2018 0309

https://emedicine.medscape.com/article/322809-overview
 Overview
 Pathophysiology
 Causes of Autonomic Dysreflexia
 Prognosis
 Patient education
 Consultations
 Prevention
 Epidemiology
 History and Physical Examination
 Physical Therapy
 Occupational Therapy
 Recreational and Speech Therapies
 Treatment of Autonomic Dysreflexia
 Prevention of Autonomic Dysreflexia
 Show All
 References

Autonomic Dysreflexia in Spinal Cord

Injury
Updated: Jan 29, 2018
Author: Ryan O Stephenson, DO; Chief Editor: Milton J Klein, DO, MBA more...

Overview
Autonomic dysreflexia is a potentially dangerous and, in rare cases, lethal clinical
syndrome that develops in individuals with spinal cord injury, resulting in acute,
uncontrolled hypertension. All caregivers, practitioners, and therapists who interact with
individuals with spinal cord injuries must be aware of this syndrome, recognize the
symptoms, and understand the causes and treatment algorithm. [1, 25]
Briefly, autonomic dysreflexia develops in individuals with a neurologic level of spinal
cord injury at or above the sixth thoracic vertebral level (T6). Autonomic dysreflexia
causes an imbalanced reflex sympathetic discharge, leading to potentially life-threatening
hypertension. It is considered a medical emergency and must be recognized immediately.
If left untreated, autonomic dysreflexia can cause seizures, retinal hemorrhage,
pulmonary edema, renal insufficiency, myocardial infarction, cerebral hemorrhage, and,
ultimately, death. Complications associated with autonomic dysreflexia result directly
from sustained, severe peripheral hypertension. (See the image below.)
(A) A strong sensory input (not necessarily noxious) is carried into the spinal cord via
intact peripheral nerves. The most common origins are bladder and bowel. (B) This
strong sensory input travels up the spinal cord and evokes a massive reflex sympathetic
surge from the thoracolumbar sympathetic nerves, causing widespread vasoconstriction,
most significantly in the subdiaphragmatic (or splanchnic) vasculature. Thus, peripheral
arterial hypertension occurs. (C) The brain detects this hypertensive crisis through intact
baroreceptors in the neck delivered to the brain through cranial nerves IX and X. (D) The
brain attempts two maneuvers to halt the progression of this hypertensive crisis. First, the
brain attempts to shut down the sympathetic surge by sending descending inhibitory
impulses. These impulses are unable to travel to most sympathetic outflow levels because
of the spinal cord injury at T6 or above. Inhibitory impulses are blocked in the injured
spinal cord. In the second maneuver, the brain attempts to bring down peripheral blood
pressure by slowing the heart rate through an intact vagus (parasympathetic) nerve;
however, this compensatory bradycardia is inadequate and hypertension continues. In
summary, the sympathetics prevail below the level of neurologic injury, and the
parasympathetic nerves prevail above the level of injury. Once the inciting stimulus is
removed, reflex hypertension resolves.

https://emedicine.medscape.com/article/322809-overview#a2

Pathophysiology
The autonomic nervous system is the division of the peripheral nervous system that
carries motor information to the visceral organs and glands. It is made up of the
sympathetic and parasympathetic autonomic nervous systems. The sympathetic fibers are
responsible for the fight-or-flight response and divert blood flow away from the
gastrointestinal tract and skin through the process of vasoconstriction. As a result, blood
flow to skeletal muscles and lungs is significantly enhanced (by as much as 1200% in the
case of skeletal muscles). [2] This also causes bronchiolar dilatation of the lung, which
allows for greater alveolar oxygen exchange and increases the heart rate and contractility
of cardiac myocytes.
The parasympathetic fibers typically act in opposition of the sympathetic autonomic
nervous system through negative feedback control. This action is a complementary
response, causing a balance of sympathetic and parasympathetic responses. Overall, the
parasympathetic outflow results in conservation and restoration of energy, reduction in
heart rate and blood pressure, facilitation of digestion and absorption of nutrients, and
excretion of waste products. This parasympathetic response is primarily mediated through
cranial nerve X, the vagus nerve, and the S2, S3, and S4 spinal nerves.
In individuals with intact central and peripheral nervous systems, a noxious stimulus
results initially in a sympathetic response, leading to elevation in heart rate and blood
pressure primarily through spinal reflexes. This response is modulated by the central
nervous system and peripheral baroreceptors through the parasympathetic nervous
system; this results in heart rate and blood pressure control both through direct responses
by the vagus nerve and through inhibitory spinal cord signals. An appropriate balance of
sympathetic and parasympathetic outflow is attained and modulated by both the central
and peripheral nervous systems.
In those with a spinal cord injury at the level of T6 and above, a noxious (or otherwise
strong) stimulus below the level of injury results in an unbalanced physiologic response.
The strong stimulus causes a peripheral sympathetic response through spinal reflexes,
resulting in vasoconstriction below the level of injury. This reflex response ascends and
descends the spinal cord and paraspinal sympathetic ganglia, causing both direct
vasoconstriction through activation of perivascular receptors and systemic/indirect
vasoconstriction through stimulation of the adrenal medulla, resulting in epinephrine and
norepinephrine release into the systemic circulation. This therefore results in
hypertension, primarily through splanchnic and peripheral vasoconstriction.

The baroreceptors in the carotid sinus and aortic arch convey appropriate responses to
hypertension through the petrosal ganglion to the nucleus ambiguous and result in strong
vagal (CN X) outflow, bradycardia, and vasodilatation above the level of injury. The
central nervous system cannot directly detect the strong or noxious signal below the level
of injury (owing to the lack continuity of the ascending sensory fibers from the
underlying spinal cord injury), and, therefore, responds to hypertension by sending a
strong inhibitory response through the spinal cord aimed at reducing the sympathetic
response. However, because of the lack of spinal cord continuity, the descending
inhibitory response only travels as far as the level of neurologic injury and does not cause
the desired response in the sympathetic fibers below the injury; therefore, the
hypertension remains uncontrolled.
As a result, there is flushing and sweating only above the level of injury, bradycardia,
pupillary constriction, and nasal congestion (unopposed parasympathetic responses); and
below the level of injury, there is pale, cool skin and piloerection due to sympathetic tone
and lack of the descending inhibitory parasympathetic modulation. [3] (However, a study
by Solinsky et al of 78 male patients with SCI who had incidents of autonomic
dysfunction found that out of 445 episodes, relative tachycardia occurred in 68.0%, far
more frequently than relative bradycardia [0.3%]. [28] )
T6 is of particular importance in the pathogenesis of autonomic dysreflexia. The
splanchnic vascular bed is one of the body’s largest reserves of circulatory volume and is
controlled primarily by the greater splanchnic nerve. This important nerve derives its
innervation from T5-T9. Lesions to the spinal cord at or above T6 allow the strong and
uninhibited sympathetic tone to constrict the splanchnic vascular bed, causing systemic
hypertension. Lesions below T6 generally allow enough descending inhibitory
parasympathetic control to modulate the splanchnic tone and prevent hypertension.
The underlying pathophysiological changes that occur in the spinal cord and in the
periphery that cause autonomic dysreflexia have not been fully elucidated in a human
model. It has been postulated that peripheral alpha-adrenergic receptors associated with
blood vessels become hyperresponsive below the level of the spinal cord lesion. This
hyperresponsiveness is secondary to a low resting catecholamine state associated with
spinal cord injury. The orphaned receptors have a decreased threshold to react to
adrenergic stimuli and react with an increased responsiveness. [4, 5, 6]

Another possible mechanism includes loss of supraspinal inhibitory control from the
medulla oblongata–bulbospinal pathways; this loss of supraspinal control may cause a
loss of the bulbospinal pathway’s inhibitory effect over serotonin in the intermediolateral
nucleus of the spinal cord. The unabated serotonin then causes strong vasoconstriction. [7]
A study by Phillips et al suggested that the brain may buffer moderate instances of
autonomic dysreflexia. During spontaneous episodes of autonomic dysreflexia in four
patients with motor-complete cervical SCI, the report found that although the mean
arterial blood pressure rose from 66 to 83 mm Hg, the cerebral blood flow and end-tidal
partial pressure of carbon dioxide remained approximately the same. [8]

https://emedicine.medscape.com/article/322809-overview#a3

Causes of Autonomic Dysreflexia

Episodes of autonomic dysreflexia can be triggered by many potential causes. [9]
Essentially, any painful, irritating, or even strong stimulus below the level of the injury
can cause an episode of autonomic dysreflexia. Bladder distension or irritation is
responsible for 75-85% of the cases. [10] Bladder irritation is commonly caused by a
blocked or kinked catheter or failure of a timely intermittent catheterization program. The
second most common cause of autonomic dysreflexia is bowel distention, usually due to
fecal impaction. This accounts for 13-19% of cases. [10] Although the list is not
comprehensive, the following events or conditions all can cause episodes of autonomic
dysreflexia:
Bladder distention
Urinary tract infection
Calculus
Cystoscopy/instrumentation
Urodynamic study [11, 24]
Epididymitis or scrotal compression
Bowel distention
Fecal impaction
Bowel instrumentation/colonoscopy
Reflux or gastritis
Gallstones
Gastric ulcers
Invasive testing
Hemorrhoids
Gastrocolic irritation
Appendicitis or other intra-abdominal pathology/trauma
Anal fissure
Menstruation
Pregnancy - Especially labor and delivery
Vaginitis
Sexual intercourse [30]
Ejaculation
Deep vein thrombosis
Pulmonary emboli
Pressure ulcers
Ingrown toenail
Burns or sunburn
Blisters
Insect bites
Contact with hard or sharp objects
Temperature fluctuations
Constrictive clothing, shoes, or appliances
Heterotopic bone
Fractures or other skeletal trauma
Surgical or diagnostic procedures
A literature review by Liu et al indicated that in patients with SCI, autonomic dysreflexia
triggers from the lower urinary tract are often associated with clinical urologic
procedures, suggesting that blood pressure monitoring should be routinely performed
during such procedures. The study found, for example, that 36.7-77.8% of patients
undergoing urodynamic testing experienced autonomic dysreflexia, with the problem also
occurring in most patients when cystoscopy, transurethral litholapaxy, or extracorporeal
shock-wave lithotripsy were performed without anesthesia. The investigators also found
that autonomic dysreflexia occurred more often in patients with cervical SCI than in
those with thoracic SCI. [12]
A study by Vírseda-Chamorro et al indicated that in performing a urodynamic exam in
patients with an SCI above T6, independent risk factors for sudden onset of autonomic
dysreflexia consist of patient age of 45 years or above and a maximum detrusor voiding
pressure of 31 cm H2O or above. [13]
A study by Xiong et al of 89 patients indicated that in individuals with SCI who undergo
cystolitholapaxy, autonomic dysreflexia is more likely to occur in those with larger or a
greater number of bladder stones, an injury level above T6, a greater hydraulic irrigation
height, and a longer surgical time. [14]

https://emedicine.medscape.com/article/322809-overview#a4

Prognosis
Complications and morbidity associated with autonomic dysreflexia result directly from
sustained, severe peripheral hypertension and include retinal/cerebral hemorrhage,
myocardial infarction, and seizures. Mortality is rare.
In a literature review, Wan and Krassioukov identified the prevalence of various causes of
life-threatening complications and death from autonomic dysreflexia in spinal cord
injury, determining that central nervous system (CNS) – related causes were the most
frequent. The investigators found that out of 32 patients identified as having either died or
suffered life-threatening complications from autonomic dysreflexia, the prevalence of
CNS-, cardiovascular-, and pulmonary-related causes were as follows [15] :
CNS: 23 patients (72%)
Cardiovascular: Seven patients (22%)
Pulmonary: Two patients (6%)
Seven patients in the study died directly owing to complications from an attack of
autonomic dysreflexia. [15]

https://emedicine.medscape.com/article/322809-overview#a5

Patient education
All medical professionals should educate the patient and family members or caregivers
about this potentially life-threatening complication of spinal cord injury. [16] Such
instruction should include prevention strategies, signs and symptoms of autonomic
dysreflexia, and proper management of the condition. Patients should be encouraged to
carry a wallet-sized card explaining symptoms and treatment for autonomic dysreflexia.
Such cards can be found from multiple sources, including the following:
Christopher and Dana Reeve Foundation
The National Spinal Cord Injury Association

https://emedicine.medscape.com/article/322809-overview#a6

Consultations
If the cause of the episode of autonomic dysreflexia is not found and blood pressure
remains elevated, emergency department care is recommended for medication
management, close monitoring, and further investigation of the possible cause. Consult
an ICU specialist for ICU monitoring and treatment of the hypertension. Physicians
specializing in physical medicine and rehabilitation are well-acquainted with the
diagnosis and management of autonomic dysreflexia and can be of assistance in both
acute management and prevention strategies of this syndrome.

https://emedicine.medscape.com/article/322809-overview#a7

Prevention
Proper bladder and bowel care (ie, preventing fecal impaction, bladder distention)
are mainstays in preventing episodes of autonomic dysreflexia. Regulation of the bladder
routine via indwelling Foley catheter or intermittent catheterization and regular
urologic follow-up is highly recommended for autonomic dysreflexia prevention. A
regular bowel program to ensure appropriate fecal movement and prevent
constipation is important. Autonomic dysreflexia caused by anorectal procedures,
including the bowel program, or from intermittent bladder catheterization may be
diminished with the use of prophylactic lidocaine or dibucaine. [9] (A study by Inskip et
al found that among patients with SCI at T7 or above, 74% experienced autonomic
dysreflexia symptoms during bowel care. [27] )
Patients with spinal cord injury should be educated to recognize the early symptoms of
autonomic dysreflexia and understand the common causes and management. Those
with recurrent symptoms should be educated on home blood pressure monitoring.

https://emedicine.medscape.com/article/322809-overview#a8

Epidemiology
Reported prevalence rates vary for autonomic dysreflexia in the United States, but the
generally accepted rate is 48-90% of all individuals who are injured at T6 and above.
Patients who have a complete injury (no motor or sensation below the level of the spinal
cord lesion) have a much higher incidence of autonomic dysreflexia (91% with complete
injury vs 27% with incomplete injury 27%). [17] In a Korean study, by Lee and Joo, 26 out
of 28 patients (93%) with SCI above T6 were found to have autonomic dysreflexia, as
measured using ambulatory blood pressure monitoring. However, several individuals
with autonomic dysreflexia appeared to be asymptomatic. Twenty-four patients had
motor-incomplete SCI, while four had motor-complete injury. [26]
The occurrence of autonomic dysreflexia increases as the patient evolves out of spinal
shock. With the return of sacral reflexes, the possibility of autonomic dysreflexia
increases. [16] Autonomic dysreflexia occurs during labor in approximately two thirds of
pregnant women with spinal cord injury above the level of T6. Spinal epidural anesthesia
can help reduce the risks of autonomic dysreflexia during pregnancy.
The male-to-female ratio for sustaining spinal cord injury is 4:1; however, autonomic
dysreflexia has no sexual predilection.

https://emedicine.medscape.com/article/322809-overview#a9

History and Physical Examination

History
The patient with autonomic dysreflexia generally gives a history of one or many of the
following symptoms: Headaches, blurry vision, spots in the visual field, nasal congestion,
blotchy skin above the level of injury, and a sense of anxiety or malaise. Feelings of
apprehension or anxiety over an impending physical problem commonly are exhibited.
Physical examination
A patient with autonomic dysreflexia may have one or more of the following findings on
physical examination:
Significant rise in systolic and diastolic blood pressure greater than 20 mm Hg
systolic or 10 mm Hg diastolic above baseline (The sudden rise in blood pressure
in autonomic dysreflexia is usually associated with bradycardia. Normal systolic
blood pressure for an individual with spinal cord injury above T6 is 90-110 mm
Hg; blood pressure of 20-40 mm Hg above the reference range for such patients
may be a sign of autonomic dysreflexia. However, patients with autonomic
dysreflexia may display no symptoms, despite elevated blood pressure.)
Profuse sweating above the level of lesion - Especially in the face, neck, and
shoulders; rarely occurs below the level of the lesion because of sympathetic
activity
Goose bumps below the level of the lesion
Flushing of the skin above the level of the lesion - Especially in the face, neck, and
shoulders; this is a frequent symptom
Blurred vision
Nasal congestion – A common symptom
https://emedicine.medscape.com/article/322809-overview#a10

Physical Therapy
Physical therapists who treat patients with SCI need to have a good understanding of
autonomic dysreflexia and be familiar with the signs and symptoms of this potentially
life-threatening condition. [16] Throughout the physical therapy sessions, the therapist
needs to monitor the urinary catheter for any blockage or twisting.
If the patient becomes hypertensive during therapy and autonomic dysreflexia is the
suspected cause, the therapist should place the patient in an upright position immediately.
This takes advantage of an orthostatic response and helps with the pooling of blood in the
lower extremities. The therapist needs to complete careful inspection to identify the
source of painful stimuli (eg, catheter, restrictive clothing, leg bag straps, abdominal
supports, orthoses). [9] A less common cause of autonomic dysreflexia during physical
therapy sessions may originate with muscle stretching, either from range-of-motion or
passive stretching.
If the patient develops autonomic dysreflexia, the physical therapist needs to treat it as a
medical emergency and be familiar with established protocols for medical management
within his or her particular setting. The individual therapy session then must be
discontinued to allow the patient to stabilize and recover. Please refer to Guidelines of the
Consortium for Spinal Cord Medicine for the management of autonomic dysreflexia if no
guidelines are available at your facility.

https://emedicine.medscape.com/article/322809-overview#a11

Occupational Therapy
Occupational therapy is another discipline involved extensively in the rehabilitation of
individuals with SCI. The occupational therapist also must be familiar with the signs and
symptoms of autonomic dysreflexia and be able to respond quickly if the condition
develops during a therapy session. [16]
Occupational therapists perform extensive training in the performance of activities of
daily living with patients who have sustained SCI. Such activities include proper bowel
and bladder management, which can help to prevent to the occurrence of autonomic
dysreflexia. The occupational therapist may be involved in establishing a regular bowel
program and may complete patient and family/caregiver education on this aspect of care.
Both occupational and physical therapists should educate the patient and family members
about autonomic dysreflexia and ensure that they are familiar with prevention strategies,
signs and symptoms, and proper management of the condition.

https://emedicine.medscape.com/article/322809-overview#a12
Recreational and Speech Therapies
Recreational therapy
Recreational therapists also are important members of the rehabilitation team, as they
help patients with SCI to become involved in recreational, community, and social
activities. As members of the SCI team, they also must be knowledgeable about
autonomic dysreflexia and know how to respond appropriately if the patient develops
symptoms during a recreational therapy session. [16]
Speech therapy
Generally, the treatment provided by the speech therapist is not associated with any
painful stimuli below the lesion that may precipitate an autonomic dysreflexia response.
However, as health care providers involved in the treatment of individuals with SCI,
speech therapists must be familiar with the manifestations of this potentially life-
threatening condition. [16]

https://emedicine.medscape.com/article/322809-overview#a13

Treatment of Autonomic Dysreflexia

Check the patient's blood pressure. If the blood pressure is elevated, have the person
sit up immediately and loosen any clothing or constrictive devices. Sitting allows some
gravitational pooling of blood in the lower extremities and reduces blood pressure.

Survey the person for instigating causes, beginning with the urinary system, the most
common cause of autonomic dysreflexia. [11, 18]

If an indwelling urinary catheter is not in place, catheterize the patient.

If the individual has an indwelling urinary catheter, check the system along its entire
length for kinks, folds, constrictions, or obstructions and for correct placement.

If the catheter appears to be blocked, gently irrigate the bladder with a small amount of
fluid, such as normal saline at body temperature. Avoid manually compressing or
tapping on the bladder. If the catheter is draining and blood pressure remains elevated,
suspect fecal impaction, the second most common cause of autonomic dysreflexia, and
check the rectum for stool, using lidocaine jelly as lubricant. If impacted, gentle
manual evacuation is recommended.
Monitor blood pressure and pulse every 2-5 minutes until the patient has stabilized;
impaired autonomic regulation can cause blood pressure to fluctuate quickly during an
episode of autonomic dysreflexia.
Use of an antihypertensive agent is recommended when the systolic blood pressure is
at or above 150 mm Hg. Once the offending agent is identified and corrected, the
autonomic dysreflexia subsides and blood pressure returns to normal (systolic, 90-110
mm Hg). For this reason, medicating with a short-acting antihypertensive is of
utmost importance.

The most commonly used agents are nifedipine and nitrates (eg, nitroglycerine paste
or sublingual nitroglycerine). [29] Nifedipine should be in the immediate-release form;
bite and swallow is the preferred method of administering the drug, not sublingual
administration. Other agents used are prazosin, captopril, terazosin, mecamylamine,
diazoxide, and phenoxybenzamine. Use antihypertensives with extreme caution in
older persons or in people with coronary artery disease. Note that men with spinal cord
injury often use cGMP-specific phosphodiesterase type 5 (PDE5) inhibitors (eg,
sildenafil, vardenafil, tadalafil.) for sexual dysfunction. Use of nitrates is
contraindicated in this situation.

If there is poor response to treatment and/or if the cause of the autonomic dysreflexia
has not been identified, the patient should be seen in an emergency department for
monitoring and pharmacologic control of blood pressure. The emergency department
has better access to the necessary tests to investigate the possible etiology of the
autonomic dysreflexia.

Monitor the individual's symptoms and blood pressure for at least 2 hours after
resolution of the autonomic dysreflexia episode to ensure that elevation of blood
pressure does not recur. Autonomic dysreflexia may resolve because of medication, not
because of resolution of the underlying cause. Unless the underlying cause is
identified and addressed, recurrence should be expected.

https://emedicine.medscape.com/article/322809-overview#a14

Prevention of Autonomic Dysreflexia

Patients who have previously experienced autonomic dysreflexia may be able to prevent
the reoccurrence by using simple prevention strategies. The prevention strategies may
mitigate further episodes of autonomic dysreflexia. Common triggers are as follows.

Bladder
Intermittent catheterization should be regular and timely; only clean catheters should
be used. Indwelling catheters should be changed routinely and regularly checked for
blockage or kinking.
Detrusor sphincter dyssynergia causing autonomic dysreflexia may be treated with
intravesicular onabotulinumtoxinA or intravesicular capsaicin. [19] A study by Fougere et
al indicated that onabotulinumtoxinA injections into the detrusor of patients with high-
level SCIs (one cycle of 200 U) can reduce the severity and frequency of episodes of
bladder-related autonomic dysreflexia. The study included 17 patients with chronic,
traumatic SCIs at the sixth thoracic level or above. Following injection, autonomic
dysreflexia was found to be less severe during urodynamic study and to occur less
frequently over a monitored 24-hour period. [20]
Other successful methods trialed to help prevent autonomic dysreflexia are sacral
denervation and sphincterotomy.

Bowels
A regular bowel program is essential for the prevention of constipation, impaction,
and ileus. Prior to a bowel procedure, an anal block helps prevent autonomic
dysreflexia. [21] Topical lidocaine may be of help.

Labor and delivery

Spinal anesthesia can help to prevent autonomic dysreflexia.

Pressure ulcers
Routine weight shifts and skin checks are necessary to prevent ulceration. Any skin
breakdown should be addressed early by a knowledgeable wound care team or
physician.

Other
A retrospective study by Del Fabro et al indicated that an intrathecal baclofen (ITB)
pump can reduce the incidence of autonomic dysreflexia in patients with SCI. The
investigators found that prior to ITB pump placement, 25 out of the 34 patients (73.5%)
in the study experienced autonomic dysreflexia, compared with two patients (5.9%)
following pump placement. [22]

References
1. Milligan J, Lee J, McMillan C, Klassen H. Autonomic dysreflexia: recognizing a
common serious condition in patients with spinal cord injury. Can Fam Physician.
2012 Aug. 58(8):831-5. [Medline]. [Full Text].
2. Roatta S, Farina D. Sympathetic actions on the skeletal muscle. Exerc Sport Sci
Rev. 2010 Jan. 38(1):31-5. [Medline].
3. Brown R, Burton A, Macefield VG. Input-output relationships of a
somatosympathetic reflex in human spinal injury. Clin Auton Res. 2009 Apr 18.
[Medline].
 4. Arnold JM, Feng QP, Delaney GA, Teasell RW. Autonomic dysreflexia in
tetraplegic patients: evidence for alpha-adrenoceptor hyper-responsiveness. Clin
Auton Res. 1995 Oct. 5(5):267-70. [Medline].
5. Bloch RF. Autonomic dysfunction in management of spinal cord. Bloch RF,
Basbaum M. Management of spinal cord injuries. Baltimore: Williams & Wilkins;
1986. 149-163.
6. Teasell RW, Arnold JM, Krassioukov A, Delaney GA. Cardiovascular
consequences of loss of supraspinal control of the sympathetic nervous system
after spinal cord injury. Arch Phys Med Rehabil. 2000 Apr. 81(4):506-16.
[Medline].

2018 0309

CHECKLIST
For
Autonomic Dysreflexia

Identify the symptom and the cause

Correct the cause
Treat the symptom and the cause
Monitor the condition
Identifying the symptom and the cause
Check for
Blood Pressure
Heart Rate

Blood Pressure
Elevated Too high
Action: sit-up immediately to allow pooling of blood in
lower extremities to reduce blood pressure.
Action: loosen clothing and restrictive devices

Survey person for instigating causes

Urinary System

Catheter
Check for
Catheter is properly in place
Kinks
Folds
Constrictions
Obstructions
Correction
Ensure
Catheter is properly in place
Clear all
Kinks
Folds
Constrictions
Obstructions
Treatment
Gentle irrigation with small amount of fluid (normal saline
at body temperature)