# Pulmonary Electrical Injury: A Case Report on an Uncommon Cause of Refractory Hypoxemia

## TL;DR

This case report describes a rare instance of severe lung issues after high-voltage electrocution, highlighting the challenges in diagnosis and treatment.

## Contribution

The paper presents a novel case of electrocution-induced pulmonary vascular injury with refractory hypoxemia and pulmonary hypertension.

## Key findings

- The patient exhibited severe hypoxemia and pulmonary hypertension disproportionate to imaging findings.
- CT pulmonary angiography identified distal subsegmental pulmonary embolism on day 4.
- The patient's condition progressed to multiorgan failure despite standard interventions.

## Abstract

Pulmonary involvement after high-voltage electrocution is rare and may present with hypoxemia and pulmonary hypertension out of proportion to imaging, suggesting a vascular/endothelial mechanism. The objective of this report is to describe a case of disproportionate hypoxemia with severe pulmonary hypertension after electrocution, highlight diagnostic pitfalls, and outline management implications.

A previously healthy 46-year-old man sustained high-voltage electrocution, required prolonged resuscitation, and developed severe hypoxemia (PaO₂/FiO₂ (ratio of arterial oxygen partial pressure to fractional inspired oxygen): 68) despite protective ventilation and proning. CT showed only mild posterior ground-glass change; echocardiography revealed preserved right ventricular function. On ICU day 4, a CT pulmonary angiogram (CTPA) identified very distal subsegmental pulmonary embolism. Pulmonary artery catheterization documented pulmonary hypertension (pulmonary artery pressure (PAP): 68/39 mmHg; mean ≈49 mmHg), high/normal cardiac index (4.19 L/min/m²), and mildly elevated pulmonary vascular resistance.

Despite prone positioning (FiO₂ 1.0, positive end expiratory pressure (PEEP) 8 cm H₂O, tidal volume (Vt) ~6 mL/kg predicted body weight (PBW)) and neuromuscular blockade, hypoxemia persisted. Inhaled vasodilators and veno-venous extracorporeal membrane oxygenation (VV-ECMO) were not available at our center. The patient progressed to multiorgan failure and died.

Electrocution may precipitate a primary pulmonary vascular phenotype with physiology that outpaces imaging. Early hemodynamic assessment can refine diagnosis and escalation. Where available, time-limited trials of inhaled vasodilators and timely consideration of VV-ECMO are reasonable.