Spinal Cord Injury
T6+
Dysreflexia Risk
Autonomic dysreflexia level
C3-C5
Phrenic Nerve
Diaphragm innervation
Low SVR
Neurogenic Shock
With bradycardia, warm dry skin
Neurogenic Shock
Loss of sympathetic tone below the level of injury causes vasodilation, hypotension, and bradycardia. The skin is warm and dry because sweat glands lose sympathetic innervation. This is fundamentally different from hypovolemic shock.
Neurogenic shock has LOW SVR and BRADYCARDIA. This differentiates it from hypovolemic shock. Treatment includes IV fluids and vasopressors. Atropine may be needed for symptomatic bradycardia.
Autonomic Dysreflexia
Occurs in injuries at T6 and above. A noxious stimulus below the injury triggers a massive, unregulated sympathetic discharge. Presents with severe hypertension, pounding headache, diaphoresis and flushing above the injury, and pallor below. This is a medical emergency that can cause seizures, stroke, or death if untreated.
Sit the patient upright immediately
Check Foley catheter for kinks or obstruction
Assess for fecal impaction
Remove tight clothing and constrictive devices
If BP remains critically elevated, administer nifedipine or apply nitropaste
Key Values to Memorize
Dysreflexia = T6 and above
C3-C5 = phrenic nerve
Neurogenic = brady + hypo
#1 trigger = full bladder
#2 trigger = fecal impaction
Sit upright FIRST
neurogenic vs hypovolemic shock is a classic CCRN trap
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Neurogenic shock has BRADYCARDIA, not tachycardia
This is the most tested distinction. Hypovolemic shock causes tachycardia as a compensatory mechanism. Neurogenic shock loses sympathetic tone below the injury, so the heart rate drops (unopposed vagal tone) and SVR drops (vasodilation). The skin is warm and dry, not cool and clammy.
Autonomic dysreflexia management starts with sitting upright
The first intervention is to sit the patient upright to allow orthostatic pooling and reduce BP. Then immediately search for and remove the trigger. The most common triggers are bladder distension (kinked catheter, full bladder) and fecal impaction.
C3 through C5 injuries threaten respiratory function
The phrenic nerve (C3, C4, C5) innervates the diaphragm. Injuries at or above this level can cause complete respiratory failure requiring mechanical ventilation. Even injuries slightly below may develop ascending edema that compromises the phrenic nerve in the first 24-72 hours.
Most common dysreflexia triggers are full bladder and fecal impaction
The exam loves to present a patient with SCI above T6 who suddenly develops severe hypertension, pounding headache, and flushing above the injury with pallor below. Check the Foley catheter first. Then check for fecal impaction. These two account for the vast majority of episodes.
Neurogenic vs Hypovolemic
Neurogenic = brady, warm, dry, low SVR. Hypovolemic = tachy, cool, clammy, high SVR. The exam WILL try to confuse these.
Dysreflexia Protocol
Sit upright FIRST. Check the catheter. Check for impaction. Remove tight clothing. If BP persists, nifedipine or nitropaste.
The spinal cord is the main wiring conduit between the brain and the body. Sympathetic signals (fight or flight) travel down through this conduit to control heart rate, blood vessel tone, and organ function.
A spinal cord injury is like a circuit breaker tripping. Below the break, sympathetic signals cannot get through. Blood vessels dilate (no tone), heart rate drops (unopposed parasympathetic), and the skin stays warm and dry. That is neurogenic shock.
In autonomic dysreflexia, a painful stimulus below the injury (full bladder, impaction) triggers a massive sympathetic response below the break. But the brain cannot send signals down to calm it because the wires are cut. BP skyrockets. The body tries to compensate above the injury with bradycardia and flushing.
For neurogenic shock, vasopressors restore tone. For dysreflexia, sit upright and remove the trigger. The alarm stops when the stimulus is gone.
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