2 95% on room air. Oral mucosa was dry. Pulmonary exam demonstrated bilateral crackles and right-sided bronchial breath sounds. Laboratory studies revealed: WBC 10.6 10^9/L, sodium 131 mmol/L, glucose 139 mg/dL, CO2 6 mmol/L, anion gap 36, b-hydroxybutyrate >5 mmol/L, and procalcitonin 6.99 ng/mL. UA showed +2 ketones, +3 glucose, and +2 protein. CT chest showed extensive right middle lobe and bilateral lower lung consolidation compatible with multifocal pneumonia. EKG showed sinus tachycardia. He was admitted with community-acquired pneumonia and euglycemic diabetic ketoacidosis (EDKA). He was started on an IV insulin drip, IV D5½ NS drip, IV ceftriaxone and azithromycin. His clinical status, acidosis, and anion gap improved and he was transitioned to basal-bolus insulin later. His initial blood cultures were positive for Streptococcus pneumoniae with negative follow-up cultures. He was discharged on subcutaneous insulin and ten days of IV ceftriaxone for pneumonia and bacteremia.

Discussion: EDKA is a life-threatening complication seen in Type 1/Type 2 DM characterized by severe metabolic acidosis, ketonemia, and glucose usually less than 250mg/dl. EDKA is a potential adverse event in some people treated with sodium-glucose cotransporter 2 inhibitors (SGLT-2), which block renal glucose absorption, causing glucosuria and a sequential carbohydrate deficit. Additional stressors such as intermittent fasting and ketogenic diet in this patient on an SGLT-2 inhibitor caused a carbohydrate starvation state precipitating decreased insulin production with breakdown of lipids and fatty acids into ketone bodies. Infection and dehydration further cause increased release of counter-regulatory hormones such as catecholamines, cortisol, and glucagon leading to EDKA. Mainstays of treatment include aggressive hydration with dextrose-containing fluids, IV insulin, and electrolyte replacement. This patient was not aware of the risk factors that lead to his hospitalization. Closing these patient education gaps could have prevented a life-threatening complication.

Conclusions: We present a patient with EDKA precipitated by recent surgery, pneumonia, ketogenic diet, and SGLT-2 inhibitor use. As SGLT-2 inhibitor usage increases in diabetic patients given the cardiovascular benefits, it is increasingly vital to educate patients on concomitant risks with their usage. These include fasting hypoglycemia and stressors such as surgery, dietary changes, and infections. Educating patients that normal glucose levels do not rule out EDKA and that further testing of urinary ketones should be performed when feeling unwell may help in early diagnosis. Pre-operative screening for SGLT-2 inhibitors and caloric restriction should warn clinicians of this potential complication. This relationship between SGLT-2 inhibitors and ketogenic diets warrants further investigation as well.