Spinal cord injury

Contents

Overview

Acute spinal cord injury (SCI) results in loss of motor, sensory, and autonomic function below the level of injury. The majority are caused by trauma — road traffic accidents, falls, sports injuries, violence — but SCI also occurs from vascular (anterior spinal artery syndrome), inflammatory (transverse myelitis), neoplastic, and iatrogenic causes. The acute phase of SCI requires careful ICU management to prevent secondary injury and manage systemic complications, particularly cardiovascular instability and respiratory failure.

Classification

Level of Injury

The neurological level of injury (NLI) is defined as the most caudal segment with normal motor and sensory function bilaterally. This is assessed using the ASIA Impairment Scale (AIS):

Grade Description
A Complete: no motor or sensory function in S4–5
B Sensory incomplete: sensory but no motor below NLI, including S4–5
C Motor incomplete: motor function below NLI, >50% of key muscles below NLI have grade <3
D Motor incomplete: motor function below NLI, ≥50% of key muscles below NLI have grade ≥3
E Normal: no SCI deficits

Clinical Syndromes

Complete cord injury (AIS A): No motor or sensory function below the injury level.

Anterior cord syndrome: Injury to anterior two-thirds of cord (anterior spinal artery territory). Loss of motor function and pain/temperature sensation below the level; preserved proprioception and vibration (posterior columns intact). Worst prognosis for motor recovery.

Central cord syndrome: Most common incomplete SCI. Injury to central grey matter, classically from hyperextension of a degenerate cervical spine in older patients. Disproportionate upper limb weakness (arms more affected than legs), with variable sensory loss and bladder dysfunction.

Brown-Séquard syndrome: Hemisection of the cord. Ipsilateral motor loss and loss of proprioception; contralateral loss of pain and temperature sensation (crossing fibres of spinothalamic tract). Best prognosis for recovery.

Posterior cord syndrome: Rare. Loss of proprioception and vibration below the level; motor and pain/temperature preserved.

Conus medullaris syndrome: Injury at L1–L2 (conus medullaris). Mixed upper and lower motor neurone signs, bowel and bladder dysfunction, sexual dysfunction.

Cauda equina syndrome: Below L1 — lower motor neurone injury with flaccid paralysis, saddle anaesthesia, bowel and bladder dysfunction. Surgical decompression is urgent.

Neurological Levels and Respiratory Implications

  • C1–C3: Diaphragm paralysed — complete respiratory failure, permanent ventilator dependence
  • C3–C5: Partial diaphragm function — high risk of early respiratory failure
  • C5–T1: Intact diaphragm, impaired intercostals — reduced vital capacity (~50%), increased secretion burden
  • T1–T8: Impaired intercostals, intact abdominal muscles — moderate respiratory impairment
  • Below T8: Near-normal respiratory function

Neurogenic Shock

Neurogenic shock results from disruption of the descending sympathetic pathways in the spinal cord above T6. Loss of sympathetic outflow to the vasculature and heart causes:

  • Hypotension: from vasodilation (loss of vasoconstrictor tone) — warm, vasodilated peripheries
  • Bradycardia: from unopposed vagal (parasympathetic) tone on the heart — note the absence of tachycardia distinguishes neurogenic from haemorrhagic shock
  • Absence of diaphoresis (sweating requires sympathetic supply)

Neurogenic shock occurs in cervical and high thoracic injuries (above T6). It is not the same as spinal shock (the transient loss of all reflex activity below the injury level, which resolves over days to weeks).

Management

Haemorrhagic shock must be excluded first — especially in traumatic SCI, where concomitant haemorrhage is common.

Fluid resuscitation: Cautious IV fluids to restore preload. Avoid excessive fluids — neurogenic shock is vasodilatory, and excessive crystalloid can cause pulmonary oedema.

Vasopressors: Noradrenaline is first-line — restores vascular tone. Target MAP ≥85–90 mmHg in acute SCI to maintain spinal cord perfusion pressure and limit secondary injury.

Atropine: For symptomatic bradycardia. Temporary pacing may be needed for refractory bradycardia.

Respiratory Complications

Respiratory failure is the leading cause of death in acute cervical SCI. The combination of diaphragm weakness, loss of intercostal and abdominal muscle function, and reduced cough efficacy leads to:

  • Reduced tidal volume and vital capacity
  • Ineffective cough → secretion retention → atelectasis and pneumonia
  • Progressive respiratory failure

Assessment

Vital capacity (VC) is the most sensitive measure. Serial VC measurements guide management:

  • VC <20 mL/kg: high risk of respiratory failure, consider elective intubation
  • VC <15 mL/kg: intubation typically required
  • VC <10 mL/kg: respiratory failure imminent

Diaphragmatic fatigue with cervical injuries may cause progressive respiratory failure over 48–72 hours even when initial presentation appears stable — a pattern of early deterioration is well recognised.

Management

Non-invasive ventilation: CPAP and BiPAP can support ventilation and reduce secretion burden. Useful in cervical SCI with adequate bulbar function. Does not address secretion clearance.

Mechanical ventilation: Required for significant respiratory failure or VC below 15 mL/kg. Early intubation (elective) is preferred over emergency intubation — improves safety and avoids crash intubation.

Secretion management: Regular chest physiotherapy is essential. Assisted cough techniques (manual abdominal thrust) augment expiratory flow. Mechanical insufflation-exsufflation (MIE, "cough assist") devices improve secretion clearance in weaned or spontaneously breathing patients.

Tracheostomy: Required for patients expected to need prolonged ventilatory support or who cannot be weaned from mechanical ventilation. Early tracheostomy is associated with improved outcomes in ventilator-dependent cervical SCI.

Weaning: Phrenic nerve pacing (diaphragmatic pacing) is an option for ventilator-dependent patients with intact phrenic nerve function (C3–C5).

Acute ICU Management

Spinal Immobilisation

Maintain full spinal precautions until bony injury has been cleared radiologically (CT of the whole spine) and clinically. In unconscious patients, the spine should remain immobilised until clinical assessment is possible or MRI has excluded ligamentous injury.

Target MAP

Maintain MAP ≥85–90 mmHg for the first 7 days to optimise spinal cord perfusion pressure and minimise secondary ischaemic injury. This is supported by current NICE and ISCI guidance, though evidence is observational.

Temperature Regulation

Patients with high SCI cannot regulate temperature (poikilothermia — dependent on ambient temperature). Monitor temperature regularly and actively warm or cool as needed.

Steroids

High-dose methylprednisolone (NASCIS III: 30 mg/kg bolus then 5.4 mg/kg/hour for 24 or 48 hours) was previously used in acute SCI but is no longer recommended. Meta-analyses show no clear neurological benefit and significant increase in complications (infection, GI haemorrhage, hyperglycaemia). Current guidelines (NICE 2016) do not recommend routine corticosteroids for traumatic SCI.

DVT and PE Prevention

Patients with SCI are at very high VTE risk (immobility, lower limb paralysis, venous stasis). LMWH should be started within 72 hours of injury if haemorrhage risk permits, in combination with compression stockings and IPC.

Nutrition

Early enteral nutrition within 24–48 hours. SCI is associated with a hypermetabolic state initially, followed by a hypometabolic state as muscle mass decreases. A dietitian should guide nutritional targets.

Complications

Pressure ulcers: High risk due to sensory loss and immobility. Two-hourly turning, pressure-relieving mattresses, skin inspection.

Urinary tract infection: Urinary retention from loss of bladder control is universal in acute SCI above sacral levels. Intermittent catheterisation is preferred to indwelling catheter for long-term management; a urethral catheter is appropriate in the acute phase.

Constipation and bowel dysfunction: Bowel programme (digital stimulation, laxatives) established early.

Heterotopic ossification: Ectopic bone formation around joints below the injury. Presents weeks to months after injury.

Pain: Neuropathic pain below the injury level is extremely common. Treated with gabapentinoids, tricyclics, and specialist pain management.

Autonomic Dysreflexia

Autonomic dysreflexia (AD) is a potentially life-threatening emergency occurring in patients with SCI at T6 or above, usually after the acute phase as spinal shock resolves (weeks to months post-injury).

A noxious stimulus below the injury level (usually bladder distension, bowel impaction, pressure sore, or urinary tract infection) triggers an unmodulated mass sympathetic discharge below the level of injury, causing:

  • Sudden severe hypertension (systolic may rise to 200–300 mmHg)
  • Bradycardia (above the injury level — reflex response to hypertension via baroreceptors and intact vagal pathways)
  • Profuse sweating, flushing, and headache above the injury level
  • Pale, goosebumped skin below the injury level (vasoconstriction, no sweating)

Hypertension can cause stroke, subarachnoid haemorrhage, MI, and pulmonary oedema if untreated.

Management: Sit the patient upright (reduces BP by orthostatic effect). Identify and remove the triggering stimulus — check catheter patency and drain the bladder; check rectum and disimpact. If BP remains dangerously elevated: glyceryl trinitrate spray sublingually or nifedipine 10 mg orally (bite and swallow) to acutely reduce BP. IV labetalol or phentolamine if persistent severe hypertension.

Viva Questions

How does neurogenic shock differ from haemorrhagic shock in a trauma patient, and how do you manage it?

The key distinguishing feature of neurogenic shock is the combination of hypotension and bradycardia — in haemorrhagic shock, hypotension is accompanied by compensatory tachycardia. In neurogenic shock, loss of sympathetic outflow above T6 removes the vasoconstrictor and chronotropic drive, leaving unopposed vagal tone. The patient is therefore warm and vasodilated with bradycardia, in contrast to haemorrhagic shock where the patient is cold, clammy, and tachycardic. However, in trauma, both can coexist — SCI with associated internal haemorrhage — and haemorrhagic shock must always be actively excluded. Bedside FAST ultrasound and clinical assessment guide this. Management of confirmed neurogenic shock involves cautious fluid resuscitation to restore preload, followed by noradrenaline as the vasopressor of choice to restore systemic vascular resistance. Target MAP ≥85–90 mmHg to maintain spinal cord perfusion. Atropine addresses symptomatic bradycardia, with temporary pacing reserved for refractory bradycardia. Corticosteroids are not indicated for acute traumatic SCI.

What are the respiratory consequences of cervical spinal cord injury and how do you decide when to intubate?

The respiratory consequences depend on the level of injury. Above C3, diaphragm function is abolished and respiratory failure is immediate — intubation is mandatory from the outset. Between C3 and C5, partial diaphragm function is preserved but inadequate — early elective intubation is usually needed. Below C5, the diaphragm is intact but intercostal and abdominal muscles are weakened or absent, reducing vital capacity to around 50% of predicted, impairing effective cough, and causing secretion retention, atelectasis, and risk of progressive respiratory failure. A well-recognised pattern is initial clinical stability in the first 24–48 hours followed by progressive respiratory failure as the diaphragm tires. Vital capacity is the most useful bedside measure: a VC below 20 mL/kg signals high risk, below 15 mL/kg typically requires intubation, and below 10 mL/kg indicates imminent respiratory arrest. Early elective intubation is safer than emergency intubation in this population — where airway management may be difficult due to spinal immobilisation, cervical injury, and cervical immobilisation devices. The decision should be made proactively, before crisis.

What is autonomic dysreflexia and how do you manage an acute episode?

Autonomic dysreflexia is a medical emergency specific to patients with spinal cord injuries at T6 or above, typically occurring weeks to months after injury once spinal shock has resolved. It is triggered by a noxious stimulus below the injury level — most commonly urinary retention, bowel impaction, or a pressure sore. The stimulus provokes a massive unmodulated sympathetic discharge through the cord below the level of injury, causing intense vasoconstriction and severe hypertension, which can reach 200–300 mmHg systolic. Above the injury level, intact baroreceptors and the vagal pathway cause reflex bradycardia and sweating, but the sympathetic surge in the trunk and legs continues unchecked as the descending inhibitory signals cannot cross the injury. The clinical picture is sudden severe hypertension, pounding headache, sweating and flushing above the injury level, and pallor and piloerection below. The immediate management is to sit the patient upright — orthostatic hypotension reduces BP by 15–20 mmHg. Then identify and eliminate the trigger: check the urinary catheter for blockage and drain the bladder; perform a rectal examination for impaction. If BP remains dangerously elevated, sublingual GTN or oral nifedipine (10 mg, bite and swallow) provides rapid vasodilation. IV antihypertensives are used for persistent severe hypertension. The hypertension typically resolves promptly once the trigger is removed.