Autonomic Dysreflexia Overview for EMS

Autonomic Dysreflexia : An Overview for EMS personnel
By Robert S. Cole, CCEMT-P
“It takes a lot of time to make things go right, but they can all go to hell in a heartbeat.”
-Walter Slovotsky
About the Author: Steve Cole has been involved in EMS and EMS education since 1990. He has worked
for a variety of EMS agencies including volunteer fire, military, hospital based, private, and third service.
He is currently employed by Ada County Paramedics (Boise, Idaho),a top-tier and often besieged Third
Service EMS.
He has no current conflicts of interest with any portion of this article, and has not received from any
commercial interest for its production. He would like to mention that he is open for some money, should a
sufficiently insane commercial enterprise wish to invest in his expansive, eclectic, and somewhat
haphazard quest for EMS excellence.
Comments are welcome. He can be reached by email at: colemedic@hotmail.com
Introduction:
Autonomic Dysreflexia (AD), sometimes known as Hyperreflexia, is a
potentially life threatening condition1
almost completely unique to patients with spinal
cord injuries (SCI). It is characterized by a severe sympathetic response, notably stroke-
level hypertension, and related symptoms. It can be triggered by the most benign and
subtle of events, and can be overlooked easily in its early stages. Fortunately, in many
cases treatment is fairly simple if AD is recognized.
The majority of this article assumes that EMS is called after the fact, and the symptoms
are severe. However, this information is also of use to those providers who transfer SCI
patients to prevent the development of AD caused by inadvertent stimulus.
Incidence and epidemiology:
AD typically occurs in approximately 85% of patient’s with spinal cord injuries above T-
5 (although some cases of T-10 injured patient’s with AD have been reported).2
While
more men than women sustain SCI, this is mainly due to lifestyle and risk-taking
behaviors. Once a cord injury occurs, there is no difference between the occurrence of
AD based on gender, age, or race.
Spinal Cord Injury itself was first discussed in a surgical papyrus dated over 5000 years
ago.3
It described two cases of high cord injury (AKA: Quadriplegia or Tetraplegia) as an
“ailment not to be treated”. Until the advent of modern medicine, however, these patients
seldom survived more than a few weeks. This has changed, with a typical patient
surviving his injury for many, many years. With this ever-increasing life span, more and
more conditions and complications of SCI are being discovered and managed. AD is one
of these conditions.
1

AD was first reported in modern medical literature in 1890, and has presumably been
present for as long as there have been a spinal cord injured patient, although prior to the
advent of modern medicine the lifespan of these patients was probably very short.4
Fortunately, prevention, patient education, and home health care greatly reduce the field
presentation of this syndrome. In fact many patients encountered may be more familiar
with this condition than most health care providers.
Basic Pathophysiology of Autonomic Dysreflexia
AD is essentially a dysfunction between two components of the Autonomic Nervous
System , the Sympathetic Autonomic Nervous System and Para-sympathetic Autonomic
Nervous system, with effects across multiple body systems. In order to better understand
the dysfunction, we must discuss the normal interaction of the CNS and PNS, and its
components.
Relevant Anatomy
The two largest divisions of the nervous system are the Central Nervous System (CNS)
and the Peripheral Nervous System (PNS) . The CNS is made up of the brain and the
spinal cord, while the PNS is pretty much everything else. The bridge between the CNS
and the PNS are the 12 cranial nerves, and numerous spinous nerves.
Overview of the Nervous System
While we mainly think of the PNS as sensory and somatic in nature, it also has important
autonomic functions as well. The autonomic portion of the PNS is known as the
Autonomic Nervous System (ANS), and is responsible for sending impulses to various
important organs in the body from the CNS, but not for receiving them5
. In fact, there is
very little “feed back” from these organs to the autonomic PNS, this is handled through
other mechanisms. An exception to this are the baroreceptors and chemoreceptors in the
carotid sinus and aortic arch. These are important in the control of heart rate, blood
pressure and respiratory activity.
2
©2007, Robert S. Cole, All rights reserved

The two branches of the autonomic PNS are the Sympathetic Autonomic Nervous System
(SANS) and the Parasympathetic Autonomic Nervous System (PANS). It is these two
components of the PNS that are responsible for AD.
The SANS, also called the adrenergic nervous system, is responsible for the “Fight or
Flight” response. Simply put, it is responsible for calling on the resources of the body for
survival. Important chemical agents of the SANS include Epinephrine and Nor-
epinephrine, and to a lesser degree, dopamine. Everyday autonomic control of blood
pressure, vasoconstriction, and heart rate come from the brain and high cord. Sympathetic
response can also be triggered by noxious stimuli of the distal sensory (pain, pressure,
etc) nerves, without “permission” from the rest of central nervous system.
Many of the symptoms of AD are directly related to stimulation of the SANS by noxious
(painful) stimuli. Most of the SANS nerve branches come directly off the spinal cord in
the cervical, thoracic, and lumbar regions.
KEY POINT
Many of the symptoms of Autonomic Dysreflexia (AD) are directly related
to stimulation of the Sympathetic Adrenergic Nervous System by noxious
stimuli.
The PANS is responsible for mediating and buffering the SANS. Known as the “Feed
and Breed” response it is responsible for the preservation and restoration of energy.
Therefore it often has an opposite effect of the SANS, and suppresses or buffers its
sympathetic effects on many organs. Its primary chemical agent is acetylcholine (Ach),
and thus the PANS is sometimes referred to as the cholinergic nervous system. Other
important chemical agents are muscarine and nicotine.
KEY POINT
The Para-sympathetic Autonomic Nervous System will often mediate,
suppress, or otherwise buffer the effects of the Sympathetic Autonomic
Nervous System on many of the body’s systems.
The PANS originates from two areas: Primary, the nerves that supply the organs of the
abdomen, heart, lungs, and skin above the waist begin at the level of the brain and very
high spinal cord (cranial nerves III, VII, IX and X). (The most important of these is the
tenth (X) cranial nerve, the Vagus nerve. This nerve directly affects heart rate during AD,
and will be discussed later.) And secondarily, the nerves that supply the reproductive
organs, pelvis, and leg begin at the sacral level.
3

Table: Comparing The Sympathetic And Para-Sympathetic
Autonomic Nervous Systems.
Organ Sympathetic Stimulation Parasympathetic Stimulation
Heart
Increased heart rate beta1 (& beta2) Decreased heart rate
Increased force of contraction
beta1 (& beta2)
Decreased force of contraction
Increased conduction velocity Decreased conduction velocity
Arteries
Constriction (alpha1)
Dilation
Dilation (beta2)
Veins
Constriction (alpha1)
Dilation (beta2)
Lungs
Bronchial muscle relaxation
(beta2)
Bronchial muscle contraction
Increased bronchial gland secretions
Gastro-
intestinal tract
Decreased motility (beta2) Increased motility
Contraction of sphincters (alpha) Relaxation of sphincters
Liver
Glycogenolysis (beta2 & alpha)
Glycogen synthesisGluconeogenesis (beta2 & alpha)
Lipolysis (beta2 & alpha)
Kidney Renin secretion (beta2)
Bladder
Detrusor relaxation (beta2) Detrusor contraction
Contraction of sphincter (alpha) Relaxation of sphincter
Uterus
Contraction of pregnant uterus
(alpha) There are very few para-sympathetic
receptors in the uterusRelaxation of pregnant and non-
pregnant uterus (beta2)
Eye Dilates pupil (alpha)
Constricts pupil
Increased lacrimal gland secretions
Submandibular &
parotid glands
Viscous salivary secretions (alpha) Watery salivary secretions
4

When one nervous system becomes two
As discussed earlier, normally the SANS and the PANS work together to maintain a
balance in the body, and to facilitate vital functions. However, in a cord-injured patient,
this synergy no longer occurs.
When a patient has a cord injury above T-6, typically the moderating effects of the PANS
on the SANS are inhibited. Simply put, the impulses from the brain to the PANS to
trigger a para-sympathetic response are interrupted through-out most of the PANS.
Remember that the PANS originates in the brain and is controlled through a number of
the cranial nerves (with the exception of some nervous function in the sacrum). After a
spinal cord injury, the parasympathetic nerves that begin at the brain continue to work,
even during the phase of spinal shock. When AD occurs, the parasympathetic nerves
attempt to control rapidly increasing blood pressure by slowing down the heart.
By contrast the SANS originates and is controlled mainly from the spinal cord (T1
through L2). While the SCI will inhibit the SANS response to everyday control of blood
pressure, heart rate, and similar vegetative functions (which arise from the brain and high
cord), it does not effect the SANS response to noxious stimuli (which come from distal
sensory nerves). This is why the SCI patient will develop chronic hypotension, and be
prone to orthostatic changes (resulting from poor autonomic control) yet can still have a
significant hypertensive response (from the SANS below the point of injury) to even
mild noxious stimuli.
KEY POINT
Normally the SCI patient lives with chronic hypotension due to lack of
autonomic control. This changes with noxious stimulation, which
stimulates the SANS and causes hypertension.
Therefore, when a cord injury occurs, the parasympathetic response is partially inhibited
while the sympathetic response largely is not. The higher the cord injury, the more
SANS is affected in this way.
KEY POINT
When the Para-sympathetic Autonomic Nervous System is interrupted or
inhibited by a cord injury, the Sympathetic Autonomic System is
unopposed.
5

So What Is Autonomic Dysreflexia?
AD occurs after the acute phase of the injury to the spinal chord, typically about a week.
It occurs most commonly and unpredictably within the first year of the injury. As
discussed in detail earlier in this article, it is the PANS and the SANS that are of most
importance in AD. Simply put, the SANS causes most of the life threatening symptoms,
while the PANS is responsible for many other signs.
In the normal non-SCI pt, when a painful/noxious stimulus occurs, the SANS is activated
and the “Fight or Flight” response is directly stimulated. The blood pressure raises, the
heart rate increases, and peristalsis decreases (as a result of vasoconstriction in the gut).
Norepinephrine, Epinephrine, and Dopamine are released.
The PANS would ideally mediate this response, doing so with mechanisms of its own. It
directly mediates the sympathetic response by slowing the heart rate (thus the associated
bradycardia with AD) and vasodilatation.
In the normal patient this happens every day to a variety of stimuli, and due to the
constant balancing act of homeostasis we often never notice a difference. In the SCI pt
however, the site of injury prohibits free movement of parasympathetic responses. Thus
as the SANS is activated, the massive vasculature in the body in general and the gut in
particular vasoconstict, raising the blood pressure (most of the S/S in AD are directly
related to this auto transfusion of blood or to the resultant hypertension). The SANS
essentially has free rein, with the parasympathetic impulses blocked at the level of SCI.
KEY POINT
Most of the symptoms of autonomic dysreflexia are related to sympathetic-
induced vasoconstriction and related hypertension. Therefore vasodilators play
an important role in treatment of refractory AD.
Often the only mediating response remaining in SCI is bradycardia (secondary to
stimulation of the vagus nerve) and general vasodilatation above the injury (causing the
sweating, nasal stuffiness, and flushed appearance) while the SANS causes its effects
below the level of SCI. These remaining PANS impulses are usually inadequate to
combat the work of the SANS.
6

KEY POINT
When AD occurs, the parasympathetic nerves attempt to control rapidly
increasing blood pressure by slowing down the heart. This is often the only
significant means remaining to the PANS to combat AD. Therefore the relative
hypertension of autonomic dysreflxia is often accompanied by bradycardia
instead of sympathetic induced tachycardia.
Signs and Symptoms of Autonomic Dysreflexia
As mentioned, most of the symptoms of AD are related to unmediated sympathetic
response to noxious stimuli, specifically hypertension and vasoconstriction. It is useful to
think that these s/s share much in common with hypertensive crisis and eclampsia,
although similar to eclampsia, relative hypertension is as dangerous as actual
hypertension.
KEY POINT
AD shares many common symptoms with PIH/eclampsia and hypertensive crisis,
although the treatments differ.
Common Presentations:
• Hypertension: Significant increase in both systolic and diastolic pressures usually
associated with bradycardia. Blood pressure may be much greater than 200/100,
however remember that a SCI pt may normally have a systolic BP as low as 90
mm Hg, so an increase in 30-40 mm Hg above this may be a warning sign. Most
clinical guidelines agree to a blood pressure threshold of 150 mm hg for severe
cases requiring aggressive treatment, although s/s can occur at lower pressures.
Blood pressures should be done in a sitting or simi-fowlers position when possible
for an accurate assessment of AD.
• Pounding headache (secondary to both sympathetic induced hypertension and
para-sympathetic vasodilatation)
• Flushed (reddened) face (secondary to vasodilatation)
• Red blotches/flushed appearance to the skin above level of spinal injury
(secondary to vasodilatation)
• Sweating above level of spinal injury (secondary to vasodilatation)
• Nasal stuffiness (secondary to vasodilatation)
7

• Nausea (secondary to vagal/parasympathetic stimulation)
• Blurred Vision/Visual disturbances.
• Bradycardia - slow pulse <60 beats per minute - (secondary to Vagal
parasympathetic stimulation)
• Signs of Congestive Heart Failure secondary to the hypertension.
• Piloerection ("goose bumps") : These can occure above or below the level of
injury.
• Cold, clammy skin below level of spinal injury
KEY POINT
When assessing for autonomic dysreflexia, blood pressures should typically be
taken in a semi-fowlers or sitting position rather than laying flat. In addition, a
blood pressure threshold of 150 mm Hg systolic is typically required prior to
aggressive (pharmacological) treatment. .
Treatment and Care
First line treatment in AD is addressing underlying causes. Simply put: remove the
noxious stimuli and the sympathetic response will subside.
KEY POINT
First line treatment of AD is to remove the underlying noxious stimuli. This should
be attempted prior to pharmacological therapy in all but the most severe cases.
To understand the causes, one must understand that while SCI pts have had to adapt to
serious lifestyle changes, most still try to live as much of a normal life as possible. They
undergo training to have regular bowel and bladder habits using “Quick Caths” and
digital removal of stool (consider the alternative to these programs before laughing), they
can have sexual intercourse, and even become pregnant. They are still subject to life’s
daily functions, like menstrual cycles (and cramps), ulcers, and other illness. Remember
that they may not be able to “feel” the pain, but that doesn’t mean that the injury
/condition is not painful at the neurological level. All of these activities and/or illness can
lead to AD.
KEY POINT
The most common cause of AD is catheter problems and bowel/bladder issues.
Pressure sores and skin related discomfort are often causes as well.
8

Any stimuli that would be uncomfortable to a non-SCI patient could cause
AD.
The most common causes of AD are either a catheter/bladder problem and/or a bowel
impaction. These are often due to a noncompliance with a bowel/bladder program, but
may be secondary to an equipment malfunction. Another common cause is skin
breakdown and discomfort.
In general however ANY stimuli that would potentially cause pain and discomfort
to a normal person may be considered suspect.
A summarized list includes:
• Bladder (most common) - from overstretch or irritation of bladder wall
o Urinary tract infection
o Kidney Stones
o Urinary retention
o Blocked catheter
o Overfilled collection bag
o Non-compliance with intermittent catheterization (Quick Cath) program
• Bowel - over distention or irritation
o Constipation / impaction
o Distention or discomfort during bowel program/digital stimulation.
o Hemorrhoids or anal fissures
o Infection or irritation (e.g. appendicitis, cellulitis)
• Skin-related Disorders
o Any direct irritant below the level of injury (e.g. - prolonged pressure by
object in shoe or chair, cut, bruise, abrasion)
o Pressure sores (decubitus ulcer)
o Ingrown toenails
o Burns (e.g. - sunburn, burns from using hot water)
o Tight or restrictive clothing or pressure to skin from sitting on wrinkled
clothing
• Sexual Activity
o Over stimulation during sexual activity [stimuli to the pelvic region which
would ordinarily be painful if sensation were present]
o Ejaculation
o Menstrual cramps
• Other
o Heterotopic ossification ("Myositis ossificans", "Heterotopic bone")
o Acute abdominal conditions (gastric ulcer, colitis, peritonitis)
o Skeletal fractures
o Invasive procedures
o Contact against hard/sharp objects
o Pulmonary Emboli
9

o Deep Vein Thrombosis
Basic treatment
The general concept of treatment is first to identify the cause and if possible, eliminate
the noxious stimulus. This often will rapidly resolve the problem. If however the cause
can either not be identified or not be treated in the field, the more aggressive measures
are called for.
KEY POINT
Removing the cause of the noxious stimuli will often resolve the problem rapidly.
Loosen all constricting/restricting clothing wherever possible. A simple bunched up or
constricting belt line can precipitate AD.
Identify and remove the offending stimulus whenever possible. Often, this alone is
successful in allowing the syndrome to subside without need for pharmacological
intervention. It is also good for the person with the symptoms to be sitting up with
frequent blood pressure checks until the episode has resolved.
Suspected cause = bladder? Check catheter - remove kinks if found, empty
urinary collection bag, irrigate catheter. If catheter is not draining, replace it
immediately. If an intermittent catheterization program is in place, a straight
catheterization should be performed immediately with slow drainage to prevent
bladder spasms. If this is unsuccessful, consider flushing the catheter, or outright
replacement. Use an anesthetic ointment to suppress the noxious stimulus, if
available. The patient, home health aids, or family are often able to assist with
this.
Suspected cause = bowel? Unless a provider is experienced in digital removal of
feces it should not be attempted as the AD can be aggravated. If episode occurred
during digital stimulation/bowel evacuation, often stopping stimulation will allow
symptoms to subside. Consider use of a prescribed anesthetic ointment to
suppress the noxious stimulus, if available. If the issue is impacted stool,
disimpact if feasible. If it occurs while doing a bowel program in bed, try
commode-based bowel evacuation. Consider use of abdominal massage instead of
digital stimulation.
Suspected cause = skin? Loosen clothing. Check for source of potential
offending stimulus - check for pressure sores to the back, heels, sacral area,
toenail problems, soles of the feet.
Routine assessment and management: Repeated V/S every 5 minutes may be indicated
to observe for fluctuations and rebound hypertension.
Elevate head 30-45 degrees. Similar to care in CVA and hypertensive crisis, this
promotes venous drainage and decreases ICP related effects. In addition placing the
10

patient in a semi-fowlers position or higher may cause small reduction in the blood
pressure.
Pharmacological Therapies
The general concept of treatment is first to identify the cause and if possible, eliminate
the noxious stimulus. This often will rapidly resolve the problem. If however the cause
can either not be identified or not be treated in the field, the more aggressive measures
are called for.
KEY POINT
If the cause can not be identified, not treated in the field, or if removing the
noxious stimuli is unsuccessful, then more aggressive treatments are needed.
This usually means pharmacological intervention.
Current clinical guidelines recommend a blood pressure threshold of 150 mm Hg
systolic prior to considering aggressive pharmacological treatment (basic measures can
be initiated at anytime however). Most therapies are focused on addressing
vasoconstriction and hypertension rather than blunting sympathetic response.
Pre-hospital EMS usually is limited to nitrates in their available drugs to treat AD,
however the patient will often have his preferred pharmacological treatment with him.
Frequently, either poor motor function or rapid progression of the AD prevents the
patient from self medicating without assistance. While Nitrates are effective, use of the
patients own medication should be strongly considered. When possible, contact medical
control for guidance.
Common pharmacological interventions are discussed below:
Calcium Channel Blockers: Ca Channel Blockers are potent vasodilators. One of the
more common (and effective) ones is Procardia.
• Procardia 10 mg sublingual, may be repeated in 10-60 minutes.
11

Nitrates: Nitrates are effective, short acting, and relatively simple vasodilators.
• NTG 0.4 mg sublingual every 3-5 minutes
• NTG Paste 1 inch to non-hairy area of chest.
Vasodilators: Hydralazine is a potent vasodilatator with little cardiac effects. It tends to
last approximately 12 hours, so its effects may last longer than the AD episode.
• Hydralazine 10-20 mg PO/IV/IM
Alpha-2 adrenergic blockers: The most common of these is Clonidine. Clonidine is used
both acutely for AD symptoms, and chronically for prevention.
• Clonidine 0.1 mg to 0.2 mg p.o.
Lidocaine based Lubricant: In the event that a catheter has to be replaced, or that the
patient, family, or EMS may be placing a catheter, it is recommended that a 2%
Lidocaine lubricant (such as commonly used during endotracheal intubation) be used
instead of the more common water based lubricants without Lidocaine. In addition if
digital dis-impaction is to be performed, then a lidocaine containing lubricant may be
desired as well. Lidocaine should reduce the noxious stimulation to the SANS, reducing
sympathetic response to the procedure. When used the Lidocaine lubricant should be
allowed to “soak” for about 5 minutes prior to the procedure to achieve maximum effect.
AD and Pregnancy
Quite a few SCI injured patients go on to live a relatively normal life after the initial
injury. This includes holding a job, enjoying many recreational activities, and even
having children. Unfortunately, there is very little research into the field of SCI and
pregnancy, and even less on proper management of AD in this situation. This is
complicated by the number of pregnancy induced hypertension (PIH) disorders that can
occur in pregnancy.
About two thirds of pregnant SCI patients will develop AD during labor and delivery.
False labor, as well as other painful conditions (like abrupted placenta) can precipitate
AD. Complicating this is that PIH/eclampsia may be mistaken for AD, and visa versa.
This is especially troublesome since while the s/s are similar, the treatment is different.
Usually, other than urine screening, angioedema and history are the most important
methods to tell the difference when determine treatment, but when possible medical
control should be consulted.
KEY POINT
AD is often difficult to discern from PIH/Eclampsia in the SCI pregnant patient. All
such patients should be transported for further evaluation, regardless if
symptoms and suspected causes are resolved.
12

When Has AD Resolved?
The primary indicator of the resolution of AD is absence of the primary c/c, such as
headache, stuffy nose, blurred vision, etc. Ideally the cause of the AD would have been
identified. In addition, the blood pressure should have returned to baseline (typically 90-
110 mm/hg in a quadriplegic patient who is sitting up). Finally, the heart rate should have
returned to normal (no bradycardia).As discussed earlier, the patient must maintain this
for at least 2 hours.
KEY POINT
End points for resolution of AD are:
- Asymptomatic for 2 hours
- Systolic Blood pressure returned to baseline (typically 90-110 mm Hg)
- No bradycardia
- The cause of the noxious stimuli has been identified
Occasionally, after a noxious stimuli has been resolved, or if a medication proves too
effective, a symptomatic hypotension may develop. This hypotension is usually transient.
If needed, this can usually be treated by simply laying the patient supine. Further
treatment, such as fluid boluses or vasopressors, are unlikely to be needed.
Treat and Release Considerations
Often, if AD is rapidly resolved, the patient will feel comfortable in remaining at home
under the care of his home health service and family. This is complicated by both the
patients and the family having both experience and a stronger knowledge base in AD than
many health care providers who do not routinely deal with SCI (like EMS).
Currently clinical guidelines recommend that the patient who has suffered an episode of
AD be observed for at least 2 hours prior to release. In addition to monitoring for rebound
hypertension, a screening would be done to evaluate potential causes and complications.
Most of these evaluations are beyond the capability of EMS services.
KEY POINT
Observation is recommended for at least two hours post AD, to observe for
recurrent hypertension. Therefore transport is strongly encouraged.
Still, many patients and families will want to decline transport. Assuming that the patient
has the legal and mental capacity to do so, such cases should always be against medical
advice (AMA) and accompanied by a tactful explanation of risks and need for further
evaluation. Document thoroughly.
13

In addition, EMS should attempt to ensure that the patent is accompanied in the presence
of a responsible party who can assist him if his AD should recur. EMS should also offer
to contact the patient’s home health service, or otherwise facilitate his personal medical
care, prior to release.
Routine Transport of the SCI patient.
Most of this article has focused on treatment of AD after it has begun. It is worth
mentioning the importance of preventing AD during a routine patient contact.
Probably the single most important consideration is simple catheter care. Laying on a
narrow uncomfortable cot, covered by blankets and sheets, amid the everyday
distractions of even routine transport, it is a simple thing for an SCI patient to have his
catheter kinked, elevated to allow back flow of urine, or even tugged. Special care should
be taken to allow the catheter to drain freely, remain secure, and not place tension on the
catheter itself. If the patient routinely straight caths himself, accommodations should be
made to allow the patient to do this to prevent bladder distention and/or UTIs.
Patient position on the cot is also of importance. Don’t allow clothes to constrict pt.
Don’t allow clothes or linen to wad up under the pt. Keep the patient off of pressure sores
as much as feasible. Over long transports (30 minute to an hour) turn the pt from one
side to another (use pillows) to prevent pressure sores.
Summary
Autonomic Dysreflexia can have devastating, even fatal, effects on the pt., ranging from
stroke to death. However, when treated quickly and appropriately, the pt. may have no
long-term consequences. Therefore, education of patients, caregivers, and healthcare
providers is imperative. This syndrome occurs suddenly and treating it must be given a
priority. AD is a medical Emergency, addressing it must be a priority.
Autonomic Dysreflexia can occur anytime after spinal shock has been resolved and can
occur anytime after discharge. Pt’s may seek medical help at any emergency room or
through any EMS. Furthermore Pt’s may present with this disorder during routine
medical transport or contact for unrelated reasons. Therefore, it is important that all
healthcare professionals, not just those who work with clients with SCI, become aware of
this disease process.
14

References
15

1
Travers, Patricia L.. "Autonomic Dysreflexia: A Clinical Rehabilitation Problem."
www.rehabnurse.org (1999) 29 MAR 2007 <http://rehabnurse.org/ce/010299/auto.htm>.
2
"Other Complications Of Spinal Cord Injury: Autonomic Dysreflexia (Hyperreflexia)." RehabSite.
1998. Louis Calder Memorial Library of the University of Miami/Jackson Memorial Medical
Center. 29 Mar 2007 <http://calder.med.miami.edu/pointis/automatic.html>.
3
Consortium for Spinal Cord Medicine, "Acute Management of Autonomic Dysreflexia: Adults
with Spinal Cord Injury Presenting to Health-Care Facilities." Clinical Practice Guidelines 2nd
editionJul 2001 29 MAR 2007 <http://www.pva.org/site/DocServer/AD2.pdf?docID=565>.
4
Campagnolo, Denise I. "Autonomic Dysreflexia in Spinal Cord Injury." www.emedicine.com. 05
OCT 2006. 29 Mar 2007 <http://www.emedicine.com/pmr/topic217.htm>.
5
Bakewell, S.. "The Autonomic Nervous System ." Update in Anesthesia Issue 5, Article 6(1995)
1-2. 29 MAR 2007 <http://www.nda.ox.ac.uk/wfsa/html/u05/u05_010.htm>.

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