Traumatic Asphyxia

Traumatic asphyxia, also called compressive asphyxia or Perthes syndrome, is the result of a sudden, severe crushing force to the chest or upper abdomen with a closed glottis. It causes a classic pattern of facial cyanosis, subconjunctival haemorrhage and petechiae.

Epidemiology. It is rare and occurs in industrial accidents, vehicle crush injuries, crowd crushes, trapping under machinery and collapse of structures. Children are affected more than expected, since their chest wall is pliable.

Pathophysiology. Compression with a closed glottis causes a sudden surge in intrathoracic pressure, which is transmitted by valveless veins to the head, neck and upper chest. Capillaries rupture and tissue shows cyanosis and petechiae. Duration of compression is the main determinant of brain injury and outcome. The cyanosis is caused by venous congestion and not by hypoxaemia.

Presentation is deep purple blue discoloration with petechiae over the face, neck and upper chest, sparing the area covered by the compressing object. There is subconjunctival haemorrhage, facial and conjunctival oedema, proptosis, epistaxis, tinnitus, reduced consciousness, seizures and retinal haemorrhage. Associated injuries include rib fractures, pulmonary contusion, pneumothorax, cardiac contusion, liver, spleen and spinal injury.

Red flags.

• Altered consciousness, seizures or focal neurological signs.
• Stridor, airway oedema or respiratory failure.
• Associated crush injury with limb compression.

Trauma assessment with CT head, cervical spine, chest, abdomen and pelvis as indicated. Check arterial gas, lactate, troponin, ECG, creatine kinase, potassium, creatinine and urine myoglobin. Do fundoscopy and eye examination for retinal haemorrhage and vision.

Differential diagnosis. Strangulation or hanging, superior vena cava obstruction, drowning, seizure with prolonged cyanosis and primary cardiac disease.

There is no specific treatment for the syndrome, and care is supportive with full trauma assessment.

Airway and breathing. Maintain the airway and anticipate swelling. Intubate for airway oedema, coma or respiratory failure, using a plan for a difficult airway. Give oxygen. Treat pneumothorax and haemothorax.

Position. Raise the head to 30 degrees when spinal injury is excluded or with spinal precautions in reverse Trendelenburg tilt.

Circulation. Treat shock for associated bleeding, and look for crush syndrome if limbs were compressed.

• Crush syndrome: 0.9% sodium chloride 1 to 1.5 L/h before and during release, then 200 to 500 mL/h, targeting urine output of 200 to 300 mL/h. Stop fluid if overload develops. Treat hyperkalaemia with calcium gluconate 10% 30 mL IV and insulin 10 units with glucose 25 g IV.

Brain. Treat seizures with lorazepam 0.1 mg/kg IV (maximum 4 mg). Manage raised intracranial pressure by head elevation, normocapnia and osmotherapy (mannitol 0.25 to 1 g/kg IV, or 3% sodium chloride 2 to 3 mL/kg) if there is herniation.

Other measures. Analgesia, ophthalmology review and tetanus prophylaxis. Most patients recover fully when compression lasts under 4 to 5 minutes, with neurological outcome determined by duration of hypoxia and hypotension.

Monitoring. Neurological observations, respiratory function, urine output and vision for 24 to 48 hours.

Referral and escalation. Trauma team and intensive care for coma, airway compromise or major associated injury. Ophthalmology for retinal haemorrhage or visual loss.

Special groups. In children, signs can be severe despite limited internal injury and observation is advised.