A 74-year-old female with a medical history of hypertension and type 2 diabetes mellitus was admitted to ICU following severe trauma from a road traffic accident. On admission, her home medications included empagliflozin, gliclazide, metformin, ramipril, amlodipine, and esomeprazole.
Initially, the patient presented with no hemorrhagic shock or organ failure. Her Glasgow Coma Scale (GCS) score was 14 upon arrival at the trauma center.
A computed tomography (CT) scan revealed:
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Mild traumatic brain injury with brain contusion hemorrhage and subarachnoid hemorrhage.
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Facial bone fractures.
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Thoracic trauma (Thoracic Trauma Score = 11) with a left-sided hemopneumothorax, which did not require drainage.
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American Association for the Surgery of Trauma (AAST) grade 3 traumatic splenic injury.
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Non hemorrhagic, non surgical pelvic trauma.
None of these injuries necessitated surgical intervention. An occipital scalp wound was debrided and sutured. Apart from esomeprazole, none of her long-term medications were resumed upon initial management. The patient’s initial medical course was favorable. Consequently, on Day 4, oral antidiabetic medications, including empagliflozin, were reintroduced.
From Day 5, the patient developed an unexplained fever without deterioration in her general condition.
By Day 7, while awaiting discharge from the ICU, her overall condition acutely deteriorated. She presented with a decreased level of consciousness (GCS 7/15), atrial fibrillation (heart rate 150–160 bpm), hemodynamic instability (90/54 mmHg), tachypnea (25–30 breaths per minute), hyperthermia (40 °C), and facial and left arm edema.
Arterial blood gas analysis revealed severe metabolic acidosis (pH 6.99, bicarbonate 6 mmol/L, pCO2 15 mmHg, pO2 105 mmHg, base excess − 23.4 mmol/L) with a lactate concentration of 1.8 mmol/L and a glucose concentration of 13.7 mmol/L.
Management initiated for septic shock included fluid resuscitation, vasopressor therapy, and broad-spectrum antibiotics. Subsequent cranial and thoraco-abdomino-pelvic CT scans revealed dermo-hypodermitis of the face, secondary to an occipital skin wound infection.
Further laboratory analysis showed a serum creatinine level of 55 µmol/L, discordant with her profound metabolic acidosis. This biochemical dissociation excluded acute kidney injury as the primary etiology, prompting evaluation for alternative causes such as diabetic ketoacidosis or toxic-mediated acidosis. In this context, a plasma ketone measurement was performed, revealing a level greater than 6 mmol/L. This strongly supported a diagnosis of EDKA associated with SGLT2i use.
All oral antidiabetic drugs, including empagliflozin, were discontinued. After achieving hemodynamic stability with aggressive crystalloid fluid resuscitation and correction of hypokalemia, a continuous intravenous insulin infusion was initiated, concurrently with a 10% dextrose infusion to prevent hypoglycemia.
Microbiological analysis confirmed methicillin-susceptible Staphylococcus aureus bacteremia, with positive blood cultures for nearly six days. Based on the antibiogram, antibiotic therapy was adjusted, and cloxacillin was subsequently introduced. A mitral valve endocarditis, characterized by a 12 mm mobile vegetation with renal and splenic emboli, developed as a secondary complication of the bacteremia. The patient was deemed unsuitable for surgical treatment due to her head trauma, which contraindicated extracorporeal circulation.
The shock resolved after 4 days, leading to the discontinuation of norepinephrine. After 5 days of insulin therapy, the patient’s acidosis resolved, and serum ketone bodies were negative. The continuous intravenous insulin infusion was then transitioned to a basal-bolus insulin regimen.
Ultimately, the clinical course of this infectious episode was favorable under well-managed antibiotic therapy for 6 weeks. The patient was transferred to a rehabilitation center after a 62-day ICU stay.