Synopsis
Recognise a time-critical compressive myelopathy, localise its level and coordinate imaging, spinal precautions and cause-specific decompression before irreversible cord injury develops.
- Compression may arise from trauma, tumour, epidural abscess, epidural haematoma, a large disc, degenerative stenosis, vertebral collapse or an intradural mass; treatment depends on the cause.
- Pain often precedes neurological loss and may be local, radicular or mechanical, but painless compression occurs and must not be dismissed when objective cord signs are present.
- Cord dysfunction produces bilateral upper-motor-neurone signs below the lesion, a sensory level and autonomic disturbance; early spinal shock can temporarily cause flaccidity and absent reflexes.
Key red flags
Bilateral weakness and long-tract sensory change occur below a definable truncal level with brisk reflexes or extensor plantars once spinal shock has passed, often accompanied by retention or constipation.
Investigation priorities
Show cord or cauda-equina compression, lesion extent, cord signal and epidural, vertebral or intradural pathology.
Management branches
Acute or progressive cord signs make external compression possible.
- Perform ABCDE, give titrated analgesia, check glucose, document a timed neurological baseline and use spinal precautions when trauma, collapse or movement-related instability is plausible.
- Call the local spinal or neurosurgical service and radiology immediately, identifying respiratory, bladder, cancer, infection and bleeding features that determine urgency and imaging coverage.
Key medicines
Cause-specific dexamethasoneUse the NICE metastatic-compression regimen only when that cause and indication apply, not generically.
Empiric intravenous antimicrobialsChoose immediately after cultures using the local spinal infection and sepsis protocol, then narrow to results.