Scrolling through my dash a little bit ago, I saw a question about autonomic dysreflexia (AD).
AD can be somewhat confusing the first time around, but AD is an emergency situation and it is critical to know the signs and symptoms to be aware of and how to respond to this potentially life threatening situation… so here’s my measly little mind’s breakdown for ya…
Autonomic dysreflexia occurs in patients who have a SCI at or above T6 and also incur some type of sustained stimuli at or below T6. Such stimuli could include a UTI, a pressure ulcer, full bladder, restrictive clothing, constipation, fecal impaction, cystitis, gall stones, hemorrhoids, and the list goes on.
The noxious stimuli produces an afferent impulse that triggers a generalized sympathetic response. The pathways are blocked at the level of the SCI and therefore prevents the body’s normal compensatory mechanisms from responding appropriately. The sympathetic response causes release of neurotransmitters [norepi, dopamine, etc] which causes vasoconstriction, pallor, and piloerection.
The severe vasoconstriction results in sudden increase in blood pressure and vasodilation above the level of injury. This vasodilation causes the patient to become flush and diaphoretic above the level of injury, while remaining pale and cool below the level of injury. The body attempts to lower the BP through compensatory bradycardia. However, these compensatory mechanisms are insufficient. The sustained stimuli must be found and alleviated in order to control the paroxysmal HTN. 

Scrolling through my dash a little bit ago, I saw a question about autonomic dysreflexia (AD).

AD can be somewhat confusing the first time around, but AD is an emergency situation and it is critical to know the signs and symptoms to be aware of and how to respond to this potentially life threatening situation… so here’s my measly little mind’s breakdown for ya…

Autonomic dysreflexia occurs in patients who have a SCI at or above T6 and also incur some type of sustained stimuli at or below T6. Such stimuli could include a UTI, a pressure ulcer, full bladder, restrictive clothing, constipation, fecal impaction, cystitis, gall stones, hemorrhoids, and the list goes on.

The noxious stimuli produces an afferent impulse that triggers a generalized sympathetic response. The pathways are blocked at the level of the SCI and therefore prevents the body’s normal compensatory mechanisms from responding appropriately. The sympathetic response causes release of neurotransmitters [norepi, dopamine, etc] which causes vasoconstriction, pallor, and piloerection.

The severe vasoconstriction results in sudden increase in blood pressure and vasodilation above the level of injury. This vasodilation causes the patient to become flush and diaphoretic above the level of injury, while remaining pale and cool below the level of injury. The body attempts to lower the BP through compensatory bradycardia. However, these compensatory mechanisms are insufficient. The sustained stimuli must be found and alleviated in order to control the paroxysmal HTN. 

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