Traumatic asphyxia is a condition resulting from a severe sustained compressive force on the thorax. Ollivier is credited for the ﬁrst autopsy description of a syndrome of cranial cyanosis, subconjunctival hemorrhage, and vascular engorgement of the head, which was observed in a person crushed to death by a panicked crowd in Paris. The syndrome was termed masque ecchymotique. This form of crush injury occurs in association with vehicle crashes, industrial accidents, uncontrolled crowd conditions and trampling, and any type of trauma characterized by a heavy object falling onto the chest, such as an individual working under a car that slips off the jack or a child pinned under a garage door. The syndrome is also seen with side wall collapse at an excavation site or may be seen with deep-sea divers from underwater explosions. The pathogenesis of traumatic asphyxia is attributed to a sudden compression of the heart between the anterior chest wall and vertebral column, generating a pressure surge in the right side of the heart that is decompressed by reverse blood ﬂow into the superior vena cava and its major branches, which lack valves. The subsequent massive capillary engorgement and rupture throughout the head, neck, shoulders, and upper thorax results in stagnation of blood, which desaturates and results in the characteristic bluish discoloration of the skin. There may be intense swelling of the face and neck, as well as petechial hemorrhages of the skin of the face and conjunctiva. It is postulated that deep inspiration and transient airway obstruction exaggerate the superior vena cava hypertension. These events may occur as a reﬂex in the victim’s anticipating the impact.
Traumatic asphyxia can be fatal, but the prognosis for those surviving to reach the hospital is good. It is critical to examine the patient for other potentially lethal associated injuries, such as pulmonary or cardiac contusion and injury to the spinal cord, brain, liver, or spleen. Rib fractures and visual changes are common. Approximately one-third of patients with traumatic asphyxia experience loss of consciousness or other neurologic ﬁndings. Interestingly, despite the alarming appearance, many patients have relatively few complaints. Occasionally, there is permanent loss of vision caused by retinal hemorrhage or transient vision changes from retinal edema. There is no speciﬁc treatment for traumatic asphyxia, but elevation of the head of the bed 30 degrees to minimize venous hypertension and supplemental oxygen to hasten absorption of air within the mediastinum are recommended. Ninety percent of patients who survive the ﬁrst few hours after injury will recover, but survival rates vary depending on the prevalence and degree of associated injuries.