Autonomic dysreflexia

Diagram illustrating how autonomic dysreflexia occurs in a person with spinal cord injury. The afferent stimulus, in this case a distended bladder, triggers a peripheral sympathetic response, which results in vasoconstriction and hypertension. Descending inhibitory signals, which would normally counteract the rise in blood pressure, are blocked at the level of the spinal cord injury. The roman numerals (IX, X) refer to cranial nerves. 

Mechanism of autonomic dysreflexia in a person with spinal cord injury (at the level of T6 or above). An afferent stimulus (e.g., distended bladder or fecal impaction) triggers a peripheral sympathetic response that results in widespread vasoconstriction and subsequent hypertension. Baroreceptors in blood vessels detect this hypertensive crisis and signal the brain via cranial nerve IX and X. Descending inhibitory signals normally respond to counteract the rise in blood pressure with slowed heart rate and vasodilation. However, vasodilation is blocked at the level of the spinal cord injury. This results in unregulated hypertension, flushed/warm skin, and sweating above the level of the lesion. Below the level of the lesion, cold/pale extremities and piloerection may be seen.

Management
What causes it? 
The most common cause is over-distension of the bladder, accounting for 75%-85% of episodes.
The“6Bs”are a reminder of possible triggers to consider in the emergency scenario: 
1. Bladder (urinary tract infection or retention, stones, or distension caused bycatheter blockage)
2. Bowel(constipation, impaction)
3. Boils (skin damage)
4. Bones(fractures)
5. Babies(pregnancy,sexualintercourse, breastfeeding)
6. Back passage (haemorrhoid or fissure)

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