Spinal-cord injury level and neurogenic shock

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

Acute spinal-cord injury is a neurological and physiological emergency. Maintain the safest alignment and minimise movement, but never let a collar or transfer delay airway and breathing support. High cervical lesions weaken diaphragm and accessory muscles, while lower cervical and thoracic lesions reduce intercostal and abdominal strength. Observe respiratory pattern, voice, cough, secretion clearance and carbon dioxide; deterioration may precede desaturation after supplemental oxygen.

Neurological localisation uses a reproducible segmental examination. Test key upper- and lower-limb myotomes and light touch and pinprick dermatomes bilaterally, then assess sacral sensation, deep anal pressure and voluntary contraction when appropriate. The single neurological level and separate right and left motor and sensory levels are derived from the complete pattern. Document factors that limit testing, such as fracture, pain, sedation or peripheral nerve injury.

Sacral sparing distinguishes incomplete from complete injury. Preserved S4–5 sensation, deep anal pressure or voluntary anal contraction indicates some continuity across the lesion. Absence at an early examination can be confounded by spinal shock, sedation and examination quality, so repeat using the International Standards for Neurological Classification of Spinal Cord Injury. Avoid premature prognostic statements based on a rushed trauma-bay assessment.

Neurogenic shock is circulatory failure from sympathetic interruption, most often with cervical or high thoracic injury. Vasodilatation reduces vascular resistance and venous return; loss of cardiac sympathetic drive produces relative bradycardia. The skin may be warm rather than vasoconstricted. These clues are not exclusion tests for bleeding. Search chest, abdomen, pelvis, retroperitoneum and long bones, use blood when haemorrhage is suspected and reassess response before starting a vasopressor-led pathway.

Imaging proceeds from CT to MRI. CT defines fracture, translation, canal fragments and alignment across the relevant spine, with whole-spine review for high-risk or ankylosed patterns. MRI demonstrates cord oedema or haemorrhage, disc prolapse, ligament disruption and epidural haematoma. NICE recommends MRI after CT when a neurological abnormality could be attributable to cord injury. Early spinal-surgeon discussion determines decompression, reduction and stabilisation timing.

Perfusion treatment is individualised in a specialist environment. Correct hypoxia, bleeding, hypothermia and significant bradycardia; avoid repeated excessive crystalloid. After adequate circulating volume and haemorrhage control, a titrated vasopressor such as noradrenaline may support pressure under local spinal critical-care protocol. Exact targets depend on injury, comorbidity and current specialist guidance. NICE advises against methylprednisolone, nimodipine and naloxone as neuroprotective treatments.

Early whole-person care prevents secondary complications. Use pressure-relieving surfaces, turning compatible with spinal stability, venous-thromboembolism assessment, bladder drainage, bowel care, nutrition, temperature control and respiratory physiotherapy. Involve a spinal-cord-injury centre early, even when surgery occurs locally. Communicate neurological level, completeness, respiratory function, shock phenotype and pending imaging at every transfer.

Key points

Protect alignment while prioritising airway and breathing; high cervical injury can retain a normal early saturation despite falling ventilation and ineffective cough.
Document a structured motor and sensory examination, including perianal sensation, deep anal pressure and voluntary anal contraction when clinically appropriate to determine sacral sparing.
The neurological level is the most caudal segment with normal sensory and antigravity motor function under the ISNCSCI method; do not infer it from one weak limb.
Complete injury has no sacral sensory or motor sparing; preserved sacral function defines incomplete injury and carries different prognostic implications.
Neurogenic shock is haemodynamic hypotension from sympathetic loss, often with relative bradycardia and warm skin; spinal shock is transient areflexia and flaccidity below the lesion.
Exclude and control haemorrhage before attributing hypotension to neurogenic physiology; mixed shock is common after high-energy trauma.
Use CT to define bone and alignment, then MRI urgently when neurological abnormality may arise from cord, disc, ligament or epidural pathology.
Avoid methylprednisolone, nimodipine and naloxone for acute traumatic cord neuroprotection under NICE guidance; preserve oxygenation, perfusion, temperature and timely decompression instead.

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

Fracture or dislocation

Cervical and thoracolumbar translation, burst, flexion-distraction and fracture-dislocation can compress, contuse or transect cord and roots.

Cord injury without obvious fracture

Disc prolapse, ligament injury, epidural haematoma and central cord injury can produce major neurology despite no acute bony lesion on CT.

Penetrating or vascular injury

Direct tract damage, arterial disruption and cord infarction cause focal or complete deficits and may coexist with external haemorrhage.

Degenerative vulnerability

A stenotic older cervical canal can sustain central cord injury after hyperextension with disproportionately weak arms and relatively preserved legs.

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

1
Primary neural damage
Mechanical compression, haemorrhage and axonal disruption determine the initial injury at impact and cannot be reversed by later pharmacological neuroprotection.
2
Secondary injury cascade
Hypoxia, hypotension, oedema, inflammation, excitotoxicity and impaired microvascular flow expand tissue loss around the initial cord lesion.
3
Sympathetic interruption
Cord injury above the major sympathetic outflow reduces vascular tone and cardiac sympathetic drive, producing vasodilatation, pooling and relative bradycardia.
4
Respiratory muscle weakness
High cervical lesions impair diaphragm, intercostal and abdominal muscle function, reducing ventilation and cough and causing secretion retention.

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

High cervical injury

Neck pain, tetraparesis, diaphragmatic breathing, weak cough, low voice and rising carbon dioxide indicate respiratory muscle compromise and possible urgent ventilation.

Central cord pattern

Arm weakness greater than leg weakness after cervical hyperextension, often in an older stenotic spine, suggests central cord injury despite limited CT abnormality.

Complete injury pattern

No motor or sensory sacral sparing on a reliable repeated ISNCSCI examination supports complete injury, with careful allowance for confounders.

Incomplete injury pattern

Preserved perianal sensation, deep anal pressure or voluntary anal contraction shows sacral sparing and residual long-tract continuity.

Neurogenic shock

Hypotension, relative bradycardia and warm peripheries after high cord injury supports sympathetic failure only after bleeding and obstructive causes are addressed.

Mixed shock

Pelvic, thoracic or abdominal trauma plus high spinal injury can produce simultaneous blood loss and vasodilatation, requiring blood, source control and specialist vasopressor support.

Red flags requiring action

Diaphragmatic breathing, weak cough, falling vital capacity, hypercapnia or high cervical weakness requires early anaesthetic and critical-care support before oxygen saturation falls.
Hypotension with relative bradycardia and warm peripheries suggests neurogenic shock, but chest, abdominal, pelvic, vascular and long-bone bleeding must be excluded and treated first.
New weakness, sensory level, sacral sensory loss, reduced anal contraction or priapism indicates spinal-cord or cauda equina injury requiring urgent spinal specialist and MRI assessment.

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
First-line structured neurological examinationFirst stepFirst line
Why
Localise level, completeness and change over time.
Interpretation and limitations
Use ISNCSCI key motor, light-touch, pinprick and sacral examination, recording untestable segments and repeating after resuscitation or surgery.
02
Preferred CT spinePreferred
Why
Define fracture, translation, canal bone and alignment rapidly.
Interpretation and limitations
Image indicated regions with complete junction coverage and review the whole spine in high-risk patterns; CT cannot show all cord and ligament injury.
03
MRI after CT
Why
Identify cord compression, oedema, haemorrhage, disc, ligament and epidural pathology.
Interpretation and limitations
Obtain urgently for attributable neurological abnormality and use the result with spinal specialists to plan decompression and stabilisation.
04
Blood gas and respiratory monitoring
Why
Detect hypoventilation and respiratory muscle fatigue.
Interpretation and limitations
Rising carbon dioxide, falling vital capacity or cough strength and secretion retention can precede saturation decline and should accelerate airway support.
05
Haemorrhage assessment
Why
Exclude the common competing cause of post-traumatic hypotension.
Interpretation and limitations
Use serial examination, blood gas, haemoglobin, eFAST or CT according to stability and response; never diagnose neurogenic shock by bradycardia alone.
06
ECG and focused echocardiography
Why
Assess bradyarrhythmia, cardiac injury and filling when shock remains unclear.
Interpretation and limitations
Findings can guide pacing or vasoactive support, but do not replace source-directed trauma assessment.

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

Haemorrhagic shock

Cool vasoconstricted skin, tachycardia, bleeding mechanism and transient response support volume loss, but mixed haemorrhagic and neurogenic shock can coexist.

Spinal shock

Transient areflexia and flaccidity below the lesion describes neurological reflex suppression, not the haemodynamic vasodilatation of neurogenic shock.

Peripheral nerve or plexus injury

Deficit limited to a named nerve or one limb without a sensory level or sacral change may arise outside the cord.

Brain injury or sedation

Reduced movement and respiratory effort can reflect consciousness or drugs, requiring GCS, cranial, limb and medication assessment in parallel.

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

01ImmediateProtect cord and ventilationFirst stepTrauma produces weakness, sensory level, sacral change or high-risk spinal pain.

1Run ABCDE with coordinated spinal protection, give oxygen when required and call anaesthetic support for weak cough, hypoventilation or high cervical injury.
2Document a structured motor, sensory and sacral examination before and after transfers or reduction whenever feasible.
3Search for and control haemorrhage, correcting hypoxia, hypothermia and inadequate volume before labelling hypotension neurogenic.
4Arrange complete CT and urgent spinal-surgeon consultation, followed by MRI for neurological abnormality attributable to the cord.

02ShockTreat neurogenic physiology after exclusionHypotension persists with a high cord injury after bleeding and obstruction are addressed.

1Confirm adequate circulating volume and reassess chest, abdomen, pelvis and long bones for mixed haemorrhage.
2Use monitored specialist vasopressor support according to the current spinal critical-care protocol, titrated to the agreed organ-perfusion objective.
3Treat clinically significant bradycardia with senior critical-care input and prepare pacing capability when recurrent severe episodes occur.
4DefinitiveTrend lactate, urine output, temperature, cardiac rhythm, skin and neurological findings while definitive decompression and stabilisation proceed.

03OngoingPrevent secondary complicationsNeurological level and acute operative plan are established.

1Transfer or liaise early with a spinal-cord-injury centre and communicate ISNCSCI findings, respiratory function, haemodynamics and skin status.
2Use pressure relief, coordinated turns, respiratory physiotherapy, bladder and bowel plans, nutrition and VTE prevention compatible with bleeding risk.
3Repeat neurological classification after resuscitation and surgery and investigate any new loss immediately.
4Begin patient-centred rehabilitation, psychological support and education about skin, autonomic, respiratory and thrombotic complications.

Key medicines and prescribing safety1 treatment · regimens, roles and cautions

Supports vascular tone and arterial pressure when sympathetic failure persists after reversible volume loss and obstructive causes have been treated.

Noradrenaline infusion for selected neurogenic shock

Start only in a monitored critical-care setting after adequate volume and haemorrhage control, using the local standard concentration and titrating the intravenous infusion to the spinal-team perfusion target; there is no single safe fixed trauma dose.

Central access is preferred for sustained use; monitor rhythm, limb perfusion, extravasation and lactate, and do not let vasopressor response conceal ongoing haemorrhage.

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

Respiratory failure and pneumonia

Weak ventilation and cough cause atelectasis, secretion plugging, infection and delayed intubation risk, especially during transfer or sedation.

Pressure injury and thrombosis

Loss of sensation, immobility and vasomotor change cause rapid skin injury and high venous-thromboembolism risk without organised prevention.

Bladder, bowel and autonomic dysfunction

Urinary retention, ileus, temperature dysregulation and later autonomic dysreflexia require structured spinal rehabilitation, surveillance and emergency planning.

Permanent neurological loss

Complete or incomplete motor, sensory and sphincter impairment affects mobility, independence, respiration, sexual function and psychological health.

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

Repeat ISNCSCI motor, sensory and sacral findings after resuscitation, imaging, surgery and any reported neurological change.
Trend respiratory rate, cough, secretion burden, blood gas carbon dioxide and bedside spirometry where feasible in cervical and upper thoracic injury.
Monitor pressure, rhythm, perfusion, lactate, temperature and urine output continuously during neurogenic-shock treatment.
Inspect skin and pressure points and document coordinated turning, bladder, bowel and VTE plans from the first day.
Reassess medicines and devices daily, including vasopressor need, catheter indication and timing of pharmacological thromboprophylaxis.

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

Two shocks share one word

Spinal shock describes reflex suppression; neurogenic shock describes haemodynamic sympathetic failure, and they require different observations.

Warm skin does not clear bleeding

A high cord lesion can mask vasoconstriction while abdominal or pelvic haemorrhage continues simultaneously.

Oxygen saturation can lag

Supplemental oxygen may preserve saturation while ventilation and cough fail, making carbon dioxide and respiratory mechanics essential.

Sacral sparing changes classification

A small preserved S4–5 sensory or motor function distinguishes incomplete from complete injury when the examination is reliable.

CT and MRI answer different questions

Bone alignment on CT cannot exclude cord oedema, disc compression, ligament disruption or epidural blood.

11Common pitfallsFrequent interpretation and management errors.

01
Calling hypotension neurogenic before excluding chest, abdominal, pelvic and long-bone haemorrhage.
02
Using spinal shock and neurogenic shock as interchangeable terms.
03
Recording a neurological level without sacral examination or documenting untestable muscles.
04
Waiting for oxygen desaturation before supporting a weak high-cervical respiratory pattern.
05
Stopping after normal CT despite objective cord signs that require MRI.
06
Using high-dose methylprednisolone for routine neuroprotection despite NICE advice.