Crush asphyxia is caused by a sudden compressive trauma to the thoracoabdominal region and presents with facial cyanosis and edema, hyposphagmata and petechial hemorrhages of the face, neck and upper chest . It is typically associated with transient ischemic neurological deficits and injuries to the thorax, abdomen and limbs.
Traumatic asphyxia was first described over 170 years ago, by Ollivier in his observations on the cadavers of people trampled upon during crowd upheavals in Paris on Bastille day . Later, Perthes added some other characteristics, such as mental dullness, hyperpyrexia, hemoptysis, tachypnea and ‘contusion pneumonia’ to the initial description . Other terms for this condition are Ollivier’s syndrome, Perthes’ symptom complex, compression cyanosis, traumatic cyanosis, cervicofacial static cyanosis and cervicofacial cutaneous asphyxia.
A review of the literature indicates that traumatic asphyxia is a rare condition, since it might go unrecognized or not be even reported. Laird and Borman found only seven cases out of 107,000 hospital and clinic patients in a 30-month period, of whom 75,000 had been involved in major accidents . Dwek reported only one case out of a total of 18,500 accident victims in an area with heavy military traffic .
Our patient suffered from traumatic asphyxia due to prolonged compression between the ground and a sizeable heavy object, a mechanism quite common in similar published reports. In particular, cases of crush asphyxia are mainly a consequence of motor vehicle crashes, crushing among other bodies in a panicked crowd, entrapment beneath vehicles or falling down in a narrow space . Other causes include injuries from machines and furniture, blast injury, a python tightened around the thorax and, rarely, deep-sea diving, weightlifting, epileptic seizures, difficult obstetric delivery and asthmatic attack. The typical range of the duration of compression is between two and five minutes . The duration and the amount of pressure affect the outcome after traumatic asphyxia. Significant weight can be tolerated for a short time, whereas a relatively modest weight applied for a longer period may result in death . In our case, the duration of compression could not be confirmed, but it is estimated as fairly long, although this is loosely consistent with the rapid and full recovery of the patient.
The diagnosis is reached from the physical appearance, clinical examination, history and trauma mechanism . Superior vena cava (SVC) obstruction and basilar skull fracture have features that closely resemble the appearance of traumatic asphyxia. Yet, the history of traumatic injury should rule out SVC obstruction, while skull fractures are rare in traumatic asphyxia, unless the force of compression is applied to the head . Our patient had no head injury, as verified by the imaging studies.
The exact pathophysiologic mechanism of traumatic asphyxia remains controversial. It is generally considered that a compressive force to the thoracoabdominal region together with the ‘fear response’ (deep breath and closing of the glottis) cause a huge increase in the central venous pressure. This induces reversal of venous blood flow from the heart through the SVC into the innominate and jugular veins of the head and neck. The back transmission of the elevated central venous pressure to the head and neck venules and capillaries, while arterial flow is continued, results into capillary stasis and rupture, producing the characteristic upper body petechial and subconjunctival hemorrhages . These features are often more prominent on the eyelids, nose and lips . The lack of petechiae in the lower body may be due to the compressive obstruction of the inferior vena cava in the chest or abdomen. Furthermore, the fact that the lower part of the body is protected from back transmission of venous pressure by a series of valves could be another mechanism, since the SVC, innominate and jugular veins have no valves .
Associated injuries, such as pulmonary, cardiac, neurologic, ophthalmic, abdominal and orthopedic trauma, were not apparent in our patient. As has been concluded from Rosato et al., cardiac injuries during traumatic asphyxia are extremely rare. Only two cases of cardiac contusion and one of ventricular rupture have been reported so far, within the last three years . A normal electrocardiogram does not rule out blunt cardiac injury. Another rare consequence of traumatic asphyxia is delayed myocardial infarction due to coronary artery contusion . Myoglobinuria, rhabdomyolysis and acute renal tubular necrosis (crush syndrome) present only in cases of associated injury and ischemia of large muscle groups .
After awakening and despite the normal findings on brain imaging, our patient was in a state of agitation and confusion that lasted for four days. According to Perthes, neurological injury in traumatic asphyxia includes cerebral hypoxia or anoxia, ischemia, venous hypertension, cerebral vascular congestion, rupture of small vessels, petechial hemorrhages and hydrostatic edema . However, the rapid full recovery discouraged us from requesting further brain imaging studies, such as magnetic resonance imaging, that were not expected to influence the treatment plan. The vision may be affected with the same mechanism: retinal hemorrhage, retrobulbar hemorrhage and vitreous exudates (Purtscher’s retinopathy) . A hearing deficit can be caused by edema of the Eustachian tubes, or a hemotympanum. Other neurologic manifestations of the syndrome are loss of consciousness, prolonged but self-limiting confusion, disorientation, agitation, restlessness, seizures, visual disturbances, blurred vision, papillary changes, optic nerve atrophy, exophthalmos, diplopia and hearing loss . Often, the neurologic status improves during transfer to the emergency room . The suggested mechanism for loss of consciousness and prolonged confusion associated with traumatic asphyxia includes cerebral hypoxia, ischemia and venous hypertension, which lead to cortical dysfunction. This dysfunction resolves within the following 24 to 48 hours. Intracranial hemorrhage has seldom ever been evident in a patient . CT scans of the brain are usually normal, whereas in fatal cases, autopsy shows only petechiae and congestion, suggesting brain injury at the cellular level .
Despite the dramatic appearance of the ‘ecchymotic mask’, mortality in crush asphyxia is low. However, it may be influenced by the severity, nature and duration of the compressive force and the presence of concomitant injuries, which can be useful markers of the severity of compression . The proposed algorithm for the management of all trauma patients on arrival and during the initial phases of treatment is the ABCDE (Airway, Breath, Circulation, Disability, Environment) algorithm, described in the Advanced Trauma Life Support guidelines by the American College of Surgeons Committee on Trauma. The outcome is improved by airway control and cervical spine protection, rapid restoration of ventilation, oxygenation and circulation by thoracic decompression, fluid resuscitation and prevention of renal complications secondary to rhabdomyolysis and other secondary causes . Management of these patients may be complicated by severe upper airway edema, and the possibility of a difficult intubation should thus be considered early. The prognosis is good if the patient survives the initial few hours following injury, although a prolonged thoracic compression could lead to cerebral anoxia and permanent neurological sequelae .