Diffuse Alveolar Haemorrhage Masquerading as Worsening ARDS in a Young Polytrauma Patient: Diagnostic Reasoning and a...

Diffuse alveolar haemorrhage (DAH) is a rare, under-recognised complication of blunt polytrauma. In patients with severe acute respiratory distress syndrome (ARDS), new airway bleeding may be mistaken for pulmonary contusion, ventilator-associated pneumonia or transfusion-related acute lung injury (TRALI), delaying appropriate treatment. The timing of definitive fracture fixation also remains uncertain.

A previously healthy man in his mid-20s sustained blunt polytrauma (Injury Severity Score 29; Glasgow Coma Scale 8), including multiple open comminuted fractures, a T11 compression fracture and bilateral pulmonary contusions. After emergency external fixation, he was transferred in haemorrhagic shock and respiratory failure, with severe ARDS (PaO₂/FiO₂ 78 mmHg), lactate 7.0 mmol/L and creatine kinase 4443 U/L. On day 4, he developed bloody endotracheal secretions, recurrent hypoxaemia, and abrupt decreases in haemoglobin (114 to 76 g/L) and platelets (139 to 65 × 10⁹/L). Bronchoscopy showed diffuse, non-focal mucosal oozing. Vasculitis and cytokine panels were negative. Targeted next-generation sequencing of bronchoalveolar lavage fluid detected high burdens of Acinetobacter baumannii and Klebsiella pneumoniae, low-abundance Pseudomonas aeruginosa, and multiple carbapenemase and extended-spectrum β-lactamase genes. Presumed non-immune post-traumatic DAH with possible TRALI contribution was diagnosed. Treatment included withholding further transfusion, methylprednisolone 1 mg/kg/day, lung-protective ventilation, four prolonged prone-positioning sessions, antimicrobial therapy and damage-control orthopaedics, with definitive fixation on day 17. Tracheostomy was decannulated on day 28, and he was discharged to rehabilitation. At follow-up, he walked independently without recurrent DAH or ARDS.

In polytrauma patients, new diffuse airway bleeding, disproportionate anaemia and worsening hypoxaemia should prompt consideration of non-immune DAH, particularly after transfusion. In this single case, recovery followed a combined strategy of bronchoscopic assessment, restrictive transfusion, corticosteroids, prone ventilation and physiology-guided orthopaedic management. However, concurrent interventions and the absence of histological confirmation preclude causal attribution; the findings are hypothesis-generating.