Abstract Introduction Stress-induced diabetic ketoacidosis (DKA) is an uncommon but serious metabolic complication that may occur in adults without prior diabetes, particularly under extreme physiologic stress. High-altitude exposure is known to affect glucose metabolism by modulating insulin sensitivity and β-cell function through hypoxia-inducible mechanisms. Moreover, hypobaric hypoxia can alter immune surveillance, predisposing individuals to respiratory infections. This report describes a case of acute stress-related DKA following return from high altitude, triggered by severe polymicrobial pneumonia, and resolved with complete metabolic recovery. Case Presentation A 28-year-old previously healthy woman from sea level presented with altered mental status, tachypnea, and dehydration one week after returning from a 5-day stay at 3,400 m altitude. Symptoms began with cough, fever, and malaise, progressing to polyuria, polydipsia, and dyspnea. On admission: heart rate 122 bpm, respiratory rate 30/min, blood pressure 145/90 mmHg, SpO2 89% on room air, and Glasgow Coma Scale 13/15. Laboratory tests confirmed DKA (pH 7.09, glucose 548 mg/dL, bicarbonate 6.1 mmol/L, anion gap 26 mEq/L, ketonuria). WBC was 17,890/µL and CRP 25.3 mg/L. HbA1c = 9.0%. Autoimmune antibodies (GAD65, IA-2, ZnT8) were negative, and C-peptide 2.1 ng/mL confirmed preserved β-cell function. CT revealed multifocal consolidation, cylindrical bronchiectasis, and air trapping. She was intubated for respiratory failure and received standard DKA management with intravenous insulin, fluids, and electrolyte replacement. Bronchoscopy on ICU day 2 revealed purulent secretions and erythematous mucosa. BAL multiplex PCR detected Parainfluenza virus, Rhinovirus/Enterovirus, Haemophilus influenzae, Staphylococcus aureus, and Moraxella catarrhalis; Candida albicans was cultured. Cefuroxime, clindamycin, and fluconazole were administered. She was extubated on day 4, discharged from ICU on day 7, and completed a 14-day antibiotic course. Insulin was tapered and discontinued by month 5, with HbA1c 5.6%. Pulmonary function normalized by 6 months. Discussion This case highlights the synergistic interaction between hypobaric hypoxia, immune dysregulation, and severe infection as triggers of transient stress-induced DKA. High-altitude exposure likely impaired respiratory mucosal defenses, predisposing to polymicrobial pneumonia upon return to sea level. Viral-bacterial co-infection may have intensified systemic inflammation, while cortisol and catecholamine surges disrupted insulin signaling and β-cell responsiveness. The absence of autoantibodies and full glycemic recovery confirm reversible β-cell dysfunction rather than autoimmune diabetes. Early bronchoscopy with molecular diagnostics proved critical for pathogen identification and targeted therapy, expediting recovery. Clinicians should recognize high-altitude travel and severe coinfection as potential precipitants of metabolic decompensation in non-diabetic adults. This abstract is funded by: NO FUNDING
Briones-Zamora et al. (Fri,) studied this question.