Pulmonary complications after electrical injury are uncommon and are most often interpreted as parenchymal forms of lung damage, including non-cardiogenic pulmonary edema, diffuse alveolar hemorrhage, or focal thermal injury. However, recent case-based observations suggest that this may not be the only pattern. In some patients, severe hypoxemia and pulmonary hypertension appear to be greater than expected from the extent of radiographic abnormalities. In a recently published case of high-voltage electrocution, profound refractory hypoxemia (PaO₂/FiO₂ 68), markedly elevated pulmonary artery pressures (68/39 mmHg), preserved right ventricular function, and only mild posterior ground-glass opacities on CT pulmonary angiography raised the possibility of a vascular-dominant form of acute lung injury. In that setting, physiological severity was difficult to explain by alveolar flooding alone.

This commentary proposes a clinical and pathophysiological framework for understanding this pulmonary vascular phenotype after electrical trauma. Electrical current may contribute to lung injury through several converging mechanisms, including electroporation-related membrane disruption, thermal microvascular damage, endothelial barrier dysfunction, maladaptive pulmonary vasoconstriction, impaired hypoxic vasoregulation, and microthrombotic perfusion defects that may remain below the resolution of routine CT imaging. Recognizing this pattern could be clinically relevant. It may help clinicians avoid anchoring on incidental distal subsegmental pulmonary embolism, encourage early echocardiographic and hemodynamic assessment, support carefully monitored trials of inhaled pulmonary vasodilators as physiologic probes, and prompt timely referral for extracorporeal support when hypoxemia remains refractory despite optimized conventional care. Future studies should clarify how often this phenotype occurs, identify biomarkers of endothelial and microvascular injury, and determine which patients may benefit from vascular-targeted supportive strategies.

Electrocution, Electrical injury, Acute lung injury, Pulmonary hypertension, Endothelial dysfunction, Ventilation–perfusion mismatch, Microthrombosis, Refractory hypoxemia, VV-ECMO