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Associated injuries and mechanism of atlanto-occipital dislocation caused by trauma
1Department of Neurosurgery, Sapporo City General Hospital, Japan.
Insights
Traumatic atlanto-occipital dislocation (AOD) is often fatal, especially in traffic accidents. Associated severe injuries, not AOD itself, frequently cause early death in these critical craniocervical trauma cases.
Area of Science:
- Traumatology
- Neurology
- Radiology
Background:
- Traumatic atlanto-occipital dislocation (AOD) is a severe injury with high mortality.
- Understanding the associated injuries and mechanisms is crucial for diagnosis and treatment.
Observation:
- Analysis of 11 patients with fatal traumatic AOD, primarily from traffic accidents.
- Common findings included unconsciousness, respiratory/cardiac arrest, retropharyngeal space enlargement, and skull/cervical fractures.
- CT revealed subarachnoid hemorrhage and ventricular hematoma in most patients.
Findings:
- Subarachnoid hemorrhage and ventricular hematoma were linked to craniocervical injury.
- Associated injuries included head trauma, chest trauma, and intraperitoneal bleeding.
- Early mortality was often attributed to severe associated injuries rather than AOD alone.
Implications:
- The mechanism of AOD likely involves a distractive force to the craniocervical joint via hyperextension-flexion.
- While mandibular injuries are known associations, diverse trauma can lead to AOD.
- The poor prognosis highlights the critical nature of these injuries and the need for rapid, comprehensive assessment.
Abstract:
Injuries associated with traumatic atlanto-occipital dislocation (AOD) leading to death were analyzed in 11 patients, nine injured by traffic accidents, of which five were victims of car-pedestrian accidents. On admission, unconsciousness and respiratory arrest were noted in all patients, and cardiac arrest in nine. Skull and cervical roentgenograms revealed enlargement of the retropharyngeal space due to injury of the vertebral artery or its branches in nine patients, atlanto-axial dislocation (C-1-C-2 separation) in four, and skull fracture in four. Computed tomography demonstrated subarachnoid hemorrhage (SAH) in the upper cervical and posterior fossa in nine patients, fourth ventricular hematoma in seven, and atlas fracture in three. SAH and ventricular hematoma were due to craniocervical injury. Other common injuries were injury of face and head excluding the mandibular region in 10 patients, mandibular fracture in three, severe chest injuries in eight, and intraperitoneal bleeding in two. The overall outcome was poor. Nine patients died within 13 hours of admission, one was diagnosed as brain dead 8 days after the accident, and the other one survived in a persistent vegetative state. Early death is probably caused by associated severe injuries, i.e. chest injuries and intraperitoneal bleeding rather than AOD. Although injury of the mandibular region is known to be associated with AOD, head, breast, and abdominal trauma may also lead to neck hyperextension-flexion in various directions. Whatever the direct cause, a distractive force to the craniocervical joint by hyperextension-flexion appears to be important in the mechanism of AOD.