Autonomic Dysreflexia (AD)
is a life-threatening condition that can occur in persons with spinal cord
AD is an acute episode of exaggerated sympathetic reflex response.
It occurs because SCI disrupts inhibitory feedback
mechanisms to the cord below the injury. Without inhibitory feedback, afferent
(sensory) stimuli travel uninhibited between reflex centers. It is often
brought on by visceral stimuli that normally cause pain or discomfort in the
abdominal or pelvic region. It is uncommon for AD to occur until spinal shock
has resolved, usually about 6 months after injury. It is most unpredictable
during the first year following injury, but can occur throughout the person's
AD is usually characterized
by hypertension ranging from mild (20 mm hg above baseline) to severe hypertension
as high as 300/160, bradycardia and headache ranging from dull to severe and
most often occurs within the first 6 months after injury.
AD is associated with injuries
at T6 and above. An injury below T6, usually allows sufficient cerebral vasomotor
inhibition to control sympathetic reflexes. The inverse is true for injuries at
or above T6, uninhibited sympathetic release of norepinephrine and dopamine below
the level of injury causes vasospasm, hypertension, skin pallor and gooseflesh
associated with the piloerector response. At the same time, baroreceptor function
and parasympathetic control of heart rate remain intact. Hypertension
produces a baroreflex-mediated vagal slowing of heart rate to bradycardic levels.
Accompanying that is a baroreflex-mediated vasodilatation, causing the flushed
skin and profuse sweating above the level of injury, along with sudden onset of
a pounding headache, nasal stuffiness and feelings of anxiety.
The stimuli for AD to occur
a full bladder or rectum;
these are the most common causes.
stimulation of pain receptors,
as occurs with pressure ulcers, ingrown toenails, a dressing change and diagnostic
or operative procedures.
such as ejaculation, bladder spasms and uterine contractions.
urinary tract infections,
or a bladder stone.
AD is a clinical emergency
and can occur very quickly. Without prompt and adequate treatment convulsions,
loss of consciousness, intracerebral hemorrhage and death can occur. The most basic treatment includes
monitoring the blood pressure, while removing or correcting the initiating cause.
Place in upright position
and loosen restrictive clothing.
These actions promote
venous pooling of blood and reduce venous return to the heart. This decreases
Catheterize the bladder;
use an intermittent catheter, and/or check to see if indwelling Foley catheter
or condom catheter is draining or kinked.
Remove stool from the
rectum manually, using numbing ointment.
Check skin for pressure
If BP remains elevated,
follow protocols for the administration of: nifedipine, nitroglycerine, phenoxybenzamine,
mecamylamine hydrochloride or diazoxide
Monitor BP for several
hours after it stabilizes.
SCI patients and their families
should be thoroughly prepared to recognize the possible onset of an episode
of AD, and trained to intervene. It is also recommended that both providers
and patients take advantage of any opportunities to educate their community
about AD, and look to their state's SCI resource center for further information.