What is Neurogenic Shock and How to Diagnose It
Neurogenic shock is a distributive form of circulatory shock resulting from loss of sympathetic nervous system control following spinal cord injury (SCI) above T6, characterized by the classic triad of hypotension, bradycardia, and warm/dry skin due to peripheral vasodilation. 1, 2
Pathophysiology
Neurogenic shock occurs when SCI disrupts descending sympathetic pathways from higher centers to spinal sympathetic neurons (originating in T1-L2 cord segments), resulting in:
- Loss of sympathetic tone below the injury level with unopposed parasympathetic (vagal) outflow 2
- Profound peripheral vasodilation from decreased peripheral vascular resistance 3
- Loss of vascular capacitance in some patients 3
- Bradycardia from unopposed vagal activity 2, 4
The hemodynamic profile is actually more complex than traditionally taught—one study found that only 33% had pure decreased peripheral vascular resistance, while 22% had loss of vascular capacitance, 33% had mixed mechanisms, and 11% had primarily cardiac dysfunction 3.
Clinical Diagnosis
Classic Presentation (The Triad)
You diagnose neurogenic shock by identifying:
- Systolic blood pressure <100 mmHg 5
- Heart rate <80 beats per minute 5
- Spinal cord injury at or above T6 level (most commonly cervical) 6, 5
Critical Diagnostic Considerations
The incidence varies dramatically based on injury level:
- Cervical SCI: 19.3% develop neurogenic shock 5
- Thoracic SCI: 7% develop neurogenic shock 5
- Lumbar SCI: 3% develop neurogenic shock 5
Important timing caveat: Neurogenic shock may not be immediately apparent on ED arrival—fewer than 20% of cervical SCI patients show classic signs initially, as the hemodynamic changes develop over time 5. The condition is part of "spinal shock," which is a broader transitory suspension of function and reflexes below the injury level 2.
Distinguishing from Hypovolemic Shock
This is the most critical diagnostic challenge. One study found that hypovolemia was the primary factor causing inconsistent incidence reports between studies 6.
Key differentiating features:
- Neurogenic shock: Hypotension + bradycardia + warm/dry extremities
- Hypovolemic shock: Hypotension + tachycardia + cool/clammy extremities
The optimal diagnostic approach combines hemodynamic AND laboratory criteria to exclude hypovolemia before confirming neurogenic shock 6. Check for:
- Hematocrit/hemoglobin levels to rule out blood loss
- Lactate levels (may be elevated in both but more pronounced in hypovolemic shock)
- Response to fluid resuscitation (neurogenic shock requires vasopressors, not just fluids)
Hemodynamic Monitoring Requirements
Maintain continuous invasive arterial blood pressure monitoring in suspected neurogenic shock 7, 1. This is essential because:
- Blood pressure targets are difficult to achieve (patients spend 25% of time below target MAP) 7
- Accurate real-time monitoring guides vasopressor titration 1
- Dissection-related arterial occlusion can give falsely low readings in affected limbs 7
Blood Pressure Management Targets
Maintain mean arterial pressure (MAP) ≥70 mmHg during the first week post-injury to prevent secondary neurological deterioration 7. This recommendation is based on:
- Correlation between MAP >70-75 mmHg and neurological improvement (only significant for 2-3 days post-admission) 7
- Spinal cord perfusion pressure >50 mmHg correlates with better 6-month neurological outcomes 7
- Avoid all episodes of systolic BP <90 mmHg through day 5-7 7
Before injury assessment is complete, maintain systolic BP >110 mmHg to reduce mortality 7.
Common Pitfalls to Avoid
Do not confuse neurogenic shock with spinal shock:
- Spinal shock is the broader phenomenon of areflexia and loss of function below injury level, lasting 3-6 months (up to 1-2 years) 1
- Neurogenic shock is specifically the hemodynamic instability component 2, 4
Do not perform accurate neurological assessment during acute neurogenic/systemic shock 7. Cognitive impairment from shock reduces examination accuracy 7. Wait until hemodynamic stabilization for reliable baseline neurological grading.
Do not assume all hypotension in SCI is neurogenic—always rule out hemorrhagic/hypovolemic shock first, especially in polytrauma 6, 5.
Do not rely on heart rate and blood pressure changes alone—markers of sympathetic outflow showed no correlation to hemodynamic profiles in one study 3, emphasizing the need for comprehensive assessment including injury level confirmation.