Abstract
Odontoid fractures are typically associated with low rates of acute neurologic deficit and morbidity/mortality in nonelderly patients. In the patient in this case, traumatic injury triggered by a syncopal event led to a combined C1-C2 fracture and a fatal spinal cord injury with apnea, quadriplegia, and cardiovascular instability. We briefly review the anatomical basis for the pathophysiology of cardiac dysfunction following high-cervical spine injury and present an example of a worst-case scenario.
Highlights
C2 fractures account for 20% of acute cervical spine fractures
They are associated with low rates of acute neurologic deficit and mortality in younger patients (8.5% and 2.4%, resp.), whereas in the elderly (>65 years old) morbidity and mortality approach 50 and 10%, respectively [1, 2]
Type III odontoid fractures rarely cause neurologic deficit [3]; type III odontoid fractures make up 20% of C1-2 combination injuries and suggest more structural and mechanical injury than do isolated C1 or C2 injuries [3]
Summary
Odontoid fractures are typically associated with low rates of acute neurologic deficit and morbidity/mortality in nonelderly patients. In the patient in this case, traumatic injury triggered by a syncopal event led to a combined C1-C2 fracture and a fatal spinal cord injury with apnea, quadriplegia, and cardiovascular instability. We briefly review the anatomical basis for the pathophysiology of cardiac dysfunction following high-cervical spine injury and present an example of a worst-case scenario
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