Neurologic injury because of trauma after type II odontoid nonunion.
Academic Article
Overview
abstract
BACKGROUND CONTEXT: Treatment of Type II odontoid fractures remains controversial, whereas nonoperative treatment is well accepted for isolated Type III odontoid fractures. Little is known about long-term sequelae of nonoperative management or risk of recurrent injury after nonsurgical treatment. We hypothesize that a substantial proportion of odontoid fractures assumed to be acute are actually chronic injuries and have a high rate of late displacement resulting in neurologic injury. PURPOSE: To identify patients presenting with previously unrecognized odontoid fracture nonunions and to document the incidence of new neurologic injury after secondary trauma in this population. STUDY DESIGN: Retrospective case series. PATIENT SAMPLE: One hundred thirty-three patients with Type II odontoid fractures presenting to a Level I trauma center. OUTCOME MEASURES: Computed tomography (CT) and magnetic resonance imaging (MRI) scans, American Spinal Injury Association Motor Score (AMS), and neurologic examination. METHODS: All patients presenting after traumatic injury to a Level I trauma center from May 2005 to May 2010 with a Type II odontoid fracture on CT scan were included. Patients aged less than 18 years and those with pathologic fractures were excluded. Fractures were classified as chronic or acute based on CT evidence of chronic injury/nonunion including fracture resorption, sclerosis, and cyst formation. Magnetic resonance imaging was then examined for evidence of fracture acuity (increased signal in C2 on T2 images). Patients without evidence of acute fracture on MRI were considered to have chronic injuries. Computed tomography and MRI scans were interpreted independently by two reviewers. Chart review was performed to document demographics, AMS, and new-onset neurologic deficit associated with secondary injury. RESULTS: One hundred thirty-three patients presented with Type II odontoid fractures and no known history of cervical fracture with an average age of 79 years. Based on CT criteria, 31/133 (23%) fractures were chronic injuries. Nine additional fractures appeared acute on CT but were determined to be chronic by MRI findings. The overall number of chronic fractures was therefore 40 (30%). Interobserver reliability analysis for classification of fractures as chronic demonstrated κ=0.65 representing substantial agreement. Of the 40 chronic fractures, 7 patients (17.5%) had new-onset neurologic deficits after secondary injury including 4 motor deficits, 2 sensory deficits, and 1 combined deficit. Although the chronic injury group as a whole had similar AMS to the acute injury group (89 vs. 84, p=.27), the seven patients with new-onset neurologic deficit had an average AMS of 52.4. CONCLUSIONS: A substantial proportion of patients presenting after cervical trauma with Type II odontoid fractures have evidence of nonacute injury. Of these patients, 17% presented with a new neurologic deficit caused by an "acute-on-chronic" injury.