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Author: Denise I Campagnolo, MD, MS; Chief Editor: Robert H Meier III, MD more...

Updated: Apr 24, 2013

Overview
Autonomic dysreflexia (AD) is a syndrome of massive imbalanced reflex sympathetic discharge occurring in patients
with spinal cord injury (SCI) above the splanchnic sympathetic outflow (T5-T6). Anthony Bowlby first recognized this
syndrome in 1890 when he described profuse sweating and erythematous rash of the head and neck initiated by
bladder catheterization in an 18-year-old patient with SCI. Guttmann and Whitteridge completed a full description of the
syndrome in 1947.

This condition represents a medical emergency, so recognizing and treating the earliest signs and symptoms
efficiently can avoid dangerous sequelae of elevated blood pressure. SCI patients, caregivers, and medical
professionals must be knowledgeable about this syndrome and its management.[1] (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 (Vagus). (D) The brain attempts 2 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 do not get 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.

Prognosis

Complications associated with autonomic dysreflexia result directly from sustained, severe peripheral hypertension
and include retinal/cerebral hemorrhage, myocardial infarction, and seizures. Morbidity related to autonomic dysreflexia
is associated with hypertension, which can cause retinal/cerebral hemorrhage, myocardial infarction, or seizures.
Mortality is rare.

Patient education

All medical professionals should educate the patient and family members or caregivers about this potentially
life-threatening complication of SCI.[2] Such instruction should include prevention strategies, signs and symptoms of
AD, and proper management of the condition.

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Consultations

If the cause of the AD episode is not found and blood pressure remains elevated, recommend that the patient go to
the nearest emergency department for close monitoring and further investigation of the possible cause. Consult an
intensive care specialist for intensive care unit (ICU) monitoring and treatment of the hypertension.

Etiology
Autonomic dysreflexia (AD) occurs after the phase of spinal shock in which reflexes return. Individuals with injury
above the major splanchnic outflow may develop AD. Below the injury, intact peripheral sensory nerves transmit
impulses that ascend in the spinothalamic and posterior columns to stimulate sympathetic neurons located in the
intermediolateral gray matter of the spinal cord. The inhibitory outflow above the SCI from cerebral vasomotor centers
is increased, but it is unable to pass below the block of the SCI.

This large sympathetic outflow causes release of various neurotransmitters (norepinephrine, dopamine-b-hydroxylase,
dopamine), causing piloerection, skin pallor, and severe vasoconstriction in arterial vasculature.[3] The result is sudden
elevation in blood pressure and vasodilation above the level of injury. Patients commonly have a headache caused by
vasodilation of pain-sensitive intracranial vessels.

Vasomotor brainstem reflexes attempt to lower blood pressure by increasing parasympathetic stimulation to the heart
through the vagus nerve to cause compensatory bradycardia. The fact that this reflex action cannot compensate for
severe vasoconstriction is explained by the Poiseuille formula, which demonstrates that pressure in a tube is affected
to the fourth power by a change in radius (vasoconstriction); the pressure is affected only linearly by a change in flow
rate (bradycardia). Parasympathetic nerves prevail above the level of injury, which may be characterized by profuse
sweating and vasodilation with skin flushing.

Cameron and colleagues found that site-directed genetic manipulation of fiber sprouting in the spinal dorsal horns in a
cord compression rat model could alter the extent of hyperreflexia after bowel distention, indicating that endogenous
spinal cord circuitry/neural sprouting plays a role in the pathophysiology of AD.[4]

Causes of autonomic dysreflexia

Episodes of AD can be triggered by many potential causes.[5] Essentially any painful, irritating, or even strong stimulus
below the level of the injury can cause an episode of AD. Although the list is not comprehensive, the following events
or conditions all can cause episodes of AD:

Bladder distention
Urinary tract infection
Cystoscopy
Urodynamics [6]
Detrusor-sphincter dyssynergia[7]
Epididymitis or scrotal compression
Bowel distention
Bowel impaction
Gallstones
Gastric ulcers or gastritis
Invasive testing
Hemorrhoids
Gastrocolic irritation
Appendicitis or other abdominal pathology trauma
Menstruation
Pregnancy - Especially labor and delivery
Vaginitis
Sexual intercourse
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

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Heterotopic bone
Fractures or other trauma
Surgical or diagnostic procedures
Pain

Good bladder and bowel care (ie, preventing fecal impaction, bladder distention) are mainstays in preventing episodes
of autonomic dysreflexia.

Epidemiology
Reported prevalence rates vary for autonomic dysreflexia (AD) in the United States, but the generally accepted rate is
48-90% of all individuals who are injured at T6 and above. Some incidence has been reported in SCI as low as T10.

The occurrence of AD increases as the patient evolves out of spinal shock. With the return of sacral reflexes, the
possibility of AD increases.[2] AD occurs during labor in approximately two thirds of pregnant women with SCI above
the level of T6.

The male-to-female ratio for sustaining SCI is 4:1; therefore, autonomic dysreflexia is primarily a male phenomenon.

History and Physical Examination

History

The patient with autonomic dysreflexia (AD) generally gives a history of blurry vision, headaches, and a sense of
anxiety. Feelings of apprehension or anxiety over an impending physical problem commonly are exhibited.

Physical Examination

A patient with AD may have 1 or more of the following findings on physical examination:

Sudden, significant rise in systolic and diastolic 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 cholinergic activity
Goose bumps above, or possibly 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
Spots in the patient's visual field
Nasal congestion – A common symptom

With regard to the first item above, the sudden rise in blood pressure in AD is usually associated with bradycardia.
Normal systolic blood pressure for SCI above T6 is 90-110 mm Hg; blood pressure 20-40 mm Hg above the
reference range for such patients may be a sign of AD. However, patients with AD may display no symptoms, despite
elevated blood pressure. Differentials for AD include essential hypertension and pheochromocytoma.

Physical Therapy
Physical therapists who treat patients with SCI need to have a good understanding of autonomic dysreflexia (AD) and
be familiar with the signs and symptoms of this potentially life-threatening condition.[2] When completing physical
therapy sessions, the therapist needs to monitor the urinary catheter for any blockage or twisting.

If the patient becomes hypertensive during therapy, he/she should be placed in an upright position immediately rather
than remain in a supine or reclining position. The therapist needs to complete careful inspection to identify the source
of painful stimuli (eg, catheter, restrictive clothing, leg bag straps, abdominal supports, orthoses).[5] A less common
cause of AD during physical therapy sessions may originate with muscle stretching, either from range of motion or
passive stretching.

If the patient develops AD, the physical therapist needs to treat it as a medical emergency and be familiar with
established protocols for medical management within his/her particular setting. The individual therapy session then
must be discontinued to allow the patient to stabilize and recover.

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 (AD) and be able to

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respond quickly if the condition develops during a therapy session.[2]

The occupational therapist performs 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 AD. The occupational therapist may be involved in establishing a regular bowel program and also may
complete patient and family/caregiver education on this aspect of care.

The occupational and physical therapists should educate the patient and family members about AD and ensure that
they are familiar with prevention strategies, signs and symptoms, and proper management of the condition.

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 and social activities. As members of the SCI team, they also must be knowledgeable
about autonomic dysreflexia (AD) and know how to respond appropriately if the patient develops symptoms during a
recreational therapy session.[2]

Speech therapy

Generally, the treatment provided by the speech therapist is not associated with any painful stimuli below the lesion
that may precipitate an AD 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 complication.[2]

Treatment of High Blood Pressure

Check the patient's blood pressure. If the blood pressure is elevated and the person is supine, have the person sit up
immediately and loosen any clothing or constrictive devices. Sitting leads to pooling of blood in the lower extremities
and may reduce blood pressure. 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 (AD). Survey the person for instigating causes, beginning with the urinary system, the most common cause
of AD.[8, 6]

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 AD, and check the rectum
for stool, using lidocaine jelly as lubricant.

Use an antihypertensive agent with rapid onset and short duration while the causes of AD are being investigated if the
blood pressure is at or above 150 mm Hg systolic. The most commonly used agents are nifedipine and nitrates (eg,
nitroglycerine paste). 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 mecamylamine, diazoxide, and
phenoxybenzamine. Use antihypertensives with extreme caution in older persons or in people with coronary artery
disease.

Monitor the individual's symptoms and blood pressure for at least 2 hours after resolution of the AD episode to ensure
that elevation of blood pressure does not recur. AD may resolve because of medication, not because of resolution of
the underlying cause.

If there is poor response to treatment and/or if the cause of the AD has not been identified, send the patient to the
emergency room (ER) for monitoring, maintenance of pharmacologic control of blood pressure, and investigation of
other possible causes of the AD. Remember to document the episode of AD.

Patients who have previously experienced episodes of AD are treated with antihypertensives prior to procedures
known to cause their episodes.

A Taiwanese study indicated that in patients with SCI who have detrusor sphincter dyssynergia, using a combination of
fluoroscopy and electromyography to localize the external urethral sphincter, with a Foley catheter employed to
visualize vesicourethral anatomy, makes transperineal injection of botulinum toxin type A into the external urethral
sphincter safe, accurate, and easy to perform.[7] Such injections have been shown to reduce the occurrence and
degree of autonomic dysreflexia, as well as of vesicoureteral reflux, hydronephrosis, and urinary tract infection.

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Contributor Information and Disclosures

Author
Denise I Campagnolo, MD, MS Director of Multiple Sclerosis Clinical Research and Staff Physiatrist, Barrow
Neurology Clinics, St Joseph's Hospital and Medical Center; Investigator for Barrow Neurology Clinics; Director,
NARCOMS Project for Consortium of MS Centers

Denise I Campagnolo, MD, MS is a member of the following medical societies: Alpha Omega Alpha, American
Association of Neuromuscular and Electrodiagnostic Medicine, American Paraplegia Society, Association of
Academic Physiatrists, and Consortium of Multiple Sclerosis Centers

Disclosure: Teva Neuroscience Honoraria Speaking and teaching; Serono-Pfizer Honoraria Speaking and teaching;
Genzyme Corporation Grant/research funds investigator; Biogen Idec Grant/research funds investigator;
Genentech, Inc Grant/research funds investigator; Eli Lilly & Company Grant/research funds investigator; Novartis
investigator; MSDx LLC Grant/research funds investigator; BioMS Technology Corp Grant/research funds
investigator; Avanir Pharmaceuticals Grant/research funds investigator

Specialty Editor Board

Milton J Klein, DO, MBA Consulting Physiatrist, Heritage Valley Health System-Sewickley Hospital and Ohio
Valley General Hospital

Milton J Klein, DO, MBA is a member of the following medical societies: American Academy of Disability Evaluating
Physicians, American Academy of Medical Acupuncture, American Academy of Osteopathy, American Academy of
Physical Medicine and Rehabilitation, American Medical Association, American Osteopathic Association, American
Osteopathic College of Physical Medicine and Rehabilitation, American Pain Society, and Pennsylvania Medical
Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College
of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Kat Kolaski, MD Assistant Professor, Departments of Orthopedic Surgery and Pediatrics, Wake Forest University
School of Medicine

Kat Kolaski, MD is a member of the following medical societies: American Academy for Cerebral Palsy and
Developmental Medicine and American Academy of Physical Medicine and Rehabilitation

Disclosure: Nothing to disclose.

Chief Editor
Robert H Meier III, MD Director, Amputee Services of America; Active Medical Staff, Presbyterian/St Luke's
Hospital, Spalding Rehabilitation Hospital, Select Specialty Hospital; Consulting Staff, Kindred Hospital

Robert H Meier III, MD is a member of the following medical societies: American Academy of Physical Medicine
and Rehabilitation and Association of Academic Physiatrists

Disclosure: Nothing to disclose.

References
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patients with spinal cord injury. Can Fam Physician. Aug 2012;58(8):831-5. [Medline]. [Full Text].

2. Schottler J, Vogel L, Chafetz R, et al. Patient and caregiver knowledge of autonomic dysreflexia among youth
with spinal cord injury. Spinal Cord. Mar 10 2009;[Medline].

3. Brown R, Burton A, Macefield VG. Input-output relationships of a somatosympathetic reflex in human spinal
injury. Clin Auton Res. Apr 18 2009;[Medline].

4. Cameron AA, Smith GM, Randall DC, et al. Genetic manipulation of intraspinal plasticity after spinal cord injury
alters the severity of autonomic dysreflexia. J Neurosci. Mar 15 2006;26(11):2923-32. [Medline]. [Full Text].

5. Krassioukov A, Warburton DE, Teasell R, et al. A systematic review of the management of autonomic
dysreflexia after spinal cord injury. Arch Phys Med Rehabil. Apr 2009;90(4):682-95. [Medline].

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6. Huang YH, Bih LI, Liao JM, Chen SL, Chou LW, Lin PH. Blood pressure and age associated with silent
autonomic dysreflexia during urodynamic examinations in patients with spinal cord injury. Spinal Cord. Dec 11
2012;[Medline].

7. Tsai SJ, Ying TH, Huang YH, et al. Transperineal injection of botulinum toxin A for treatment of detrusor
sphincter dyssynergia: localization with combined fluoroscopic and electromyographic guidance. Arch Phys
Med Rehabil. May 2009;90(5):832-6. [Medline].

8. McMahon D, Tutt M, Cook AM. Pharmacological management of hemodynamic complications following spinal
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Medscape Reference © 2011 WebMD, LLC

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