Acute spinal cord compression

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

The fixed spinal canal leaves little reserve for an expanding mass, displaced bone or collapsing vertebra. Venous congestion, oedema and arterial compromise then amplify mechanical injury. Symptoms depend on level and tempo: cervical lesions affect hands, legs and sometimes breathing; thoracic lesions produce a truncal sensory level and paraparesis; lesions around the conus add early sphincter and saddle dysfunction. A root-predominant lumbar syndrome is considered separately as cauda equina disease.

History should establish exact onset, maximal severity, pain quality, trauma, cancer, infection and bleeding risk. Fever, injecting drug use, diabetes, immunosuppression, bacteraemia or recent spinal procedure raises abscess. Anticoagulation, coagulopathy or neuraxial intervention raises haematoma. Cancer and progressive nocturnal or mechanical pain raise metastasis. Examination documents respiratory function, segmental power, tone, reflexes, plantar responses, a reproducible sensory level, sacral sensation and bladder function without repeated painful or unnecessary intimate testing.

Management proceeds in parallel: stabilise, immobilise if instability is plausible, image, identify cause and prepare definitive treatment. Neurosurgery or spinal orthopaedics, radiology, oncology, infection, haematology and critical care are involved according to the lesion. Steroid, antimicrobial, reversal, decompression and radiotherapy decisions are cause-specific. Pressure care, bladder drainage, thrombosis prevention and rehabilitation begin while definitive treatment is arranged.

Key points

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.
High cervical compression threatens diaphragmatic function and can impair cough before oxygen saturation falls; serial vital capacity and critical-care review may be needed.
MRI is the definitive first-line study in most non-traumatic cases and should cover the clinically relevant region, commonly the whole spine when multifocal disease is possible.
CT defines fractures and bony alignment when trauma or instability is suspected, but it cannot reliably exclude cord, epidural soft-tissue or cauda-equina compression.
Do not give corticosteroid reflexively to every compression. Dexamethasone has a defined role in suspected metastatic compression with neurological signs, not routine traumatic injury, haematoma or untreated epidural infection.
Epidural abscess requires blood cultures, prompt antibiotics after appropriate sampling and urgent spinal surgical discussion; neurological deficit must not wait for a completed microbiology work-up.
Epidural haematoma requires urgent anticoagulant reversal where relevant and decompression assessment, balancing haemorrhage control against the original antithrombotic indication.
Neurological status at treatment strongly predicts outcome, so repeated examination and rapid escalation are more important than finding a single perfectly specific red flag.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Traumatic and degenerative compression

Fracture, dislocation, disc prolapse and severe degenerative narrowing can reduce canal space abruptly or progressively; instability may allow continuing mechanical injury during movement.

Malignant disease

Vertebral metastasis, epidural tumour or pathological collapse can compress the cord, often after progressive night, mechanical or radicular pain in a person with known or occult cancer.

Spinal epidural infection

Haematogenous infection or recent spinal intervention can produce epidural pus and inflammatory swelling; fever may be absent, particularly after antibiotics or during immunosuppression.

Spinal epidural haemorrhage

Anticoagulation, coagulopathy, trauma or neuraxial procedures can cause rapidly expanding epidural blood, typically with sudden severe pain followed by evolving motor and sensory loss.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Canal space loss
Bone, disc, tumour, pus or blood occupies the fixed spinal canal and directly deforms the cord while potentially destabilising the vertebral column.
2
Venous congestion and oedema
Compression impairs venous drainage and disrupts the blood–cord barrier, producing oedema that further raises tissue pressure and extends injury beyond the original lesion.
3
Arterial compromise
Continuing pressure reduces spinal perfusion and causes ischaemia, axonal failure and necrosis, converting potentially reversible conduction block into permanent tract and segmental damage.
4
Tract and autonomic failure
Corticospinal, sensory and autonomic pathways fail below the lesion, while anterior-horn or root injury at the level may add flaccid segmental weakness.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Cord-level syndromeRed flag

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.

Epidural infectionRed flag

Severe focal spinal pain with fever, systemic illness, raised inflammatory markers or infection risk progresses to radicular symptoms and neurological deficit; the complete classic triad may be absent.

Epidural haemorrhageRed flag

Sudden severe neck or back pain is followed by rapidly evolving motor and sensory loss after anticoagulation, coagulopathy, trauma or a neuraxial procedure.

Traumatic instabilityRed flag

A high-energy mechanism, midline tenderness, deformity or neurological deficit raises fracture-dislocation and requires movement restriction and trauma imaging even if the patient can move limbs initially.

High cervical threatRed flag

Tetraparesis, weak cough, shallow breathing, accessory-muscle use, bradycardia or hypotension suggests cervical cord compromise with respiratory and autonomic risk.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Urgent MRI spine with contrast when appropriateFirst step
Why
Show cord or cauda-equina compression, lesion extent, cord signal and epidural, vertebral or intradural pathology.
Interpretation and limitations
Sequence and coverage follow the suspected cause; image the whole spine when tumour, infection or multifocal disease is plausible. A radiologist should report the study urgently to the treating spinal team.
02
CT spine in trauma or bony disease
Why
Define fracture, alignment, collapse, calcification and surgical anatomy rapidly, including when MRI is initially unsafe or unavailable.
Interpretation and limitations
CT complements rather than replaces MRI for neural and epidural soft tissues. Maintain precautions and escalate if neurological findings exceed the CT explanation.
03
Serial neurological and respiratory examination
Why
Detect ascent or deterioration and provide the baseline against which decompression outcome is judged.
Interpretation and limitations
Record myotomal power, tone, reflexes, plantars, sensory level, sacral function, gait only if safe, and forced vital capacity for high lesions; avoid vague labels such as legs weak.
04
Blood count, inflammatory markers and cultures
Why
Support an infectious cause and obtain organisms before antibiotics when this can be done without delaying treatment.
Interpretation and limitations
Normal temperature or inflammatory markers do not exclude early abscess. Take at least two blood-culture sets when feasible and arrange targeted tissue culture during drainage.
05
Coagulation, group and save and medicine review
Why
Identify reversible bleeding risk and prepare for urgent intervention in suspected haematoma or operative compression.
Interpretation and limitations
Record the exact anticoagulant, last dose, renal function and antiplatelet exposure; reversal follows agent-specific emergency and haematology guidance.
06
Bladder scan and complication baseline
Why
Quantify autonomic dysfunction and protect the patient while imaging and transfer occur.
Interpretation and limitations
A raised residual supports but a low residual does not exclude early cord or cauda-equina compromise. Record renal function, skin, thrombosis and haemodynamic risks.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Transverse myelitis

An inflammatory cord syndrome can produce a similar level and sphincter dysfunction, but urgent contrast MRI is required to exclude mechanical, infective and neoplastic compression before immunotherapy is assumed appropriate.

Spinal cord infarction

A deficit maximal within minutes, often with severe back pain and relative dorsal-column sparing, supports vascular injury; diffusion imaging and vascular context refine the diagnosis.

Guillain–Barré syndrome

Symmetrical areflexic weakness without a sensory level favours polyradiculoneuropathy, whereas early bladder dysfunction, local spinal pain and later pyramidal signs point towards cord disease.

Cauda-equina syndrome

Root compression below the conus causes radicular pain, saddle sensory change, areflexia and lower-motor-neurone weakness rather than a clear upper-motor-neurone syndrome below a cord level.

Additional chapter-specific clues

Inflammatory mimicRed flag

Transverse myelitis, spinal-cord infarction and metabolic myelopathy can produce a level without external compression; MRI distinguishes intramedullary and extrinsic patterns and redirects treatment.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01First responseStabilise and preserve anatomyFirst stepAcute or progressive cord signs make external compression possible.

1Perform ABCDE, give titrated analgesia, check glucose, document a timed neurological baseline and use spinal precautions when trauma, collapse or movement-related instability is plausible.
2Call the local spinal or neurosurgical service and radiology immediately, identifying respiratory, bladder, cancer, infection and bleeding features that determine urgency and imaging coverage.
3Arrange urgent MRI, adding CT for fracture or bony definition, and create a monitored transfer plan that avoids unnecessary movement or delays for routine investigations.
4Prevent pressure injury and venous thrombosis when safe, drain clinically significant retention and keep the patient nil by mouth if urgent surgery is likely.

02Infection pathwayControl epidural sepsisFocal spinal pain, systemic infection risk and imaging suggest epidural abscess or vertebral infection with neural compression.

1Take blood cultures and urgent laboratory tests, but begin local sepsis antibiotics promptly after sampling when the patient is unstable or neurological function is threatened.
2Discuss immediate drainage and decompression with spinal surgery and microbiology or infection specialists; obtain operative tissue for culture whenever intervention occurs.
3Tailor antimicrobial choice and duration to organism, source, bone or disc involvement and drainage, while searching for endocarditis or another bacteraemic focus where indicated.

03Bleeding or traumaReverse, decompress and reassessImaging shows haematoma, fracture-dislocation or another mechanically unstable cause.

1For haemorrhage, stop the implicated antithrombotic and implement agent-specific reversal with haematology input while surgical assessment proceeds rather than sequentially.
2For trauma, follow major-trauma imaging and haemodynamic guidance, maintain alignment and involve the appropriate regional spinal injury centre early.
3Proceed to decompression and stabilisation when indicated, then repeat neurological, respiratory and autonomic assessment and begin specialist spinal rehabilitation.

Key medicines and prescribing safety4 treatments · regimens, roles and cautions

Reduces oedema around malignant cord compression while definitive surgery or radiotherapy is organised.

Cause-specific dexamethasone

Use the NICE metastatic-compression regimen only when that cause and indication apply, not generically.

Avoid routine use in traumatic cord injury, epidural haematoma or uncontrolled infection; monitor glucose, mental state, gastric and infectious complications and taper if MSCC is excluded.

Treats epidural abscess or vertebral infection while drainage and source control are arranged.

Empiric intravenous antimicrobials

Choose immediately after cultures using the local spinal infection and sepsis protocol, then narrow to results.

Cover likely staphylococci and context-specific Gram-negative infection without delaying surgery; adjust for renal function, allergy, CNS or bone penetration and microbiology advice.

Limits haematoma expansion and enables safer urgent decompression when clinically significant anticoagulant effect contributes to compression.

Anticoagulant reversal

Stop further anticoagulant and use the haematology-selected reversal strategy and dose in the current local major-haemorrhage or emergency-surgery protocol.

Confirm the drug, last dose and renal function; options and licensed or NICE-funded indications differ between agents and bleed sites. Monitor haemostasis and thrombosis and document later anticoagulation reassessment.

Reduces severe pain during immobilisation, imaging and transfer without substituting for definitive decompression.

Analgesia

Titrate multimodal analgesia to comfort and safe examination using local acute-pain guidance.

Sedation and hypotension can obscure neurological or respiratory decline; NSAIDs and opioids have renal, bleeding, bowel and delirium risks.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Permanent paralysis and sensory loss

Prolonged mechanical and ischaemic injury destroys cord tissue, leaving spastic weakness, neuropathic pain and loss of protective sensation even after successful decompression.

Respiratory failure

High cervical compression can weaken the diaphragm, cough and accessory muscles before oxygen saturation falls, creating urgent ventilatory and airway risk.

Bladder, bowel and sexual dysfunction

Autonomic pathway injury causes retention, incontinence, constipation and sexual dysfunction; overdistension and infection add avoidable renal and functional harm.

Immobility complications

Weakness and bed rest increase venous thrombosis, pressure injury, chest infection, contracture and deconditioning, so protective care and rehabilitation begin alongside definitive treatment.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Repeat level-specific power, sensation, reflexes, sacral and bladder findings at a frequency matched to tempo and document exact times before and after intervention.
Monitor respiratory rate, cough, forced vital capacity and blood gases when cervical or high thoracic disease is present; do not wait for desaturation.
Check bladder volume, urine output, bowel function, skin and pressure areas and venous-thromboembolism risk throughout immobilisation and transfer.
Follow temperature, cultures, inflammatory markers and organ function in infection, or coagulation and haemoglobin in haemorrhage, against a cause-specific plan.
After surgery or radiotherapy, reassess stability, mobilisation instructions, pain, wound, sphincters and rehabilitation goals with the spinal service.
Escalate any new weakness, ascending level, respiratory change, hypotension, fever or loss of bladder sensation immediately rather than waiting for a routine ward round.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Spinal shock masks long tracts

An acute cord lesion may initially be flaccid and areflexic, so absent brisk reflexes do not prove a peripheral process.

Pain response is irrelevant

Relief after opioid or positioning does not exclude ongoing mechanical compression or remove the need for definitive imaging.

A level can mislead upward

The perceived sensory boundary may lie below the anatomical lesion, so imaging should not stop at the first dermatome suggested by the patient.

Steroid is not universal

The same neurological syndrome can arise from tumour, pus, blood or trauma, and indiscriminate corticosteroid can delay or complicate the correct treatment.

CT cannot see everything

Excellent bony images do not reliably exclude an epidural collection, cord oedema or disc-related neural compression.

Outcome is time dependent

Preserved walking and sphincter function at definitive treatment predict recovery, making repeated examination and rapid coordination central interventions.

11Common pitfallsFrequent interpretation and management errors.

01
Waiting for the complete triad of pain, weakness and sphincter dysfunction before arranging emergency imaging.
02
Removing spinal precautions after a normal plain radiograph despite trauma, midline tenderness and neurological deficit.
03
Giving blanket high-dose steroid before distinguishing malignant, infective, haemorrhagic and traumatic causes.
04
Delaying antibiotics or decompression for epidural abscess until every culture result is final.
05
Using one normal bladder scan to exclude early cauda-equina or cord compromise.
06
Documenting paraparesis without a timed myotomal, sensory, reflex, sacral and respiratory baseline.