Neurogenic Shock

Quick Answer

Neurogenic shock is distributive shock caused by loss of sympathetic tone following acute spinal cord injury (SCI) at ≥T6 level, resulting in unopposed parasympathetic activity. The classic triad is:

1. Hypotension (loss of vasoconstriction)
2. Bradycardia (unopposed vagal tone)
3. Warm, dry peripheries (vasodilation)

Key Management:

• MAP target: 85-90 mmHg for 7 days (AOSpine 2017 guidelines)
• Noradrenaline first-line vasopressor (α + β effects)
• Atropine for symptomatic bradycardia (HR below 50 with hypotension)
• Avoid excessive fluids → pulmonary oedema risk
• Methylprednisolone NOT recommended (NASCIS trials refuted)
• Monitor for autonomic dysreflexia (SCI ≥T6)

Prognosis: Resolves over days-weeks as spinal shock resolves and spinal reflexes return. Autonomic dysreflexia risk persists lifelong in injuries ≥T6.

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CICM Exam Focus

High-Yield Topics

Common SAQ Themes

1. Pathophysiology: Explain the haemodynamic changes in neurogenic shock following C5 SCI
2. Management: Outline resuscitation priorities in a hypotensive patient with acute cervical SCI
3. Vasopressors: Compare and contrast vasopressor options in neurogenic shock
4. Autonomic dysreflexia: Describe the pathophysiology, triggers, and management of autonomic dysreflexia
5. Evidence: Discuss the evidence for MAP targets and steroid use in acute SCI

Viva Scenarios

• 25-year-old with C5 SCI, BP 80/40, HR 45 → Identify neurogenic shock, initiate resuscitation, apply MAP targets
• Differentiating neurogenic shock from haemorrhagic shock in polytrauma
• Managing refractory hypotension despite vasopressors
• Recognizing and managing autonomic dysreflexia (BP 220/120, headache, sweating in T4 paraplegic)

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Key Points

1. Neurogenic shock = distributive shock from loss of sympathetic tone after SCI ≥T6
2. Classic triad: Hypotension + bradycardia + warm peripheries (vs cold peripheries in hypovolaemic shock)
3. Pathophysiology: Loss of sympathetic outflow (T1-L2) → vasodilation, unopposed vagal tone
4. Level matters:
   • ≥T6: Risk neurogenic shock + autonomic dysreflexia
   • under T6: Partial sympathetic preservation, less severe
5. MAP target: 85-90 mmHg × 7 days (AOSpine 2017 guidelines for spinal cord perfusion)
6. Vasopressor: Noradrenaline first-line (α + β effects overcome bradycardia)
7. Bradycardia: Treat if symptomatic (HR below 50 + hypotension) with atropine 0.5 mg IV
8. Fluid management: Avoid overload → pulmonary oedema (loss of venous tone)
9. Steroids: NOT recommended (NASCIS trials refuted by AANS/CNS 2013, AOSpine 2017)
10. Autonomic dysreflexia: Life-threatening hypertensive crisis in SCI ≥T6 (bladder/bowel distension triggers)
11. Duration: Resolves over days-weeks as spinal shock resolves and spinal reflexes return
12. Differential: Must exclude haemorrhagic shock in trauma (FAST, CT, serial Hb)

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Introduction

Definitions

Neurogenic Shock

• Distributive shock caused by loss of sympathetic tone following acute spinal cord injury (SCI)
• Results in vasodilation, venous pooling, and unopposed parasympathetic (vagal) activity
• Characterized by hypotension, bradycardia, and warm peripheries

Spinal Shock

• Neurological phenomenon of flaccid paralysis and areflexia below the level of SCI
• Occurs immediately after SCI, lasts days-weeks
• Neurogenic shock often occurs during spinal shock but they are distinct entities
• Spinal shock resolves when spinal reflexes return (bulbocavernosus reflex, anal wink)

Autonomic Dysreflexia

• Life-threatening hypertensive crisis in SCI ≥T6 due to uncontrolled sympathetic reflex to noxious stimulus below injury level
• Occurs after spinal shock resolves (weeks-months post-injury)
• Triggered by bladder/bowel distension, pressure sores, procedures

Distinction: Neurogenic vs Spinal Shock

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Epidemiology

Incidence

• Spinal cord injury (SCI): ~40-50 cases per million population annually (Australia/NZ)
• Neurogenic shock: Occurs in 20-30% of acute SCI patients
• Higher risk with:
  • Cervical SCI (50-70% neurogenic shock)
  • High thoracic SCI (T1-T6) (30-40% neurogenic shock)
  • Complete injuries (ASIA A) vs incomplete (ASIA B-D)
  • Penetrating trauma vs blunt trauma

Demographics

• Age: Bimodal distribution
  • "Peak 1: 15-30 years (motor vehicle crashes, sports)"
  • "Peak 2: greater than 60 years (falls, elderly)"
• Sex: Male predominance (4:1 ratio)
• Mechanism:
  • Motor vehicle crashes (40-50%)
  • Falls (20-30%, higher in elderly)
  • Sports injuries (10-15%, diving, rugby, equestrian)
  • Violence (10-15%, penetrating trauma)
  • Other (5-10%, iatrogenic during spine surgery)

Risk Factors for Neurogenic Shock

Key References:

• Summers et al. (2011). Injury. PMID: 21129739 - Acute SCI epidemiology in Australia
• Ahn et al. (2017). J Trauma Acute Care Surg. PMID: 28375881 - Neurogenic shock incidence and outcomes
• Levi et al. (2010). Neurosurgery. PMID: 20404772 - SCI epidemiology global perspective

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Pathophysiology

Sympathetic Nervous System Anatomy

Sympathetic Outflow:

• Cell bodies: Intermediolateral cell column (IML) of spinal cord T1-L2
• Cardiac sympathetic innervation: T1-T4 (chronotropy, inotropy)
• Splanchnic circulation: T5-L2 (vasoconstriction, venous tone)
• Adrenal medulla: T10-L1 (catecholamine release)

Normal Cardiovascular Regulation:

• Sympathetic tone maintains:
  • Vascular smooth muscle contraction → peripheral vascular resistance
  • Venous tone → venous return and preload
  • Cardiac contractility and heart rate (T1-T4)
• Parasympathetic (vagal) tone (cranial nerve X) provides opposing influence on heart rate

Mechanisms of Neurogenic Shock

Primary Mechanism: Loss of Sympathetic Tone

1. SCI ≥T6 disrupts sympathetic outflow from T1-L2
2. Loss of vasoconstrictor tone → arterial and venous vasodilation
3. Venous pooling → reduced preload and cardiac output
4. Loss of cardiac sympathetic innervation (T1-T4) → reduced contractility (if C-spine or high T-spine injury)
5. Unopposed parasympathetic (vagal) activity → bradycardia

Haemodynamic Consequences:

Level of Injury and Severity:

Secondary Injury

Primary Injury:

• Mechanical trauma to spinal cord (contusion, laceration, compression)

Secondary Injury:

• Hypotension → spinal cord ischaemia → expansion of injury zone
• Hypoxia → metabolic failure
• Inflammation, oedema, oxidative stress → further tissue damage
• Rationale for MAP targets: Maintain spinal cord perfusion to limit secondary injury

Key Evidence:

• AOSpine 2017 guidelines: MAP 85-90 mmHg × 7 days to optimize spinal cord perfusion (PMID: 28466278)
• Hawryluk et al. (2015): Higher MAP associated with improved neurological recovery (PMID: 26214766)

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Clinical Presentation

Classic Triad of Neurogenic Shock

1. Hypotension (SBP below 90 mmHg or MAP below 65 mmHg)
2. Bradycardia (HR below 60 bpm, often 40-50 bpm)
3. Warm, dry peripheries (vasodilation) — vs cold, clammy skin in hypovolaemic shock

History

Trauma Mechanism:

• Motor vehicle crash, fall from height, diving accident, sports injury, penetrating trauma
• High-impact deceleration, axial loading, hyperflexion/hyperextension

Immediate Symptoms:

• Loss of motor function below injury level
• Loss of sensation (light touch, pain, temperature)
• Loss of bowel/bladder control (neurogenic bladder/bowel)
• Respiratory difficulty (if cervical injury, diaphragm C3-C5)

Associated Injuries (Polytrauma):

• Traumatic brain injury (15-60% of SCI patients)
• Chest trauma (rib fractures, pneumothorax, haemothorax)
• Abdominal trauma (solid organ injury, hollow viscus injury)
• Long bone fractures, pelvic fractures

Examination

General Appearance:

• Warm, dry skin (vasodilation) vs cold, clammy (hypovolaemia)
• Pink/well-perfused peripheries vs pale (haemorrhagic shock)
• Respiratory distress (cervical SCI, loss of intercostals/abdominals)

Vital Signs:

• Hypotension: SBP 70-90 mmHg (may be relative in previously hypertensive patients)
• Bradycardia: HR 40-60 bpm (unopposed vagal tone)
• Normothermia or hypothermia (poikilothermia — inability to thermoregulate)
• Respiratory rate: May be normal or increased (compensatory, or reduced if high cervical injury)

Neurological Examination (ASIA Score):

ASIA Impairment Scale:

• A (Complete): No motor or sensory function in S4-S5
• B (Sensory incomplete): Sensory but no motor function below injury level, including S4-S5
• C (Motor incomplete): Motor function below injury, greater than 50% key muscles below level below 3/5 strength
• D (Motor incomplete): Motor function below injury, ≥50% key muscles below level ≥3/5 strength
• E (Normal): Normal motor and sensory function

Cardiovascular Examination:

• JVP: Low or normal (reduced preload)
• Heart sounds: Normal (no murmurs unless pre-existing)
• Peripheral pulses: Bounding (vasodilation, low SVR)
• Capillary refill: Brisk (warm peripheries)

Respiratory Examination:

• Cervical SCI (C3-C5): Diaphragmatic breathing only, paradoxical abdominal breathing
• High thoracic SCI: Loss of intercostals → reduced vital capacity, weak cough
• Auscultation: Clear if isolated SCI, crackles if pulmonary oedema (fluid overload)

Abdominal Examination:

• Distension: Neurogenic ileus (loss of sympathetic innervation)
• Tenderness: May be absent despite intra-abdominal injury (loss of sensation)
• Rectal tone: Absent (spinal shock)

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Differential Diagnosis

Distinguishing Neurogenic from Other Shock States

Critical Distinction in Trauma:

• Neurogenic shock + haemorrhagic shock can coexist in polytrauma
• Assume haemorrhagic shock until proven otherwise (ATLS principles)
• Warm peripheries + bradycardia suggest neurogenic component
• Cold peripheries + tachycardia suggest haemorrhagic shock
• Perform FAST, CT, serial Hb to exclude bleeding

Other Causes of Hypotension + Bradycardia

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Investigations

Bedside Tests

Vital Signs:

• Continuous ECG monitoring: Identify bradycardia, heart block (rare)
• Blood pressure: Invasive arterial line preferred for continuous MAP monitoring
• Temperature: Poikilothermia (inability to thermoregulate)
• Urine output: Foley catheter, target greater than 0.5 mL/kg/h

Neurological Assessment:

• ASIA score: Document motor/sensory level, completeness of injury
• Rectal examination: Tone, voluntary contraction, bulbocavernosus reflex

Laboratory Tests

Key Points:

• Lactate may be normal or mildly elevated (good peripheral perfusion despite hypotension)
• Serial Hb to exclude ongoing bleeding (haemorrhagic shock)

Imaging

Spinal Imaging (All Patients with SCI):

Trauma Imaging (Polytrauma):

• FAST (Focused Assessment with Sonography for Trauma): Exclude haemoperitoneum
• CT head: Exclude TBI (15-60% of SCI patients)
• CT chest/abdomen/pelvis: Exclude solid organ injury, haemothorax, pneumothorax
• CXR: Exclude pneumothorax, haemothorax, aspiration

Cardiovascular Monitoring:

• Echocardiography: Assess LV function, preload (IVC collapsibility), exclude tamponade
• Cardiac output monitoring: FloTrac, LiDCO, or pulmonary artery catheter (if refractory shock)

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Management

Initial Resuscitation (ATLS Principles)

A — Airway:

• C-spine immobilization (hard collar, blocks, tape)
• Early intubation if:
  • C1-C5 injury (high risk respiratory failure, phrenic nerve C3-C5)
  • GCS below 8 (TBI)
  • Respiratory distress (hypoxia, hypercapnia)
  • Inability to protect airway
• Technique: Manual in-line stabilization (MILS), avoid hyperextension
• Consider awake fibreoptic intubation if difficult airway + unstable C-spine

B — Breathing:

• Supplemental oxygen: Target SpO₂ 94-98%
• Ventilation: If cervical SCI (C3-C5), loss of diaphragm → mechanical ventilation
• Chest drain: If pneumothorax/haemothorax

C — Circulation:

• IV access: 2 × large-bore peripheral cannulae (14-16G)
• Fluid resuscitation:
  • "Initial bolus: 500-1000 mL crystalloid (0.9% NaCl or Hartmann's)"
  • "Caution: Avoid excessive fluids → pulmonary oedema (loss of venous tone)"
  • "Goal: MAP 85-90 mmHg (AOSpine 2017), not normotension"
• Vasopressors: Start early (within 1 hour) if fluids insufficient
• Invasive BP monitoring: Arterial line for continuous MAP monitoring

D — Disability:

• GCS: Exclude TBI
• Pupillary response: Brainstem function
• ASIA score: Motor/sensory level, completeness

E — Exposure:

• Log roll (C-spine precautions)
• Examine back: Spine deformity, step-off, penetrating wounds
• Rectal examination: Tone, voluntary contraction, bulbocavernosus reflex

Haemodynamic Goals

MAP Target: 85-90 mmHg × 7 Days (AOSpine 2017 Guidelines)

• Evidence: Hawryluk et al. (2015) — higher MAP associated with improved neurological recovery (PMID: 26214766)
• Duration: 7 days post-injury to optimize spinal cord perfusion
• After 7 days: Wean MAP target to 65-70 mmHg (standard ICU target)

Heart Rate Target:

• Avoid severe bradycardia (HR below 50 with hypotension)
• Treat with atropine if symptomatic (see below)

Urine Output:

• Target: greater than 0.5 mL/kg/h (marker of end-organ perfusion)

Fluid Management

Principles:

• Avoid excessive fluids → pulmonary oedema (loss of venous tone, venous pooling)
• Initial fluid bolus: 500-1000 mL crystalloid (assess response)
• Limited response to fluids: Start vasopressors early

Fluid Type:

• Crystalloid: 0.9% NaCl or Hartmann's (balanced crystalloid preferred to avoid hyperchloraemic acidosis)
• Colloid: Not routinely recommended (no mortality benefit, SAFE study)
• Blood products: If haemorrhagic shock (Hb below 70 g/L, massive transfusion protocol)

Monitoring:

• CVP: May be low (venous pooling), not reliable for fluid responsiveness
• Echocardiography: IVC collapsibility, LV filling
• Cardiac output monitoring: Guide fluid vs vasopressor therapy

Vasopressor Therapy

First-Line: Noradrenaline

• Mechanism:
  • "α₁-agonist: Vasoconstriction → ↑ SVR, ↑ BP"
  • "β₁-agonist: ↑ inotropy, ↑ chronotropy (overcomes bradycardia)"
• Dose: Start 0.05-0.1 mcg/kg/min, titrate to MAP 85-90 mmHg
• Advantages: Overcomes bradycardia (β₁), restores SVR (α₁)
• Monitoring: Invasive BP, cardiac output if refractory

Second-Line Options:

Avoid Phenylephrine Monotherapy:

• Pure α₁-agonist → vasoconstriction but no chronotropic effect
• Reflex bradycardia → worsens existing bradycardia in neurogenic shock
• May be used in combination with noradrenaline if tachycardia is a concern

Key Evidence:

• Inoue et al. (2014). J Trauma Acute Care Surg. PMID: 24977772 — Noradrenaline vs dopamine in neurogenic shock
• Popa et al. (2010). J Neurotrauma. PMID: 19705964 — Vasopressor use and neurological outcomes

Management of Bradycardia

Indications for Treatment:

• Symptomatic bradycardia: HR below 50 with hypotension or inadequate perfusion
• Severe bradycardia: HR below 40 bpm
• Asystolic pauses greater than 3 seconds

First-Line: Atropine

• Dose: 0.5 mg IV bolus, repeat every 3-5 minutes (max 3 mg total)
• Mechanism: Blocks vagal (parasympathetic) tone → ↑ HR
• Caution: May be ineffective if complete loss of cardiac sympathetics (T1-T4 injury)

Second-Line: Noradrenaline

• β₁-agonist effect → ↑ HR
• Preferred if atropine ineffective

Third-Line: Pacing

• Temporary transcutaneous pacing: If refractory bradycardia, haemodynamically unstable
• Temporary transvenous pacing: If prolonged bradycardia expected
• Permanent pacemaker: Rarely required (most cases resolve with spinal shock resolution)

Avoid:

• Isoprenaline: Pure β-agonist → tachycardia, arrhythmias, myocardial oxygen demand

Spinal Cord Protection

MAP Optimization:

• Target MAP 85-90 mmHg × 7 days (AOSpine 2017)
• Mechanism: Maintain spinal cord perfusion pressure, limit secondary injury

Oxygenation:

• Target SpO₂ 94-98%
• Avoid hypoxia (SpO₂ below 90%) → secondary injury

Avoid Secondary Insults:

• Hypotension (MAP below 65 mmHg)
• Hypoxia (SpO₂ below 90%)
• Hyperthermia (greater than 38.5°C)
• Hyperglycaemia (glucose greater than 10 mmol/L)
• Anaemia (Hb below 70 g/L)

Methylprednisolone: NOT RECOMMENDED

Historical Context:

• NASCIS II (1990): Methylprednisolone 30 mg/kg bolus + 5.4 mg/kg/h × 23 hours within 8 hours of injury showed modest motor improvement (PMID: 2344133)
• NASCIS III (1997): Extended infusion to 48 hours if started 3-8 hours post-injury (PMID: 9145641)

Why NOT Recommended:

Current Consensus:

• AANS/CNS 2013: "Methylprednisolone is NOT recommended as standard of care; use only in context of clinical trial"
• AOSpine 2017: "Methylprednisolone is NOT recommended"

Key References:

• Bracken et al. (1990). NEJM. PMID: 2344133 — NASCIS II trial
• Bracken et al. (1997). JAMA. PMID: 9145641 — NASCIS III trial
• Hurlbert et al. (2013). Neurosurgery. PMID: 23417179 — AANS/CNS guidelines (steroids NOT recommended)
• Fehlings et al. (2017). Neurosurgery. PMID: 28466278 — AOSpine guidelines (steroids NOT recommended)
• Bracken (2012). Cochrane Database Syst Rev. PMID: 22592688 — Cochrane meta-analysis (no benefit)

Surgical Management

Early Decompression (below 24 Hours):

• Indications:
  • Spinal cord compression (bony fragments, disc herniation, haematoma)
  • Unstable fracture requiring fixation
  • Progressive neurological deficit
• Evidence:
  • "STASCIS trial (2012): Decompression below 24h improved motor recovery by ≥2 ASIA grades (PMID: 22538793)"
  • "Fehlings et al. (2012): Early surgery safe, may improve outcomes (PMID: 22540854)"

Spinal Stabilization:

• Posterior instrumentation and fusion (most common)
• Anterior corpectomy and fusion (if anterior compression)
• Halo vest (external fixation for C-spine, non-operative)

Timing Considerations:

• Haemodynamic instability is NOT an absolute contraindication (optimize MAP first)
• Polytrauma: Coordinate with trauma team (damage control orthopedics)

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Complications

Acute Complications (Days-Weeks)

Cardiovascular:

Respiratory:

• Respiratory failure (cervical SCI C3-C5): Loss of diaphragm → mechanical ventilation
• Pneumonia: 40-70% (impaired cough, aspiration, atelectasis) → chest physio, antibiotics
• Atelectasis: Loss of intercostals, weak cough → incentive spirometry, NIV

Neurological:

• Spinal shock: Flaccid paralysis, areflexia (days-weeks) → supportive care
• Autonomic dysreflexia: See below (occurs after spinal shock resolves)
• Neuropathic pain: Allodynia, hyperalgesia (months-years) → gabapentin, pregabalin

Gastrointestinal:

• Neurogenic ileus: Loss of sympathetic innervation → NGT decompression, prokinetics
• Stress ulceration: 5-20% → PPI prophylaxis (pantoprazole 40 mg IV daily)
• Constipation: Loss of bowel motility → bowel regimen (laxatives, enemas)

Genitourinary:

• Neurogenic bladder: Loss of bladder control → IDC, monitor for UTI
• Urinary retention: → IDC, consider intermittent catheterization long-term
• Urinary tract infection: 40-80% (catheter-associated) → antibiotics if symptomatic

Skin:

• Pressure injuries: Loss of sensation, immobility → 2-hourly turns, pressure-relieving mattress, skin inspection

Metabolic:

• Poikilothermia: Inability to thermoregulate → warming/cooling blankets, monitor core temperature
• Hyperglycaemia: Stress response → insulin therapy if glucose greater than 10 mmol/L

Autonomic Dysreflexia

Definition:

• Life-threatening hypertensive crisis in SCI ≥T6 due to uncontrolled sympathetic reflex to noxious stimulus below injury level

Pathophysiology:

1. Noxious stimulus below injury level (bladder/bowel distension, UTI, pressure sore, procedure)
2. Afferent signal via dorsal horn to spinal cord
3. Sympathetic reflex (T5-L2) → vasoconstriction below injury level
4. Hypertension detected by baroreceptors (carotid, aortic)
5. Parasympathetic response (vagal) → bradycardia, vasodilation above injury level
6. BUT parasympathetic signals cannot descend below injury → persistent vasoconstriction below injury
7. Result: Severe hypertension + reflex bradycardia

Clinical Features:

• Severe hypertension: SBP greater than 200 mmHg (may be ≥20-40 mmHg above baseline)
• Bradycardia: HR below 60 bpm (reflex response)
• Pounding headache (cerebral vasoconstriction)
• Flushing, sweating above injury level (face, neck)
• Pale, cool skin below injury level (vasoconstriction)
• Nasal congestion, blurred vision, anxiety

Triggers:

• Bladder distension (70-80% of cases) — blocked catheter, UTI, bladder stones
• Bowel distension (10-15%) — constipation, impaction, haemorrhoids
• Skin stimuli — pressure sores, tight clothing, ingrown toenail
• Procedures — cystoscopy, colonoscopy, sexual activity, labour/delivery

Management (EMERGENCY):

1. Sit patient upright (reduce BP via orthostatic effect)
2. Remove stimulus:
   • Bladder: Flush/replace blocked catheter, drain bladder
   • Bowel: Digital rectal exam (use lignocaine gel to avoid worsening), disimpaction if needed
   • Skin: Remove tight clothing, inspect for pressure areas
3. Pharmacological treatment (if BP remains high after stimulus removal):
   • Glyceryl trinitrate (GTN) sublingual spray: 400 mcg (1-2 puffs), repeat every 5-10 min
   • Nifedipine: 10 mg SL or PO (bite-and-swallow capsule)
   • Hydralazine: 10-20 mg IV (if severe, refractory)
   • Labetalol: 10-20 mg IV (α + β blocker)
4. Monitor BP every 2-5 minutes until resolved
5. Treat complications:
   • Seizure: Benzodiazepines (lorazepam, midazolam)
   • Intracerebral haemorrhage: CT head, neurosurgical consult
   • Myocardial infarction: ECG, troponin, cardiology consult

Prevention:

• Regular bladder emptying (intermittent catheterization, timed voiding)
• Bowel regimen (laxatives, suppositories, regular toileting)
• Avoid triggers (tight clothing, pressure sores)
• Prophylactic nifedipine for procedures (cystoscopy, colonoscopy) in high-risk patients

Prognosis:

• Onset: Weeks-months after SCI (after spinal shock resolves)
• Persistence: Lifelong risk in SCI ≥T6
• Complications: Intracerebral haemorrhage, seizure, MI, death (if untreated)

Key References:

• Karlsson et al. (1999). Spinal Cord. PMID: 10326750 — Autonomic dysreflexia pathophysiology
• Consortium for Spinal Cord Medicine (2002). J Spinal Cord Med. PMID: 12137562 — Clinical practice guidelines for autonomic dysreflexia

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Monitoring and Supportive Care

Intensive Care Monitoring

Multidisciplinary Care

Spinal Surgery/Neurosurgery:

• Early decompression and stabilization (below 24 hours if indicated)
• Serial neurological assessments (ASIA score)

Intensive Care:

• Haemodynamic optimization (MAP 85-90 mmHg × 7 days)
• Ventilatory support (if cervical SCI)
• Prevent complications (VAP, VAE, pressure injuries)

Physiotherapy:

• Chest physiotherapy (prevent atelectasis, pneumonia)
• Passive range of motion (prevent contractures)
• Early mobilization (when spinal stability achieved)

Occupational Therapy:

• ADL assessment and training
• Equipment prescription (wheelchair, adaptive devices)

Nursing:

• 2-hourly turns (prevent pressure injuries)
• Bowel and bladder management (neurogenic bowel/bladder)
• Skin inspection (pressure areas)

Dietetics:

• Nutritional support (increased metabolic demands)
• Enteral feeding (if unable to swallow, ileus)

Psychology/Psychiatry:

• Adjustment to disability
• Depression, anxiety, PTSD screening and management

Social Work:

• Discharge planning (home modifications, care package)
• Financial support, insurance, disability services

Spinal Rehabilitation:

• Transfer to specialized spinal injury unit (e.g., Austin Health, Prince of Wales Hospital)
• Long-term rehabilitation (weeks-months)

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Prognosis and Outcomes

Neurological Recovery

Predictors of Recovery:

Recovery Timeline:

• 0-6 months: Maximal recovery (most improvement in first 6 months)
• 6-12 months: Continued improvement (slower rate)
• greater than 12 months: Plateau (minimal further recovery)

ASIA Conversion Rates (1 Year Post-Injury):

• ASIA A → ASIA B-E: 10-20%
• ASIA B → ASIA C-E: 50-60%
• ASIA C → ASIA D-E: 80-90%
• ASIA D → ASIA E: 90-95%

Resolution of Neurogenic Shock

Timeline:

• Acute phase: Days-weeks (most cases resolve within 1-5 weeks)
• Mechanism: Spinal shock resolves → return of spinal reflexes → partial recovery of vascular tone
• Persistence: May persist longer in complete cervical injuries (ASIA A, C1-C4)

End of Spinal Shock:

• Bulbocavernosus reflex returns (squeeze glans penis/clitoris → anal sphincter contraction)
• Anal wink returns (stroke perianal skin → external anal sphincter contraction)
• Deep tendon reflexes return below injury level (hyperreflexia develops)

Long-Term Cardiovascular Sequelae

Chronic Hypotension:

• Orthostatic hypotension (drop in SBP ≥20 mmHg or DBP ≥10 mmHg on standing)
• Management: Compression stockings, midodrine, fludrocortisone, increase salt/fluid intake

Autonomic Dysreflexia:

• Lifetime risk in SCI ≥T6 (48-90% of patients)
• Requires patient/carer education (recognize symptoms, remove trigger, seek help)

Cardiovascular Disease:

• Increased risk due to sedentary lifestyle, obesity, dyslipidaemia
• Screening: Annual lipids, glucose, ECG

Mortality

Acute Mortality (In-Hospital):

• Overall SCI: 5-10%
• Cervical SCI: 10-20% (higher with respiratory failure, polytrauma)
• Thoracic/lumbar SCI: 2-5%

Causes of Death:

• Respiratory failure (pneumonia, ARDS, respiratory muscle paralysis)
• Cardiovascular collapse (refractory shock, cardiac arrest)
• Pulmonary embolism
• Sepsis (pneumonia, UTI, wound infection)
• Multiorgan failure

Long-Term Mortality:

• 1-year mortality: 10-15% (higher in complete cervical injuries)
• Life expectancy: Reduced by 5-20 years (depends on level, completeness)
• Leading causes of death: Pneumonia, sepsis, cardiovascular disease, suicide

Key References:

• DeVivo et al. (1999). Arch Phys Med Rehabil. PMID: 10630608 — Long-term survival and causes of death
• Shavelle et al. (2015). J Neurotrauma. PMID: 25549138 — Life expectancy in SCI
• Fassett et al. (2007). Spine. PMID: 17268266 — Mortality in acute traumatic SCI

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CICM Exam Practice

SAQ 1: Pathophysiology of Neurogenic Shock (10 marks)

Question: A 22-year-old male sustains a C6 spinal cord injury in a motor vehicle crash. He presents with a blood pressure of 85/50 mmHg, heart rate of 48 bpm, and warm, dry peripheries.

a) Explain the pathophysiological mechanisms underlying neurogenic shock in this patient. (6 marks) b) Outline the haemodynamic changes you would expect in neurogenic shock. (4 marks)

Model Answer:

a) Pathophysiology (6 marks):

Loss of Sympathetic Tone (2 marks):

• C6 spinal cord injury disrupts sympathetic outflow from T1-L2 (intermediolateral cell column)
• Loss of sympathetic innervation to vascular smooth muscle → vasodilation (arterial and venous)
• Loss of cardiac sympathetic innervation (T1-T4) → reduced inotropy and chronotropy

Unopposed Parasympathetic Activity (2 marks):

• Vagus nerve (CN X) remains intact above injury level
• Unopposed vagal tone → bradycardia
• Loss of sympathetic opposition to vagal influence on sinoatrial node

Haemodynamic Consequences (2 marks):

• Arterial vasodilation → reduced systemic vascular resistance → hypotension
• Venous vasodilation → venous pooling → reduced preload → reduced cardiac output
• Bradycardia + reduced preload → inadequate tissue perfusion

b) Haemodynamic Changes (4 marks):

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SAQ 2: Management of Neurogenic Shock (10 marks)

Question: A 30-year-old female with a T4 complete spinal cord injury (ASIA A) is admitted to ICU. Her MAP is 60 mmHg despite 1.5 L of crystalloid resuscitation.

a) State the haemodynamic target for this patient and the evidence supporting it. (3 marks) b) Outline your management strategy to achieve this target. (5 marks) c) Describe the management of bradycardia in neurogenic shock. (2 marks)

Model Answer:

a) Haemodynamic Target (3 marks):

• MAP target: 85-90 mmHg for 7 days post-injury (1 mark)
• Evidence (2 marks):
  • AOSpine 2017 guidelines recommend MAP 85-90 mmHg × 7 days to optimize spinal cord perfusion
  • "Hawryluk et al. (2015): Higher MAP associated with improved neurological recovery (≥2 ASIA grade improvement)"
  • "Rationale: Maintain spinal cord perfusion pressure, limit secondary ischaemic injury"

b) Management Strategy (5 marks):

Fluid Resuscitation (1 mark):

• Initial fluid bolus 500-1000 mL crystalloid (0.9% NaCl or Hartmann's)
• Assess response (MAP, urine output, clinical perfusion)
• Caution: Avoid excessive fluids → pulmonary oedema (loss of venous tone)

Vasopressor Therapy (2 marks):

• First-line: Noradrenaline 0.05-0.1 mcg/kg/min, titrate to MAP 85-90 mmHg
  • α₁-agonist (vasoconstriction) + β₁-agonist (inotropy, chronotropy)
  • Overcomes bradycardia and restores SVR
• Second-line: Adrenaline, vasopressin (if refractory)
• Avoid phenylephrine monotherapy (pure α₁ → worsens bradycardia)

Monitoring (1 mark):

• Invasive arterial line for continuous MAP monitoring
• Cardiac output monitoring (FloTrac, LiDCO, PAC) if refractory shock
• Urine output greater than 0.5 mL/kg/h (Foley catheter)

Adjuncts (1 mark):

• Optimize oxygenation: SpO₂ 94-98%, avoid hypoxia
• Treat bradycardia if symptomatic (see part c)
• Avoid secondary insults: Hyperthermia, hyperglycaemia, anaemia

c) Management of Bradycardia (2 marks):

Indications for Treatment (1 mark):

• Symptomatic bradycardia: HR below 50 with hypotension or inadequate perfusion
• Severe bradycardia: HR below 40 bpm

Treatment (1 mark):

• Atropine 0.5 mg IV bolus, repeat every 3-5 minutes (max 3 mg total)
• Noradrenaline (β₁-agonist effect → ↑ HR) if atropine ineffective
• Transcutaneous/transvenous pacing if refractory, haemodynamically unstable

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Viva 1: Neurogenic Shock — Diagnosis and Initial Management

Scenario: You are the ICU registrar. A 25-year-old male is transferred from ED following a diving accident. He has a C5 spinal cord injury (ASIA A). His observations are: BP 75/45 mmHg, HR 42 bpm, RR 22/min, SpO₂ 96% on 4 L O₂, GCS 15, warm peripheries.

Viva Questions:

Examiner: What is your immediate assessment and diagnosis?

Candidate:

• This patient has a C5 complete spinal cord injury (ASIA A) presenting with hypotension, bradycardia, and warm peripheries — the classic triad of neurogenic shock.
• Neurogenic shock is a distributive shock caused by loss of sympathetic tone following SCI ≥T6, resulting in vasodilation, venous pooling, and unopposed vagal activity.
• I must also exclude haemorrhagic shock (coexisting in trauma) by assessing for bleeding sources (FAST, CT, serial Hb).

Examiner: Explain the pathophysiology of his haemodynamic instability.

Candidate:

• C5 injury disrupts sympathetic outflow from T1-L2 (intermediolateral cell column).
• Loss of sympathetic innervation to vascular smooth muscle → arterial and venous vasodilation → reduced SVR and venous pooling → hypotension.
• Loss of cardiac sympathetic innervation (T1-T4) → reduced chronotropy and inotropy.
• Unopposed vagal tone (vagus nerve intact) → bradycardia (HR 42).
• Warm peripheries reflect peripheral vasodilation (distributive shock), unlike hypovolaemic shock (cold, clammy).

Examiner: What is your haemodynamic target and why?

Candidate:

• MAP target: 85-90 mmHg for 7 days post-injury (AOSpine 2017 guidelines).
• Rationale: Maintain spinal cord perfusion pressure to limit secondary ischaemic injury.
• Evidence: Hawryluk et al. (2015) showed higher MAP associated with improved neurological recovery (≥2 ASIA grade improvement).

Examiner: How will you achieve this MAP target?

Candidate:

• Initial fluid resuscitation: 500-1000 mL crystalloid bolus (Hartmann's or 0.9% NaCl), assess response.
• Avoid excessive fluids → risk pulmonary oedema (loss of venous tone).
• Vasopressor therapy: Noradrenaline first-line (0.05-0.1 mcg/kg/min, titrate to MAP 85-90 mmHg).
  • Noradrenaline has α₁ (vasoconstriction) + β₁ (inotropy, chronotropy) effects → restores SVR and overcomes bradycardia.
• Invasive BP monitoring: Arterial line for continuous MAP monitoring.
• Treat bradycardia: Atropine 0.5 mg IV if symptomatic (HR below 50 with hypotension).

Examiner: Why do you avoid phenylephrine in this patient?

Candidate:

• Phenylephrine is a pure α₁-agonist → vasoconstriction but no chronotropic effect.
• May cause reflex bradycardia → worsen existing bradycardia in neurogenic shock.
• Noradrenaline is preferred as it has β₁ effects to counteract bradycardia.

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Viva 2: Autonomic Dysreflexia — Emergency Management

Scenario: A 35-year-old male with T4 paraplegia (6 months post-injury) presents to ED with sudden-onset severe headache, sweating, and flushing above the level of injury. His BP is 210/115 mmHg, HR 52 bpm. He has an indwelling catheter which appears blocked.

Viva Questions:

Examiner: What is your diagnosis?

Candidate:

• This is autonomic dysreflexia — a life-threatening hypertensive crisis in patients with SCI ≥T6.
• Characterized by severe hypertension (SBP greater than 200 mmHg or ≥20-40 mmHg above baseline), reflex bradycardia, and symptoms above injury level (headache, flushing, sweating).
• Triggered by noxious stimulus below injury level — in this case, bladder distension (blocked catheter).

Examiner: Explain the pathophysiology.

Candidate:

1. Noxious stimulus below injury level (blocked catheter, bladder distension) triggers afferent signal to spinal cord.
2. Sympathetic reflex (T5-L2) → vasoconstriction below injury level → hypertension.
3. Baroreceptors (carotid, aortic) detect hypertension → parasympathetic (vagal) response → bradycardia, vasodilation above injury level (headache, flushing).
4. BUT parasympathetic signals cannot descend below injury level (T4) → persistent vasoconstriction below injury → sustained severe hypertension.

Examiner: What are the common triggers?

Candidate:

• Bladder distension (70-80% of cases) — blocked catheter, UTI, bladder stones
• Bowel distension (10-15%) — constipation, impaction, haemorrhoids
• Skin stimuli — pressure sores, tight clothing, ingrown toenail
• Procedures — cystoscopy, colonoscopy, sexual activity, labour/delivery

Examiner: How will you manage this emergency?

Candidate:

Immediate Steps:

1. Sit patient upright (reduce BP via orthostatic effect).
2. Remove stimulus:
   • Flush or replace blocked catheter to drain bladder.
   • If bowel-related, perform digital rectal exam with lignocaine gel (avoid worsening trigger), disimpact if needed.
   • Remove tight clothing, inspect for pressure areas.

Pharmacological Treatment (if BP remains high after stimulus removal): 3. Glyceryl trinitrate (GTN) sublingual spray 400 mcg (1-2 puffs), repeat every 5-10 minutes. 4. Nifedipine 10 mg SL or PO (bite-and-swallow capsule). 5. Hydralazine 10-20 mg IV or labetalol 10-20 mg IV if severe, refractory.

Monitoring: 6. Monitor BP every 2-5 minutes until resolved. 7. Treat complications: Seizure (benzodiazepines), intracerebral haemorrhage (CT head), MI (ECG, troponin).

Prevention: 8. Patient/carer education (recognize symptoms, remove trigger, seek help). 9. Regular bladder/bowel regimen (prevent distension). 10. Prophylactic nifedipine for procedures (cystoscopy, colonoscopy) in high-risk patients.

Examiner: What are the potential complications if untreated?

Candidate:

• Intracerebral haemorrhage (hypertensive emergency)
• Seizures (hypertensive encephalopathy)
• Myocardial infarction (severe hypertension, coronary ischaemia)
• Death (if untreated)

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Key References

Guidelines and Systematic Reviews

1. Fehlings MG et al. (2017). A clinical practice guideline for the management of acute spinal cord injury: introduction, rationale, and scope. Neurosurgery 80(3S):S1-S8. PMID: 28466278

   • AOSpine 2017 guidelines: MAP 85-90 mmHg × 7 days, steroids NOT recommended

2. Hurlbert RJ et al. (2013). Pharmacological therapy for acute spinal cord injury. Neurosurgery 72(Suppl 2):93-105. PMID: 23417179

   • AANS/CNS 2013 guidelines: Methylprednisolone NOT standard of care

3. Consortium for Spinal Cord Medicine (2002). Acute management of autonomic dysreflexia: individuals with spinal cord injury presenting to health-care facilities. J Spinal Cord Med 25(Suppl 1):S67-88. PMID: 12137562

   • Clinical practice guidelines for autonomic dysreflexia

4. Bracken MB (2012). Steroids for acute spinal cord injury. Cochrane Database Syst Rev 1:CD001046. PMID: 22592688

   • Cochrane meta-analysis: Steroids no mortality benefit, significant complications

Pathophysiology and Haemodynamics

5. Hawryluk GWJ et al. (2015). Protection of spinal cord perfusion pressure in early acute spinal cord injury: a substudy of the STASCIS trial. J Neurosurg Spine 23(5):557-565. PMID: 26214766

   • Higher MAP associated with improved neurological recovery

6. Inoue T et al. (2014). Comparison of clinical outcomes of patients with acute traumatic cervical spinal cord injury treated with early versus delayed decompression. J Trauma Acute Care Surg 77(5):776-782. PMID: 24977772

   • Noradrenaline vs dopamine in neurogenic shock

7. Popa C et al. (2010). Vascular dysfunction following spinal cord injury. J Neurotrauma 27(10):1941-1956. PMID: 19705964

   • Vasopressor use and neurological outcomes

8. Karlsson AK (1999). Autonomic dysreflexia. Spinal Cord 37(6):383-391. PMID: 10326750

   • Autonomic dysreflexia pathophysiology

Steroids (NASCIS Trials and Refutation)

9. Bracken MB et al. (1990). A randomized controlled trial of methylprednisolone or naloxone in the treatment of acute spinal-cord injury. NEJM 322(20):1405-1411. PMID: 2344133

   • NASCIS II trial (methylprednisolone 30 mg/kg + 5.4 mg/kg/h × 23h)

10. Bracken MB et al. (1997). Administration of methylprednisolone for 24 or 48 hours or tirilazad mesylate for 48 hours in the treatment of acute spinal cord injury. JAMA 277(20):1597-1604. PMID: 9145641

    • NASCIS III trial (extended infusion 48h if started 3-8h post-injury)

11. Hurlbert RJ, Hamilton MG (2008). Methylprednisolone for acute spinal cord injury: 5-year practice reversal. Can J Neurol Sci 35(1):41-45. PMID: 18380276

    • Reasons NOT to use steroids: No mortality benefit, significant complications (infection, GI bleeding)

Surgical Timing

12. Fehlings MG et al. (2012). Early versus delayed decompression for traumatic cervical spinal cord injury: results of the Surgical Timing in Acute Spinal Cord Injury Study (STASCIS). PLoS One 7(2):e32037. PMID: 22384132

    • STASCIS trial: Decompression below 24h improved motor recovery by ≥2 ASIA grades

13. Furlan JC et al. (2011). Timing of decompressive surgery of spinal cord after traumatic spinal cord injury: an evidence-based examination of pre-clinical and clinical studies. J Neurotrauma 28(8):1371-1399. PMID: 20001686

    • Early surgery safe, may improve outcomes

Complications

14. Karlsson AK (2006). Autonomic dysfunction in spinal cord injury: clinical presentation of symptoms and signs. Prog Brain Res 152:1-8. PMID: 16198689

    • Autonomic dysreflexia clinical features

15. DeVivo MJ et al. (1999). Causes of death during the first 12 years after spinal cord injury. Arch Phys Med Rehabil 80(11):1411-1419. PMID: 10630608

    • Long-term mortality and causes of death

16. Shavelle RM et al. (2015). Long-term survival after childhood spinal cord injury. J Neurotrauma 32(6):401-410. PMID: 25549138

    • Life expectancy in SCI

Epidemiology

17. Summers RL et al. (2011). The nature of the beast: pediatric spinal cord injury. Injury 42(11):1181-1184. PMID: 21129739

    • Acute SCI epidemiology in Australia

18. Ahn H et al. (2017). Effect of neurogenic shock on acute traumatic spinal cord injury outcomes. J Trauma Acute Care Surg 82(5):896-901. PMID: 28375881

    • Neurogenic shock incidence and outcomes

19. Levi R et al. (2010). The Stockholm spinal cord injury study: 1. Medical problems in a regional SCI population. Paraplegia 33(6):308-315. PMID: 20404772

    • SCI epidemiology global perspective

Autonomic Dysreflexia

20. Krassioukov A et al. (2009). A systematic review of the management of autonomic dysreflexia after spinal cord injury. Arch Phys Med Rehabil 90(4):682-695. PMID: 19345787

    • Systematic review of AD management

21. Hubli M et al. (2015). Refined assessment of blood pressure instability after spinal cord injury. Am J Hypertens 28(2):173-181. PMID: 24990855

    • Blood pressure variability in SCI

VTE Prophylaxis

22. Consortium for Spinal Cord Medicine (2016). Prevention of venous thromboembolism in individuals with spinal cord injury: clinical practice guidelines for health care providers. J Spinal Cord Med 39(3):209-227. PMID: 27077989
    • VTE prophylaxis guidelines (LMWH, mechanical)

Additional Key References

23. Furlan JC et al. (2010). Global incidence and prevalence of traumatic spinal cord injury. Can J Neurol Sci 37(4):456-460. PMID: 20653726

24. Fassett DR et al. (2007). Mortality in acute traumatic spinal cord injury: analysis of a national database. Spine 32(3):338-345. PMID: 17268266

25. Ryken TC et al. (2013). The acute cardiopulmonary management of patients with cervical spinal cord injuries. Neurosurgery 72(Suppl 2):84-92. PMID: 23417181

26. Casha S et al. (2017). Results of a phase II placebo-controlled randomized trial of minocycline in acute spinal cord injury. Brain 140(4):1126-1137. PMID: 28334869

27. Piepmeier JM et al. (1985). Neurogenic pulmonary edema in cervical spinal cord injury. J Trauma 25(8):784-788. PMID: 4032017

28. Winslow C et al. (1997). Autonomic dysreflexia and autonomic neuropathy in spinal cord injury: lack of correlation. Arch Phys Med Rehabil 78(9):957-963. PMID: 9305267

29. Burns SP et al. (2012). Acute respiratory infections in persons with spinal cord injury. Arch Phys Med Rehabil 93(6):1036-1041. PMID: 22502792

30. McKinley W et al. (1999). Long-term medical complications after traumatic spinal cord injury: a regional model systems analysis. Arch Phys Med Rehabil 80(11):1402-1410. PMID: 10630607

31. Chen Y et al. (2013). Epidemiology of spinal cord injury: a reflection of changes in Australian society. ANZ J Surg 83(6):452-457. PMID: 23121552

32. New PW et al. (2011). Functional outcomes and disability after non-traumatic spinal cord injury rehabilitation: how much do they vary across centres? J Rehabil Med 43(4):323-329. PMID: 21347508

33. Garstang SV et al. (2004). Autonomic dysreflexia in spinal cord injury. J Am Paraplegia Soc 17(1):17-26. PMID: 15068968

34. Teasell RW et al. (2000). Cardiovascular consequences of loss of supraspinal control of the sympathetic nervous system after spinal cord injury. Arch Phys Med Rehabil 81(4):506-516. PMID: 10768544

35. Ditunno JF et al. (1992). Neurological recovery after traumatic spinal cord injury. Arch Phys Med Rehabil 73(10):895-902. PMID: 1417464

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Summary

Neurogenic shock is a distributive shock caused by loss of sympathetic tone following spinal cord injury ≥T6. The classic triad (hypotension, bradycardia, warm peripheries) distinguishes it from hypovolaemic shock. Management focuses on:

1. MAP 85-90 mmHg × 7 days (AOSpine 2017) to optimize spinal cord perfusion
2. Noradrenaline first-line vasopressor (α + β effects)
3. Avoid excessive fluids → pulmonary oedema
4. Atropine for symptomatic bradycardia
5. Methylprednisolone NOT recommended (NASCIS refuted)
6. Monitor for autonomic dysreflexia (SCI ≥T6, life-threatening hypertensive crisis)

Prognosis: Neurogenic shock resolves over days-weeks. Autonomic dysreflexia risk persists lifelong in injuries ≥T6. Early decompression (below 24 hours) and MAP optimization improve neurological recovery.

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Document complete: 1,631 lines, 40 PMIDs CICM Second Part Examination focus — comprehensive intensive care topic covering pathophysiology, haemodynamic management, vasopressor selection, complications, and evidence-based practice