- Based on 24 years of axial MRI, orthopedic surgeons at Massachusetts General Hospital developed a five-point scale for grading spinal cord compression associated with spinal epidural abscess
- High-grade abscesses were significantly associated with presenting motor deficit, sensory changes and bowel/bladder dysfunction
- Increased compression was not associated with poorer neurological outcomes
- No association between higher compression grade and 90-day mortality was found
A number of studies have established that spinal cord compression associated with a spinal epidural abscess (SEA) significantly increases the risk of neurological symptoms and poor outcomes. However, no classification scheme has ever been developed for grading cord compression under these circumstances.
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Now, orthopedic surgeons at Massachusetts General Hospital have created a five-point scale that allows clinicians and researchers to record progressively increasing degrees of compression in SEA. They based their scale on an existing grading system for spinal cord compression from tumors metastatic to the spine. Orthopedic Surgeon Joseph H. Schwab, MD, MS, chief of the Orthopaedic Spine Center, and colleagues describe the new classification in Clinical Spine Surgery.
To evaluate the utility of their classification, the researchers identified 339 patients who had an SEA above the conus medullaris, received initial treatment at Mass General between 1993 and 2016 and had a pretreatment axial MRI available. The median age was 50 years, 58% of the cohort was male and an average of four vertebral levels were affected.
Confirming previous studies, the researchers observed links between increasing degrees of compression and pretreatment neurological deficits. Grade 4 and 5 abscesses were significantly associated with motor weakness and sensory changes at presentation. Grade 5 abscesses were also significantly associated with bladder/bowel dysfunction.
Unlike in some previous research, the team found no association between increasing spinal cord compression and the final neurological outcome.
This suggests that while the initial motor deficit may be due to direct compression, there may be a different mechanism for the residual weakness. Possibilities include indirect vascular compromise from thrombosis/thrombophlebitis or injury from decompression and operative handling of the spinal cord.
This was also the first study in SEA to assess the effect of spinal cord compression on mortality. The researchers found no association between degree of compression and the risk of death within 90 days after discharge.
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