Neurogenic Shock

Definition

• Schwartz's Principles of Surgery, 11e: "Neurogenic shock refers to diminished tissue perfusion as a result of loss of vasomotor tone to peripheral arterial beds."

Pathophysiology

1. Loss of vasomotor tone → Profound arteriolar and venous dilation below the level of injury → Increased vascular capacitance → Decreased venous return → Decreased cardiac output → Hypotension
2. Loss of sympathetic cardiac innervation (injuries at or above T4) → Prevents reflex tachycardia; unopposed parasympathetic (vagal) tone → Bradycardia
3. Loss of adrenal medullary stimulation → Decreased catecholamine (epinephrine/norepinephrine) release → No compensatory vasoconstriction
4. Secondary spinal cord injury → Hypotension reduces spinal cord perfusion → Worsens the neurological injury (ischemic cascade: loss of autoregulation, vasospasm, thrombosis, free radical release)
5. Thermoregulation failure → Loss of sympathetic tone below injury level → Inability to redirect blood from periphery to core → Hypothermia

Causes

Most relevant to orthopaedics: vertebral body fractures of the cervical or high thoracic region. Incidence is ~20% in cervical-level SCI, decreasing as injury level moves caudally. Complete motor injuries are >5× more likely to require vasopressors than incomplete lesions.

Clinical Features

• Hypothermia (frequently present, often under-recognised)
• Flaccid paralysis below level of injury
• Motor and sensory deficits corresponding to the level of SCI
• Oliguria (reduced end-organ perfusion)
• Radiographic evidence of vertebral column fracture

Neurogenic Shock vs. Spinal Shock

Diagnosis

• Diagnosis of exclusion — hypotension in trauma is never presumed to be neurogenic until other causes are eliminated
• Exclude: haemorrhagic shock (most common in blunt trauma), tension pneumothorax, cardiogenic shock, cardiac tamponade
• In penetrating SCI: 74% of hypotension is from blood loss, only 7% from true neurogenic shock
• In multiply-injured patients with head injury, motor/sensory deficits may be difficult to assess

• Plain radiographs / CT spine: vertebral fracture/dislocation
• CT chest/abdomen/pelvis: exclude haemorrhage
• ECG: bradycardia, dysrhythmias
• Haemodynamic monitoring (ICU): low SVR, low/normal CO, bradycardia

Management

Step 1 — Secure Airway & Ventilation (ATLS primary survey)

Step 2 — Fluid Resuscitation

• IV volume replacement is first-line to restore venous return and cardiac output
• Most patients respond to volume resuscitation alone
• Caution: loss of pulmonary vasomotor capacity predisposes to pulmonary oedema with excessive fluids; monitor cardiac preload

Step 3 — Vasopressors (if hypotension persists despite adequate volume)

• Vasopressor requirement is typically brief (24–48 hours)
• Target MAP ≥ 85 mmHg for 7 days post-SCI (systematic review evidence) to prevent secondary spinal cord ischaemia

Step 4 — ICU Monitoring

• Continuous cardiac monitoring for dysrhythmias
• Blood pressure titration
• Temperature management (correct hypothermia)
• Urinary catheter (oliguria monitoring)

Step 5 — Definitive Spinal Management

• Surgical stabilisation or conservative management depending on fracture type
• Maintain spinal cord perfusion throughout

MAP Target — Evidence Base

• Norepinephrine for cervical and upper thoracic injuries
• Phenylephrine or norepinephrine for mid-to-lower thoracic injuries

Summary Diagram

Spinal Cord Injury (C/T1–T4)
         ↓
Sympathetic outflow interrupted
         ↓
┌──────────────────────┬──────────────────────┐
│ Peripheral vessels   │ Heart (T1–T4)         │
│ ↓ vasoconstriction   │ ↓ sympathetic drive   │
│ ↑ vascular capacity  │ Vagal predominance    │
│ ↓ venous return      │ Bradycardia           │
└──────────────────────┴──────────────────────┘
         ↓
Hypotension + Bradycardia + Warm skin
         ↓
NEUROGENIC SHOCK

• Schwartz's Principles of Surgery, 11th ed., Chapter 5
• Rockwood & Green's Fractures in Adults, 10th ed. (2025), Chapter 47
• Sabiston Textbook of Surgery, p. 934
• Mulholland & Greenfield's Surgery, 7th ed., Chapter 9
• Tintinalli's Emergency Medicine, 9th ed., Chapter 258
• Guyton & Hall Textbook of Medical Physiology

Spinal Shock

Definition

• The term was first used in 1841
• It is a neurological phenomenon, not a haemodynamic one — it must not be confused with neurogenic shock
• (Rockwood & Green's Fractures in Adults, 10th ed., 2025)

Aetiology / Precipitating Causes

• Complete or incomplete traumatic spinal cord transection
• Severe spinal cord contusion (vertebral fractures/dislocations)
• Non-traumatic: epidural haematoma, acute myelopathy, high spinal/epidural anaesthesia

Pathophysiology

• Reticulospinal tracts
• Vestibulospinal tracts
• Corticospinal tracts

"When the spinal cord is suddenly transected in the upper neck, essentially all cord functions, including cord reflexes, immediately become depressed to the point of total silence." — Guyton & Hall, Medical Physiology

• Denervation supersensitivity — upregulation of neurotransmitter receptors
• Axon-supported synapse growth — new synaptic contacts form on denervated neurons
• Eventually leading to hyperreflexia and spasticity

Clinical Features

Immediate (Shock Phase):

Note: Blood pressure may fall to as low as 40 mmHg at onset; it ordinarily returns to normal within a few days — Guyton & Hall

Duration

• Spinal shock lasts days to weeks, occasionally up to 6 months
• In subprimates: a few hours to 1 day
• In humans: 2 weeks to several months (longer in primates due to greater dependence on supraspinal input)
• In a small subset (~5/29 in Kuhn's series): permanent, with only fragmentary reflex recovery — Adams & Victor's Principles of Neurology

Phases of Spinal Shock (Ditunno et al., 2004)

Order of Reflex Return

1. Delayed plantar reflex (first pathological reflex, Phase 1)
2. Bulbocavernosus reflex (BCR) — polysynaptic, typically first to return; signifies end of spinal shock
3. Cremasteric reflex
4. Abdominal wall reflexes
5. Deep plantar response
6. Achilles reflex (ankle jerk)
7. Babinski sign
8. Patellar reflex
9. Finally → hyperreflexia and spasticity

The Bulbocavernosus Reflex (BCR) — Critical Marker

• Squeeze the glans penis or clitoris → observe anal sphincter contraction
• In catheterised patients: gentle tug on urinary catheter → anal sphincter contraction
• Assesses integrity of S2–S4 motor and sensory neurons in the conus medullaris

• While BCR is absent → spinal shock is present → cannot determine whether SCI is complete or incomplete
• A cord lesion cannot be declared "complete" until spinal shock has resolved
• Exception: injury caudal to the conus medullaris (e.g., lumbar burst fracture) → absence of BCR indicates cauda equina syndrome, not spinal shock (spinal shock does not occur with pure nerve root injuries below the cord)

Spinal Shock vs. Neurogenic Shock

Management

Clinical Significance in Orthopaedics

1. Prognostic significance: Until spinal shock resolves and BCR returns, neurological grading (ASIA classification) cannot be finalised — a seemingly complete injury may prove incomplete
2. Surgical timing: Spinal stabilisation should be performed urgently but neurological assessment for completeness awaits BCR return
3. Rehabilitation planning: Spasticity in Phase 3–4 can be utilised for functional gains (e.g., standing, gait training)
4. Autonomic dysreflexia: A late complication emerging after spinal shock resolves in T6 and above injuries — life-threatening hypertensive crisis triggered by noxious stimuli below the level of injury

• Miller's Review of Orthopaedics, 9th ed.
• Rockwood & Green's Fractures in Adults, 10th ed. (2025)
• Adams & Victor's Principles of Neurology, 12th ed.
• Bradley & Daroff's Neurology in Clinical Practice
• Guyton & Hall Textbook of Medical Physiology
• Kandel: Principles of Neural Science, 6th ed.
• Tintinalli's Emergency Medicine, 9th ed.