Rapid-onset respiratory failure following diesel aspiration at 4,200 m: a case report

Oral siphoning of diesel fuel carries substantial risks of chemical inhalation injury; however, documented cases of diesel aspiration pneumonia, especially at altitudes >2,500 m, remain rare. The synergistic effects of hydrocarbon toxicity and hypobaric hypoxia in such environments are inadequately characterized.

A 23-year-old man accidentally aspirated approximately 10 mL of diesel while siphoning a fuel line at 4,200 m altitude. Within 5 h, he developed nausea, vomiting, and dry cough, progressing to right-sided pleuritic chest pain, fever (38.2 °C), and hypoxemia (SpO₂ 84%). Arterial blood gas analysis revealed type I respiratory failure (PaO₂ 44.8 mmHg). Chest CT demonstrated patchy consolidations in the right middle lobe and left lower lobe. Laboratory findings included leukocytosis (15.9 × 10⁹/L) and elevated C-reactive protein (72.51 mg/L). Management comprised supplemental oxygen, broad-spectrum antibiotics (meropenem covering anaerobes and Gram-negative bacteria), intravenous methylprednisolone, and nebulized mucolytics.

Diesel's lipophilic and irritant properties disrupt the alveolar-capillary barrier, inciting intense inflammation and pulmonary edema. At high altitude, baseline hypoxemia (SpO₂ 85-90%) synergistically exacerbates ventilation-perfusion mismatch and accelerates respiratory failure. Hypoxia-amplified inflammatory cascades and consequent pulmonary hypertension further increase right ventricular afterload.

Diesel aspiration pneumonia may progress rapidly to life-threatening respiratory failure under hypobaric conditions. Early triple therapy (broad-spectrum antibiotics, systemic corticosteroids, supplemental oxygen) is critical to mitigate complications. This case underscores the imperative for occupational safety interventions prohibiting oral siphoning and heightened vigilance for toxic-hypoxic interactions at high altitude.