Spinal shock and autonomic dysreflexia — Rapid

Synopsis

Distinguish transient spinal areflexia from neurogenic circulatory shock, recognise autonomic dysreflexia as a hypertensive emergency, remove common triggers safely, and prevent cerebral and cardiac complications.

Spinal shock is flaccidity and areflexia below an acute cord lesion; neurogenic shock is hypotension from sympathetic loss; autonomic dysreflexia is later episodic hypertension, usually with lesions at T6 or above.
Know the person's baseline pressure because a clinically dangerous rise can occur before an absolute threshold appears striking by general-population standards.
For suspected dysreflexia, sit upright and lower legs if safe, remove tight garments and abdominal binders, and measure pressure and pulse every 2–5 minutes.
Check the urinary system first: inspect catheter tubing for kinks, bag position, blockage and displacement; use only the patient's trained irrigation or catheter-replacement pathway.
If urinary drainage is satisfactory, assess bowel, skin, pressure areas, footwear, fractures, wounds, infection and recent sexual, reproductive or procedural triggers.
Avoid digital rectal examination or manual evacuation until pressure is controlled and the spinal protocol's topical local-anaesthetic precautions are followed, because manipulation can intensify dysreflexia.
Use a prescribed rapid short-acting antihypertensive when trigger removal is insufficient and pressure remains dangerous; check PDE5-inhibitor exposure before giving nitrate.
Continue monitoring after resolution, document the trigger and successful intervention, replace emergency medication and update the patient's portable dysreflexia plan.

Key red flags

Sudden pounding headache, marked rise above usual low blood pressure, flushing or sweating above the lesion, nasal congestion, visual change and piloerection after a T6-or-higher cord lesion is autonomic dysreflexia until proven otherwise.

Blocked urinary catheter, distended bladder, bowel impaction, pressure injury, tight equipment, fracture, infection, sexual activity or labour are common triggers that must be identified without delaying pressure control.

Chest pain, severe bradycardia or tachyarrhythmia, seizure, focal deficit, reduced consciousness or persistent hypertension despite trigger removal requires critical-care escalation and investigation for end-organ injury.

Investigation priorities

First-line repeated blood pressure and rhythmFirst stepFirst line

Confirm the hypertensive change and detect dangerous bradycardia or arrhythmia.

Management branches

ImmediateLower pressure and find bladder trigger

A susceptible person develops abrupt headache, autonomic signs and blood-pressure rise.

Sit upright, lower legs when safe, loosen restrictive garments and call spinal and emergency support while recording pressure and pulse every few minutes.
Ask the patient about their usual trigger and rescue plan, current catheter, bowel routine and recent medicines including PDE5 inhibitors.
Inspect urinary tubing and bag, correct simple kinks or closed clamps and use trained local protocol for blockage, irrigation or catheter replacement.
Give the prescribed rapid short-acting antihypertensive if pressure remains dangerously raised while trigger treatment continues.

Key medicines

Glyceryl trinitrate sublingual spray for protocol-defined dysreflexiaIf the individual emergency plan specifies GTN and pressure remains dangerously high, give 1–2 metered sprays of 400 micrograms each under the tongue while seated; repeat only under the monitored local protocol, not exceeding 3 sprays in 15 minutes.Do not give with recent sildenafil, tadalafil or another PDE5 inhibitor, marked hypotension, severe aortic stenosis or nitrate allergy; continuous pressure monitoring is essential because trigger removal can cause a sudden fall.

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