Abstract
IntroductionCrush asphyxia is different from positional asphyxia, as respiratory compromise in the latter is caused by splinting of the chest and/or diaphragm, thus preventing normal chest expansion. There are only a few cases or small case series of crush asphyxia in the literature, reporting usually poor outcomes.Case presentationWe present the case of a 44-year-old Caucasian man who developed traumatic asphyxia with severe thoracic injury and mild brain edema after being crushed under heavy auto vehicle mechanical parts. He remained unconscious for an unknown time. The treatment included oropharyngeal intubation and mechanical ventilation, bilateral chest tube thoracostomies, treatment of brain edema and other supportive measures. Our patient’s outcome was good. Traumatic asphyxia is generally under-reported and most authors apply supportive measures, while the final outcome seems to be dependent on the length of time of the chest compression and on the associated injuries.ConclusionTreatment for traumatic asphyxia is mainly supportive with special attention to the re-establishment of adequate oxygenation and perfusion; treatment of the concomitant injuries might also affect the final outcome.
Highlights
Crush asphyxia is different from positional asphyxia, as respiratory compromise in the latter is caused by splinting of the chest and/or diaphragm, preventing normal chest expansion
Treatment for traumatic asphyxia is mainly supportive with special attention to the re-establishment of adequate oxygenation and perfusion; treatment of the concomitant injuries might affect the final outcome
Asphyxia is defined as any condition that leads to tissue oxygen deprivation [1]
Summary
Asphyxia is defined as any condition that leads to tissue oxygen deprivation [1]. Traumatic asphyxia is a type of mechanical asphyxia, where respiration is prevented by external pressure on the body, at the same time inhibiting respiratory movements and compromising venous return from the head. Thoracic X-ray examination revealed bilateral pneumothorax and multiple rib fractures (Figure 1) In this respect, bilateral tube thoracostomies were inserted, draining air and blood and eliciting major improvement in his hemodynamic parameters. Arterial blood gases on admission to our ICU were: pH 7.246; partial pressure of carbon dioxide: 58.3mmHg; partial pressure of oxygen: 441mmHg; bicarbonate: 21.9mEq/L; oxygen saturation: 99.9%; and lactate: 1.1mmol/L while our patient was ventilated with a frequency of 15 breaths/ min; tidal volume: 700mL; positive end-expiratory pressure: 5cmH2O; and fraction of inspired oxygen: 100% His Acute Physiology and Chronic Health Evaluation II score was 14, while his past medical history was noted to be non-significant. Alanine aminotransferase, creatine phosphokinase and lactic dehydrogenase levels decreased to normal on the seventh day and our patient was discharged from the ICU and transferred to the thoracic surgical ward
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