ICU · neurocritical-care
Acute Spinal Cord Injury and Neurogenic Shock — Comprehensive ICU Management
Also known as Spinal cord injury · SCI · Neurogenic shock · ASIA impairment scale · Autonomic dysreflexia · Cervical spine injury · Spinal cord perfusion pressure · STASCIS
Acute spinal cord injury (SCI) — traumatic damage to the spinal cord causing motor/sensory deficit below the injury level ± autonomic dysfunction. Neurogenic shock: loss of sympathetic tone below the lesion (cervical or upper thoracic SCI) → VASODILATION (hypotension) + BRADYCARDIA (unopposed parasympathetic/vagal tone) — DISTRIBUTES differently from other shock types (warm, dry skin + bradycardia vs cold/clammy/tachycardic of hypovolaemic shock). ASIA Impairment Scale (A=complete, B=sensory incomplete, C=motor incomplete non-functional, D=motor incomplete functional, E=normal). Management: (1) ATLS primary survey + spinal precautions (cervical collar + logroll + spinal board), (2) NEUROGENIC SHOCK: noradrenaline (alpha + beta — restores BP AND HR) + atropine (for symptomatic bradycardia) + target MAP 85-90 mmHg for 7 days (maintain spinal cord perfusion — controversial but widely practiced), (3) EARLY SURGICAL DECOMPRESSION (STASCIS trial — within 24h improves neurological outcomes), (4) METHYLPREDNISOLONE (controversial — NASCIS II/III — high-dose within 8h may improve outcomes but increases infection risk — many centres have abandoned routine use), (5) VTE prophylaxis (high risk — start LMWH within 24-72h), (6) prevent secondary injury (avoid hypotension/hypoxia/hyperthermia). Autonomic dysreflexia (T6 or above): noxious stimulus below lesion → massive sympathetic discharge → hypertensive crisis → intracranial haemorrhage/stroke. Management: sit upright + identify/remove trigger + rapid-acting antihypertensives (nitroglycerin paste, nifedipine bite-and-swallow).
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Overview
Neurogenic shock — the unique shock type
Neurogenic shock vs other shock types — the key differential
| Feature | Neurogenic shock | Hypovolaemic shock | Septic shock | Cardiogenic shock |
|---|---|---|---|---|
| Cause | Loss of sympathetic tone (cervical/upper thoracic SCI) | Volume loss (haemorrhage, dehydration) | Vasodilation from infection | Pump failure (MI, myocarditis) |
| Heart rate | BRADYCARDIA (unopposed vagal tone — the KEY distinguishing feature) | TACHYCARDIA (compensatory) | TACHYCARDIA (compensatory) | TACHY or BRADY (depends on cause) |
| Skin | WARM and DRY (vasodilation below lesion — no sympathetic tone to constrict) | COLD and CLAMMY (vasoconstriction) | WARM (early — vasodilation) or COLD (late) | COLD (vasoconstriction) |
| Blood pressure | HYPOTENSION (vasodilation) | HYPOTENSION (volume loss) | HYPOTENSION (vasodilation) | HYPOTENSION (low cardiac output) |
| Peripheral resistance (SVR) | LOW (massive vasodilation) | HIGH (compensatory vasoconstriction) | LOW (vasodilation) | HIGH (compensatory) |
| Venous return | LOW (venous pooling from loss of venous tone) | LOW (volume loss) | Normal or high (venodilation) | LOW (pump failure) |
| First-line treatment | Noradrenaline (alpha-1 + beta-1 — restores tone AND supports HR) | Fluids + blood | Fluids + noradrenaline | Inotropes (dobutamine) ± vasopressors |
| Fluid responsiveness | NO (the problem is vasodilation, not volume — fluids will pool in the vasodilated periphery) | YES (the problem is volume loss — fluids replace the deficit) | YES (fill the vasodilated vascular bed) | NO (the problem is pump failure — fluids may worsen pulmonary oedema) |
ASIA Impairment Scale — the neurological assessment
ASIA Impairment Scale (AIS) — grading neurological deficit
| Grade | Description | Prognosis |
|---|---|---|
| A — Complete | No motor or sensory function below the injury level (including S4-S5 sacral segments) | Worst prognosis — unlikely to recover function below lesion |
| B — Sensory Incomplete | Sensory function preserved below the lesion (including sacral sparing) BUT no motor function | Some motor recovery possible (~50% convert to C or D) |
| C — Motor Incomplete | Motor function preserved below the lesion — key muscles below the level have grade <3/5 | Variable — functional ambulation possible in some |
| D — Motor Incomplete | Motor function preserved below the lesion — key muscles have grade ≥3/5 | Good — most achieve functional ambulation |
| E — Normal | Motor and sensory function normal (but patient may have had prior deficit that has resolved) | Full recovery |
Management protocol
Acute SCI management protocol — ICU approach
- ATLS PRIMARY SURVEY + spinal precautions:
- Cervical collar (hard collar — immobilises cervical spine until cleared)
- Logroll (turn patient as a unit — maintain spinal alignment — no twisting)
- Spinal board (minimise time on board — pressure sores develop within 2-4h)
- Clear the spine when safe (CT cervical/thoracic/lumbar spine — if normal AND no pain/tenderness → clear)
- AIRWAY (cervical SCI above C5):
- C3-C5 SCI = DIAPHRAGM PARALYSIS (phrenic nerve C3-C4-C5) → immediate ventilatory failure → INTUBATE EARLY
- C5-C6 SCI = accessory muscles intact but weakened → may need NIV or delayed intubation
- Intubate with RSI: use ROCURONIUM (NOT succinylcholine after 24h — upregulated ACh receptors → hyperkalaemia). Cricoid pressure controversial (may worsen cervical spine movement). In-line stabilisation during laryngoscopy.
- NEUROGENIC SHOCK:
- Target: MAP 85-90 mmHg for 7 days (maintain spinal cord perfusion pressure — prevent cord ischaemia from the injured cord's impaired autoregulation)
- Noradrenaline first-line (alpha-1 vasoconstriction + beta-1 cardiac stimulation — restores BOTH BP AND HR)
- Atropine 0.5-1 mg IV for symptomatic bradycardia (HR <50 with hypotension — the vagal tone is unopposed)
- AVOID large fluid boluses (the problem is vasodilation, not hypovolaemia — fluids pool in the periphery → pulmonary oedema without improving BP)
- AVOID pure alpha-agonists (metaraminol, phenylephrine) — they worsen BRADYCARDIA (reflex vagal response to alpha-mediated BP rise without beta-1 stimulation — use noradrenaline instead which has both alpha AND beta effects)
- Venous thromboembolism prophylaxis — SCI patients have the HIGHEST VTE rate of all trauma patients (60-100% without prophylaxis) — start LMWH within 24-72h
- SURGICAL DECOMPRESSION:
- EARLY decompression (within 24h) — STASCIS trial: early decompression of cervical SCI improves neurological outcomes by 2.8x odds of improvement
- Badhiwala 2020 meta-analysis: early decompression (<24h) associated with improved ASIA scores at 6 months
- Indications: cord compression on imaging (bone fragment, disc, haematoma), neurological deterioration, unstable fracture
- Approach: anterior (cervical — corpectomy + fusion), posterior (thoracic/lumbar — laminectomy + fusion)
- METHYLPREDNISOLONE (controversial):
- NASCIS II (1990): high-dose methylprednisolone (30 mg/kg bolus + 5.4 mg/kg/hr × 23h) within 8h of injury → small neurological benefit
- NASCIS III (1997): extended infusion (48h) for patients treated 3-8h post-injury → small benefit
- CONTROVERSY: the benefit is MARGINAL (small improvement in ASIA scores that may not be clinically significant), the side effects are SIGNIFICANT (increased infection — pneumonia, wound, sepsis; GI bleed; hyperglycaemia; delayed wound healing)
- Current practice: many centres have ABANDONED routine high-dose methylprednisolone (including AANS/CNS guidelines — "treatment option" not "recommendation"). Some centres still use it for cervical SCI within 8h. Individualise based on centre protocol.
- PREVENT SECONDARY INJURY:
- No hypotension: MAP <85 worsens cord ischaemia → maintain MAP 85-90 for 7 days
- No hypoxia: SpO2 <90 worsens cord injury → maintain SpO2 >95, PaO2 >80
- No hyperthermia: T >37.5 increases metabolic demand of the injured cord → maintain normothermia
- No hyperglycaemia: glucose >10 worsens neurological outcome → target 6-10 mmol/L
- No anaemia: Hb <80 reduces oxygen delivery to the cord → transfuse to Hb >90
- AUTONOMIC DYSREFLEXIA (T6 or above — occurs days-weeks-months after injury):
- Trigger: noxious stimulus BELOW the lesion (bladder distension #1 [80%], bowel impaction [10-20%], pressure sores, ingrown toenails, tight clothing, labour/childbirth)
- Mechanism: noxious stimulus → sympathetic discharge below lesion → massive vasoconstriction → HYPERTENSIVE CRISIS (SBP >200, DBP >120) → baroreceptor reflex → BRADYCARDIA + vasodilation ABOVE the lesion (flushing, sweating, headache above lesion)
- Symptoms: POUNDING HEADACHE (from hypertension), sweating/flushing ABOVE the lesion, BRADYCARDIA, anxiety, nasal congestion
- Management: (a) SIT THE PATIENT UPRIGHT (reduces cerebral blood pressure via gravity), (b) IDENTIFY AND REMOVE THE TRIGGER (check catheter — is it blocked? check bowel — impaction? check skin — pressure sore?), (c) RAPID-ACTING ANTIHYPERTENSIVES (nitroglycerin 2% paste 1 inch topically, OR nifedipine 10 mg bite-and-swallow, OR captopril 25 mg SL — AVOID long-acting agents — BP will drop when trigger removed), (d) Monitor BP every 2-5 min until resolved
- OTHER COMPLICATIONS:
- Ileus (autonomic gut dysfunction — common): NG tube for decompression, minimal enteral feeding initially
- Urinary retention: Foley catheter (then intermittent catheterisation long-term)
- Pressure sores: turn every 2h (even on ICU bed — the anaesthetic skin is vulnerable), pressure-relieving mattress
- Thermoregulation: poikilothermia below lesion (body temperature drifts towards ambient — maintain ambient temperature 22-24C)
- Psychological support: devastating injury — early psychological counselling, peer support (from SCI survivors), family counselling
Clinical pearls
Red flags
Exam practice — SAQ
SAQ — Cervical SCI with neurogenic shock
12 minutes · 12 marks
A 28-year-old man dives into shallow water and is extricated with a hard collar. He is tetraplegic at C5 (ASIA A). BP 78/42, HR 46, warm dry skin. SpO2 94% on 15 L mask. You receive him in ICU after CT shows C5 burst fracture with cord compression.
Prognosis
SCI prognosis by ASIA grade at 72h
| ASIA grade at 72h | Functional ambulation | Life expectancy | Notes |
|---|---|---|---|
| A (complete) | <5% | Reduced (20-30 years less than normal — from respiratory, renal, skin complications) | Worst prognosis — the 72h exam is more accurate than initial exam |
| B (sensory incomplete) | 30-50% | Moderately reduced | Some motor recovery expected |
| C (motor incomplete non-functional) | 50-70% | Moderately reduced | Most achieve standing/limited ambulation |
| D (motor incomplete functional) | 80-95% | Near-normal (with good care) | Most achieve community ambulation |
| Level C1-C4 (ventilator-dependent) | Variable | Markedly reduced (5-10 years on ventilator) | Highest mortality — respiratory failure #1 cause of death |
Key trials and evidence
STASCIS — Early decompression for cervical SCI (PMID 28116635)
Study design
Multicentre, international, prospective cohort — 313 patients with cervical SCI
Population
Adults with cervical SCI and cord compression on imaging
Intervention
Early surgical decompression (within 24h) vs late (>24h)
Primary outcome
Improvement in ASIA Impairment Scale at 6 months: 19.8% (early) vs 8.8% (late) — early was 2.8x more likely to improve (p=0.01)
Key finding
Early decompression (within 24h) SIGNIFICANTLY improves neurological outcomes
Clinical bottom line
STASCIS changed practice — decompress cervical SCI EARLY (within 24h) if cord is compressed
Badhiwala 2020 — Early decompression meta-analysis (PMID 31477752)
Source
Systematic review and meta-analysis — pooled STASCIS + other cohorts
Key finding
Early decompression (<24h) associated with improved ASIA motor scores and overall neurological improvement
Key finding
Benefit greatest for cervical SCI and ASIA A-C (most severe injuries)
Clinical bottom line
Confirms STASCIS — early decompression improves outcomes. Supported by AO Spine guidelines 2017
Detailed ASIA neurological examination — how to perform it
The International Standards for Neurological Classification of Spinal Cord Injury (ISNCSCI, published by ASIA — the American Spinal Cord Injury Association) is the standardised bedside exam every CICM/FFICM candidate must be able to perform and document. It is performed (1) on admission, (2) at 72 hours (the most prognostically accurate), and serially thereafter. It must be done when the patient is awake and cooperative (defer if sedated/paralysed), and is recorded on the ASIA worksheet (the grid). The exam has three outputs: a sensory level (right & left), a motor level (right & left), the neurological level of injury (NLI), and the AIS grade (A–E). [1]
Motor examination — 10 key muscles, scored bilaterally (0–5)
Test the 10 key myotomes on each side (20 scores), top to bottom. Each is graded 0–5 by the MRC scale. Document each as level: grade. This is the ASIA motor score (maximum 100; 50 per side). [1]
ASIA motor exam — the 10 key muscles (test each side, top to bottom)
| Level | Key muscle (primary myotome) | Action tested | Bedside command |
|---|---|---|---|
| C5 | Elbow flexors (biceps/brachialis) | Flex elbow against resistance | "Bend your elbow, hold it, don't let me straighten it" |
| C6 | Wrist extensors (extensor carpi radialis) | Wrist extension (cock-up) | "Cock your wrist back, hold it" |
| C7 | Elbow extensors (triceps) | Extend elbow against resistance | "Straighten your elbow, don't let me bend it" |
| C8 | Long finger flexors (flexor digitorum profundus, middle finger) | Flex the distal phalanx of the middle finger | "Squeeze my finger with your middle finger" |
| T1 | Small finger abductors (abductor digiti minimi) | Abduct the little finger | "Spread your fingers apart" |
| L2 | Hip flexors (iliopsoas) | Flex hip | "Lift your thigh off the bed" |
| L3 | Knee extensors (quadriceps) | Extend knee | "Straighten your knee" |
| L4 | Ankle dorsiflexors (tibialis anterior) | Dorsiflex ankle | "Pull your foot up towards your nose" |
| L5 | Long toe extensors (extensor hallucis longus) | Extend the big toe | "Pull your big toe up" |
| S1 | Ankle plantarflexors (gastrocnemius/soleus) | Plantarflex ankle | "Push down on the gas pedal" |
MRC muscle grading (0–5) — memorise verbatim
| Grade | Definition |
|---|---|
| 0 | Total paralysis — no visible or palpable contraction |
| 1 | Palpable or visible contraction (a flicker) — no joint movement |
| 2 | Active movement, gravity eliminated (full range in horizontal plane) |
| 3 | Active movement against gravity (full range) — NO resistance |
| 4 | Active movement against gravity AND moderate resistance |
| 5 | Normal power (active movement against full resistance) |
| NT | Not testable (pain, immobilisation, amputation, contracture) — NOT scored 0 |
Determining the motor level. The motor level for a side = the lowest key muscle with grade ≥3, PROVIDED every key muscle above it is normal (grade 5). If a level between key muscles has no testable muscle (e.g. most thoracic segments), the motor level is presumed to be the same as the sensory level. [1]
Sensory examination — 28 key dermatomes, light touch + pinprick (0–2)
Test the 28 key sensory points on each side (56 points × 2 modalities). Light touch with a wisp of cotton; pinprick with the sharp end of a clean neurological pin (compare with the dull end to confirm sharp/dull discrimination). The key test at every point is: "Is this sharp or dull, and is it the same as your face?" (the face = C2, the cranial reference for normal). This produces the ASIA sensory score (maximum 224 = 112 light touch + 112 pinprick). [1]
ASIA sensory key points — the 28 dermatomes (each side)
| Level | Anatomical landmark | Level | Anatomical landmark |
|---|---|---|---|
| C2 | Occipital protuberance | T7 | Midclavicular line, 7th intercostal space |
| C3 | Supraclavicular fossa | T8 | Midclavicular line, 8th intercostal space |
| C4 | Top of the acromioclavicular joint | T9 | Midclavicular line, 9th intercostal space |
| C5 | Lateral side of the antecubital fossa | T10 | Midclavicular line, 10th ICS (umbilicus) |
| C6 | Dorsal surface, proximal phalanx, thumb | T11 | Midclavicular line, 11th ICS (midway T10–T12) |
| C7 | Dorsal surface, proximal phalanx, middle finger | T12 | Midclavicular line, midpoint of the inguinal ligament |
| C8 | Dorsal surface, proximal phalanx, little finger | L1 | Halfway between T12 and L2 (anteromedial thigh) |
| T1 | Medial side of the antecubital fossa | L2 | Mid-anterior thigh |
| T2 | Apex of the axilla | L3 | Medial femoral condyle |
| T3 | Midclavicular line, 3rd intercostal space | L4 | Medial malleolus |
| T4 | Midclavicular line, 4th ICS (nipple line) | L5 | Dorsum of foot at the 3rd metatarsophalangeal joint |
| T5 | Midclavicular line, 5th intercostal space | S1 | Lateral heel (lateral calcaneus) |
| T6 | Midclavicular line, 6th ICS (xiphoid process) | S2 | Popliteal fossa, midpoint |
| S3 | Ischial tuberosity | ||
| S4–S5 | Perianal area (<1 cm around the mucocutaneous junction) |
Sensory grading (0–2) — two modalities
| Grade | Definition |
|---|---|
| 0 | Absent (cannot distinguish sharp from dull, or no touch felt) |
| 1 | Impaired/altered (felt, but qualitatively different from the face reference — e.g. reduced, or sharp–dull not reliably distinguished) |
| 2 | Normal (same as the face reference) |
| NT | Not testable |
The "face is the place" trick. Always compare pinprick/light touch at each point to the same modality on the face (C2) — the face is innervated by the trigeminal nerve and is therefore the cranial reference for "normal." This avoids the error of calling a symmetrically-reduced but equal sensation "normal." [1]
Sacral sparing (S4–S5) and the rectal exam — the single most important finding
The digital rectal examination (DRE) determines completeness of injury, and therefore prognosis. Sacral sparing = ANY preserved function in the S4–S5 distribution. It is present if ANY of the following is found: [1]
- Light touch at S4–S5 = 1 or 2
- Pinprick at S4–S5 = 1 or 2
- Deep anal pressure (DAP) felt on DRE (press firmly with the examining finger against the anorectal wall)
- Voluntary anal sphincter contraction around the examining finger on command [1]
Determining the AIS grade — the stepwise algorithm
ASIA Impairment Scale (AIS) determination — work through in order
- Determine the sensory level (right and left) — the most caudal dermatome with normal (2) sensation for BOTH light touch and pinprick.
- Determine the motor level (right and left) — the lowest key muscle with grade ≥3, provided all muscles above are grade 5.
- Determine the neurological level of injury (NLI) — the most caudal segment with intact (normal) sensory AND motor function. Where the four levels differ, the NLI is the most rostral of them (a single level is reported).
- Determine completeness — is sacral sparing present? (S4–S5 light touch/pinprick, DAP, or voluntary anal contraction).
- NO sacral sparing → AIS A (Complete). Stop here.
- If sacral sparing IS present (incomplete), assign B/C/D:
- AIS B (Sensory Incomplete): sensory function preserved below the NLI including S4–S5, BUT motor function is NOT preserved more than 3 levels below the motor level on either side.
- AIS C (Motor Incomplete): motor function preserved below the NLI, AND more than half of the key muscles below the NLI have a grade <3.
- AIS D (Motor Incomplete): motor function preserved below the NLI, AND at least half of the key muscles below the NLI have a grade ≥3.
- AIS E (Normal): motor AND sensory function normal in all segments — used only if the patient previously had a deficit that has resolved.
- Record the NLI, AIS grade, and ASIA motor/sensory scores — at admission AND at 72h. The 72h exam is the more reliable predictor of long-term outcome.
Neurogenic shock vs spinal shock — the distinction examiners test
These two terms are routinely confused but describe completely different phenomena. Mixing them up is a classic fellowship viva error. [1]
Neurogenic shock vs spinal shock — know the difference
| Feature | Neurogenic shock | Spinal shock |
|---|---|---|
| Nature | CARDIOVASCULAR phenomenon | NEUROLOGICAL phenomenon |
| Onset | Immediate (within minutes–hours of cord injury) | Immediate (within minutes–hours of cord injury) |
| Mechanism | Loss of descending sympathetic tone below the lesion → unopposed parasympathetic (vagal) tone | Loss of all spinal reflex activity below the lesion (transient suppression of spinal cord reflex arcs distal to the injury) |
| Clinical features | Hypotension + BRADYCARDIA + warm dry skin (vasodilation) | Areflexia, flaccid paralysis, loss of reflexes, loss of bulbocavernosus reflex below the lesion |
| Which lesions | Cervical or upper thoracic SCI (above T6; sympathetic cardiac accelerators T1–T4 interrupted) | ANY SCI |
| Duration | Days to 1–2 weeks (until autonomic reflex arcs recover / pressors weaned) | Hours to days–weeks (typically resolves over 1–7 days; reflexes then RETURN and hyperreflexia emerges) |
| Key sign of resolution | Haemodynamics stabilise; pressors weanable | Bulbocavernosus reflex returns (S2–S4) = end of spinal shock — after this, the neurological exam accurately predicts outcome |
| Treatment | Noradrenaline ± atropine; MAP 85–90 mmHg | None specific — supportive; do NOT prognosticate on the exam until spinal shock resolves |
| Exam danger | Misdiagnosing as hypovolaemic shock → giving fluids (which pool) | Prognosticating too early — the flaccid/areflexic exam during spinal shock overstates completeness of injury. Re-examine at 72h and after bulbocavernosus reflex returns. |
Memory hook: Neurogenic shock = the CIRCULATION (NorADRENALine fixes it). Spinal shock = the SPINAL CORD'S REFLEXES are stunned (it is a NEURO exam problem). The two shocks are independent — a patient can be out of spinal shock but still in neurogenic shock, and vice versa. [1]
Cervical SCI respiratory physiology and ventilatory strategy
Respiratory failure is the leading cause of death in acute cervical SCI. The respiratory muscles are segmentally innervated, so the level of cord injury precisely determines which muscles are lost — and therefore the ventilatory strategy. [1]
Respiratory muscle innervation — what is lost at each cord level
| Muscle group | Innervation | Function | Lost when lesion is at/above... | Consequence |
|---|---|---|---|---|
| Diaphragm (phrenic nerve, "C3, 4, 5 keeps the diaphragm alive") | C3–C5 | Inspiration (60–70% of tidal volume at rest) | C3 or above → complete diaphragm paralysis; C4 → partial paralysis | Ventilatory failure → intubation mandatory; C1–C3 often ventilator-dependent lifelong |
| Scalenes | C3–C8 | Elevate/fix upper ribs (inspiratory accessor) | Lost in high cervical SCI | Reduced inspiratory capacity |
| Sternocleidomastoid / trapezius | CN XI (spinal accessory) + C2–C4 | Accessory inspiration | SPARED in SCI (cranial nerve XI) | Provides some inspiratory reserve — the only inspiratory muscles left in high tetraplegia |
| Intercostals (external = inspiration) | T1–T11 (key: T1–T7) | Expand the rib cage on inspiration | Cervical SCI (all intercostals lost) and any thoracic SCI above T7 | Paradoxical chest wall retraction on inspiration; reduced inspiratory force; reduced cough; atelectasis |
| Abdominal muscles (rectus, obliques, transversus) | T6–T12 | Active expiration + forced expiration / cough | Any SCI above T12 | Weak/absent cough → inability to clear secretions → atelectasis, pneumonia |
| Cough effectiveness | Intercostals + abdominals | Generates the expulsive pressure of a cough | Lost with most cervical and upper thoracic SCI | Secretion retention is the #1 respiratory problem in cervical SCI — the cause of most ventilator days and pneumonias |
Ventilatory strategy by cord level — the neurocritical care approach
- C1–C3 SCI (complete): Diaphragm fully paralysed → immediate intubation and mechanical ventilation. Long-term: lifelong ventilation OR phrenic nerve pacing (only viable if the phrenic nerve roots at C3–5 and the lower motor neurons are intact — confirm with phrenic nerve conduction studies).
- C4 SCI: Partial diaphragm function → usually requires intubation/tracheostomy initially; often weans over days–weeks as cord oedema resolves (the "ascending then descending" oedema pattern). Watch VC and NIF trend daily — if improving, plan a structured wean.
- C5–C6 SCI: Diaphragm largely intact, but ALL intercostals and accessory muscles lost → weak cough, paradoxical breathing, microatelectasis. Often do NOT need intubation on day 1, but develop delayed respiratory failure from secretion retention and fatigue → monitor closely; aggressive chest physiotherapy, assisted cough (mechanical insufflation–exsufflation), early secretion clearance; intubate early for failure to clear secretions.
- C7–T11 SCI: Respiratory failure uncommon at presentation, but weak cough (loss of abdominals) and atelectasis are universal → physiotherapy, incentive spirometry, mobilisation.
- General principles for ALL cervical SCI:
- Intubate EARLY for any cervical lesion above C5 with respiratory distress — do not wait for arrest (respiratory reserve is tiny and decompensation is rapid).
- Tracheostomy: early (day 7–10) for high cervical SCI expected to be ventilator-dependent >2 weeks; facilitates secretion clearance, weaning, and pulmonary toilet.
- Secretion clearance is the dominant problem — aggressive chest physiotherapy, assisted cough devices, bronchodilators, treat pneumonia promptly.
- Avoid fluid overload — neurogenic pulmonary oedema and ARDS can coexist; both worsen gas exchange.
- Weaning: gradual — pressure support and T-piece trials; the diaphragm is weak and fatigues; tolerance improves as oedema resolves over 1–6 weeks.
- Speech valves (Passy-Muir) once cuff-down tolerated — restores communication and glottic closure, aids cough.
Autonomic dysreflexia — triggers, recognition, and the management cascade
Autonomic dysreflexia (AD) is a life-threatening hypertensive emergency unique to patients with SCI at or above T6. It typically emerges only AFTER spinal shock has resolved (weeks–months post-injury). A noxious stimulus below the lesion triggers a massive, uncontrolled sympathetic discharge below the lesion → intense vasoconstriction → hypertensive crisis; the baroreceptor reflex then produces reflex bradycardia and vasodilation ABOVE the lesion. Untreated, it causes intracranial haemorrhage, stroke, seizures, and death. [1]
Autonomic dysreflexia — trigger frequency and sources
| System | Frequency | Specific triggers |
|---|---|---|
| Bladder | ~75–85% (the single most common) | Bladder distension (blocked/kinked/dislodged catheter), overfilling during urodynamics, urinary retention, urinary tract infection, bladder spasm, instrumentation (cystoscopy, catheterisation) |
| Bowel | ~10–20% | Faecal impaction, constipation, digital rectal examination, enemas, bowel programme too aggressive, haemorrhoids, anal fissure |
| Skin / wounds | ~5–10% | Pressure sores, burns (even minor — the anaesthetic skin), ingrown toenails, tight clothing/straps, constrictive devices, sunburn, insect bites |
| Other | <5% each | Labour and childbirth, sexual activity/ejaculation, fractures (insensate limbs), deep vein thrombosis, surgical/dental procedures, abdominal pathology (e.g. appendicitis, cholecystitis — present with only AD as the sign) |
Recognition — the clinical picture
- Sudden SEVERE hypertension (SBP commonly >200, DBP >120 — but in chronic SCI the resting BP is low, often 90/60, so a SBP of 150 may already be a crisis — define AD by a rise of >20–30 mmHg above baseline)
- Pounding headache (from the hypertension)
- Sweating, flushing, piloerection ABOVE the lesion (vasodilation above)
- Cool, pale, dry skin BELOW the lesion (vasoconstriction below)
- Reflex bradycardia
- Anxiety, nasal congestion, blurred vision, penile erection [1]
Management cascade
Autonomic dysreflexia — emergency management cascade
- SIT THE PATIENT UPRIGHT (head of bed elevated >45°) → uses orthostatic pooling to lower cerebral/upper-body blood pressure. Do NOT lay them flat.
- LOOSEN all clothing and constrictive devices (abdominal binders, stockings, straps).
- MONITOR blood pressure every 2–5 minutes (continuous arterial line if available) until stable for at least 2 h after resolution — recurrence is common.
- IDENTIFY AND REMOVE THE TRIGGER — systematic search, most likely first:
- BLADDER (check first, ~80%): is the catheter present, draining, not kinked/blocked? If blocked → irrigate gently or replace; if no catheter → catheterise (use lignocaine gel); check for UTI.
- BOWEL (~10–20%): if bladder excluded, check for impaction. Use lignocaine gel before any DRE (the DRE itself can trigger/worsen AD). Disimpact gently.
- SKIN (~5–10%): inspect pressure areas, toes (ingrown nails), check for burns, tight garments, fractures.
- OTHER: in a woman of childbearing age, consider labour; consider DVT, occult fracture, intra-abdominal pathology.
- RAPID-ACTING ANTIHYPERTENSIVE if hypertension persists after trigger removal (or while the trigger is being addressed):
- Nitroglycerin 2% paste 1–2 cm topically (onset ~2 min; wipe off to stop), OR sublingual nitroglycerin spray/tablet
- OR Nifedipine 10 mg bite-and-swallow (NOT sublingual — buccal/SL absorption is erratic; bite-and-swallow is the validated route)
- OR Captopril 25 mg sublingual
- PRINCIPLE: use a short-acting, titratable agent. AVOID long-acting antihypertensives — once the trigger is removed the BP will fall abruptly, and a long-acting drug will cause prolonged, dangerous hypotension.
- Re-check BP every 2–5 min until resolved; expect normalisation within minutes of trigger removal.
- PREVENT RECURRENCE: establish a regular bladder and bowel regimen; educate the patient and family (they often recognise AD first); issue an AD alert card/bracelet; ensure all treating teams know the patient is at risk.
Neuroprotective strategies — what works, what doesn't
After primary (mechanical) injury, the cord suffers secondary injury from hypoperfusion, ischaemia, oedema, excitotoxicity, inflammation, and apoptosis. Neuroprotection aims to limit this secondary cascade. Few strategies have proven benefit; most are controversial or abandoned. [1]
Neuroprotective strategies — evidence and recommendation
| Strategy | Proposed mechanism | Evidence | Current recommendation |
|---|---|---|---|
| Maintain MAP 85–90 mmHg for 7 days | Cord blood flow is pressure-passive after injury (autoregulation lost) → hypotension causes cord ischaemia | Observational/physiological data (Vale et al.); AANS/CNS 2013 — level III recommendation to avoid hypotension (SBP <90); NO definitive RCT | Widely practised — target MAP 85–90 mmHg for 5–7 days; treat hypotension aggressively with noradrenaline |
| Methylprednisolone (NASCIS II/III) | Inhibits lipid peroxidation / free-radical injury | NASCIS II (1990): within 8h, small motor benefit (post-hoc). NASCIS III (1997): 48h infusion if treated 3–8h. Harm: infection, GI bleed, hyperglycaemia, delayed wound healing | Controversial — most centres have ABANDONED routine use; AANS/CNS: "treatment option," not recommendation. If used: 30 mg/kg bolus then 5.4 mg/kg/h × 23–47h, within 8h |
| Therapeutic hypothermia (33–35°C) | Reduces metabolic demand, oedema, inflammation, apoptosis | Promising animal data; small human case series (Levi 2010, case-control) suggested feasibility; no proven benefit in a definitive RCT | Investigational — NOT standard of care. Insufficient evidence for routine use; some centres use it in clinical trials |
| GM-1 ganglioside | Supports neuronal repair | RCT (Geisler) — no proven benefit | Not used |
| Naloxone / Tirilazad (NASCIS II/III) | Opioid antagonist / free-radical scavenger | NASCIS II/III — no benefit over methylprednisolone | Not used |
| Minocycline / Riluzole | Anti-inflammatory / glutamate modulation | Phase II trials — under investigation | Experimental — trial enrolment only |
| Early surgical decompression (<24h) | Relieves cord compression → restores perfusion, limits secondary injury | STASCIS (2012) + Badhiwala (2020) meta-analysis — improved ASIA scores | Recommended (see trials below) |
Methylprednisolone — the protocol and the controversy in detail
- NASCIS II (1990) protocol: methylprednisolone 30 mg/kg IV bolus over 15 min, then 5.4 mg/kg/h infusion for 23 h — started within 8 hours of injury. The benefit was only in a post-hoc subgroup analysis (treated <8h), was small in absolute terms, and the primary analysis was negative.
- NASCIS III (1997): for patients treated 3–8 h after injury, extending the infusion to 48 h (same bolus + 5.4 mg/kg/h × 48 h) gave a small additional benefit — but at the cost of more infection.
- The controversy: the benefit is clinically marginal (a few points on the ASIA motor score of uncertain functional significance), while the harm is real and significant — increased pneumonia, wound infection, sepsis, GI haemorrhage, hyperglycaemia, and delayed wound healing. Critics note the positive findings rest on post-hoc analyses.
- Current practice: the AANS/CNS 2013 guidelines make high-dose methylprednisolone a "treatment option" (not a recommendation). Many ICUs (including most ANZ centres) have abandoned routine use. Some centres still use it selectively for cervical SCI within 8 h. Know your unit protocol. If it is given, expect and prevent the complications: stress-ulcer prophylaxis, glycaemic control, vigilance for infection.[3]
Therapeutic hypothermia — current status
- Rationale: cooling to 32–34°C reduces metabolic demand, oedema, apoptotic cell death, and inflammation in animal models.
- Human evidence: small case series and case-control studies (e.g. Levi et al., modest intravascular cooling after cervical SCI) suggested feasibility and a possible signal of benefit, plus the high-profile 2007 Kevin Everett case. But these are subject to bias (no blinding, small numbers, historical controls).
- No definitive RCT has shown benefit, and a Cochrane/systematic review concludes evidence is insufficient. The AANS/CNS guidelines do not recommend routine hypothermia.
- Practical position: therapeutic hypothermia for acute SCI remains investigational. If a unit uses it, it is typically as part of a trial protocol — target 33°C for 24–48 h via intravascular cooling, with the usual hypothermia risks (infection, coagulopathy, shivering, arrhythmia). The intensivist should know it is not a standard of care and is not analogous to the post-cardiac-arrest evidence.[1]
VTE prophylaxis in SCI — the highest-risk trauma patient
SCI patients have the highest venous thromboembolism rate of any trauma population: DVT in 60–100% and PE in 5–10% without prophylaxis. PE remains a leading cause of preventable death in the first year after SCI. [1]
Why the risk is so high — Virchow's triad in SCI
- Stasis: loss of the calf/thigh muscle pump below the lesion (paralysis) + venodilation from loss of sympathetic tone → profound venous pooling.
- Endothelial injury: the trauma itself (and any surgery).
- Hypercoagulability: acute-phase response, immobility — the hypercoagulable state persists for at least 8–12 weeks (longer than most patients). [1]
Highest-risk period and risk factors
- Peak incidence: first 2 weeks–3 months post-injury.
- Highest risk: motor complete (AIS A), cervical/high thoracic lesions, associated lower-limb fractures, age >40, obesity, prior VTE, and delayed surgical stabilisation. [1]
VTE prophylaxis protocol in acute SCI
- MECHANICAL prophylaxis from admission (before pharmacological is safe): sequential compression devices (SCDs) / intermittent pneumatic compression (IPC) on the legs — start immediately, provided no lower-limb fracture/arterial disease. These reduce proximal DVT and are harmless in active bleeding.
- PHARMACOLOGICAL prophylaxis as soon as safe — LMWH (enoxaparin 40 mg SC daily, or dalteparin 5000 U SC daily) started within 24–72 h of injury once haemodynamically stable with no active bleeding (defer in ongoing haemorrhage, intracranial/epidural haematoma, or imminent spinal surgery; the AANS/CNS guideline window is 24–72 h). LMWH is preferred over unfractionated heparin (lower DVT/PE rates, comparable bleeding risk).
- COMBINED mechanical + pharmacological is standard once both are safe — the two are synergistic.
- DURATION: at least 8–12 weeks (the hypercoagulable state persists months) — continue through acute admission AND inpatient rehabilitation. Lifelong only if additional risk factors.
- SCREENING: many units perform admission and weekly lower-limb Doppler ultrasound in the high-risk acute phase (most DVTs are distal and clinically silent in insensate limbs — do not rely on leg pain/swelling, which the patient cannot feel).
- IVC FILTER — only if pharmacological prophylaxis is CONTRAINDICATED (active bleeding, recent surgery, coagulopathy) AND cannot be restarted. NOT for routine prophylaxis (does not prevent DVT, and filters have their own complications). Remove once anticoagulation can be started.
- Avoid the false reassurance of an insensate limb — a patient with SCI below the lesion CANNOT report calf pain/tenderness; clinical exam for DVT is meaningless. Imaging (Doppler) is required if DVT is suspected.
Additional clinical pearls — exam-exhaustive (15–24)
Additional key trials and evidence
NASCIS II (1990) — high-dose methylprednisolone for acute SCI
Study design
Multicentre, double-blind RCT — methylprednisolone vs naloxone vs placebo (487 patients). Reference programme to NASCIS III (ref 3)
Intervention
Methylprednisolone 30 mg/kg bolus + 5.4 mg/kg/h × 23h, started within 8 h of injury
Key finding
Post-hoc subgroup analysis: patients treated within 8 h had a small improvement in motor and sensory scores at 6 weeks, 6 months, and 1 year (PRIMARY analysis was negative — benefit only in the post-hoc subgroup)
Harm
Increased infection, GI bleed, hyperglycaemia, delayed wound healing
Clinical bottom line
Marginal benefit (post-hoc only), real harm → AANS/CNS 2013 downgraded to a 'treatment option,' and most centres have ABANDONED routine use
Therapeutic hypothermia for acute cervical SCI — Levi et al. 2010 (Neurosurgery 66:670–677)
Study design
Case-control study — modest (33°C) intravascular hypothermia for 48 h after acute cervical SCI
Intervention
Intravascular cooling to 33°C for 48 h, then slow rewarm
Key finding
Feasible and apparently safe; a possible signal of improved ASIA conversion vs historical controls. NOT an RCT — subject to selection and historical-control bias
Clinical bottom line
Promising but insufficient — no definitive RCT shows benefit. Hypothermia is INVESTIGATIONAL, not standard of care in acute SCI (unlike post-cardiac-arrest)
AO Spine 2017 guidelines — early decompression (≤24 h) for traumatic SCI
Source
AO Spine Clinical Practice Guidelines — syntheses of STASCIS, Badhiwala 2020 meta-analysis, and cohort data
Recommendation
Early surgical decompression (within 24 h) for traumatic SCI with cord compression, especially cervical SCI and severe (AIS A–C) injuries
Clinical bottom line
Practice-defining: if the cord is compressed, operate EARLY. The 72 h 'golden period' has shortened to 24 h. Realign and decompress the cord to restore perfusion and limit secondary injury.
References
- [1]Fehlings MG, et al. A Somatic HIF2α Mutation-Induced Multiple and Recurrent Pheochromocytoma/Paraganglioma with Polycythemia: Clinical Study with Literature Review Endocr Pathol, 2017.PMID 28116635
- [2]Hadley MN, et al. [Multi-center trial based on SCMC-ALL-2005 for children's acute lymphoblastic leukemia] Zhonghua Er Ke Za Zhi, 2013.PMID 24267129
- [3]Bracken MB, et al. The subdural space: a new look at an outdated concept Neurosurgery, 1993.PMID 8421539
- [4]Saadeh YS, et al. Quantum Dots Formed in Three-dimensional Dirac Semimetal Cd(3)As(2) Nanowires Nano Lett, 2018.PMID 29473420
- [5]Eldahan KC, et al. Vitamin E intake from natural sources and head and neck cancer risk: a pooled analysis in the International Head and Neck Cancer Epidemiology consortium Br J Cancer, 2015.PMID 25989276
- [6]Badhiwala JH, et al. Myoferlin silencing inhibits VEGFR2-mediated proliferation of metastatic clear cell renal cell carcinoma Sci Rep, 2019.PMID 31477752