Spinal trauma and autonomic dysreflexia
Autonomic dysreflexia (AD) is a life‑threatening sympatho‑autonomic emergency that occurs in people with spinal cord injury (SCI), most commonly with lesions at T6 or above (cases reported as low as T8).
AD results from an unchecked sympathetic response to noxious stimuli below the level of the lesion, producing severe hypertension and characteristic split autonomic signs. Treat AD as a medical emergency: identify and remove the trigger, reduce blood pressure safely, monitor closely and escalate early (NICE NG211).
In suspected acute traumatic SCI follow standard trauma ABCDE principles with cervical spine protection (NICE NG41; Resuscitation Council UK). Do not compromise spinal protection to treat AD in the acute traumatic patient without senior/spinal-team advice.
Overview - key clinical pattern
- Sudden, often marked hypertension (systolic commonly >150 mmHg).
- Bradycardia (or relative bradycardia) from vagal reflex.
- Flushing, sweating and vasodilation above the lesion; pallor, cool skin and piloerection below the lesion.
Pathophysiology
- A noxious afferent stimulus below the lesion triggers a massive sympathetic outflow that cannot be modulated by supraspinal centres.
- This causes widespread vasoconstriction below the lesion and acute hypertension.
- Baroreceptor‑mediated vagal activity causes bradycardia.
- Parasympathetic vasodilatation and sweating occur only above the lesion because descending inhibitory/vasodilator pathways are blocked.
Clinical features and common triggers