Traumatic Asphyxia—Reappraised

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Abstract
A clinical and experimental appraisal of traumatic asphyxia is presented; 4 surviving patients with traumatic asphyxia, and the records of 8 fatal cases of blunt thoraco-abdominal trauma were analyzed. All patients who developed the craniocervical cyanosis characteristic of the syndrome had accidents in which there was warning of impending trauma. Surviving patients had varying degrees of transient cerebral dysfunction and hematuria or albuminuria. The ecchymotic rash in these patients cleared within 5 days. Fatal cases showed varying degrees of pulmonary and intra-abdominal congestion at autopsy; 1 had diffuse intra-cortical petechial hemorrhages and another acute meningeal congestion. In experiments on dogs, acute thoracic compression was produced with a pneumatic tourniquet placed around the chest and inflated to 750 mm Hg. Airways were controlled with cuffed endotracheal tubes and hemodynamic alterations were recorded. With chest compression for 30 sec. and airway obstruction in full inspiration, jugular and inferior vena caval pressure was markedly increased above normal, and jugular flow was rapidly diminished or actually reversed. Carotid artery flow and brachial and femoral artery pressures also decreased significantly. When the airway was unobstructed during chest compression, pressures and flows were only slightly different from controls. Airway occlusion plays an integral role in the pathophysiology of traumatic asphyxia. The individual performs a Valsalva maneuver, which if prolonged, as in a seizure, vomiting results in a marked elevation of venous pressure and reversal of venous flow with capillary stasis or rupture, producing the typical ecchymotic rash that characterizes the syndrome. This also happens if the Valsalva maneuver is accompanied by thoraco-abdominal compression.