autonomic dysreflexia

13
YAutonomic dysreflexia Autonomic dysreflexia, "AD" also known as "autonomic hyperreflexia or Hyperreflexia , is a potentially life threatening condition which can be considered amedical emergency requiring immediate attention. AD occurs most often in spinal cord-injured individuals with spinal lesions above the (T6) spinal cord level. Acute AD is a reaction of the autonomic (involuntary) nervous system to overstimulation. It is characterised by severe paroxysmal hypertension (episodic high blood pressure) associated with throbbing headaches, profuse sweating, nasal stuffiness, flushing of the skin above the level of the lesion, bradycardia , apprehension and anxiety, which is sometimes accompanied by cognitive impairment. [1] The sympathetic discharge that occurs is usually in association with spinal cord injury (SCI) or disease (e.g. multiple sclerosis ). AD is believed to be triggered by afferent stimuli (nerve signals that send messages back to the spinal cord and brain) which originate below the level of the spinal cord lesion. It is believed that these afferent stimuli trigger and maintain an increase in blood pressure via a sympathetically mediated vasoconstriction in muscle, skin and splanchnic (gut) vascular beds (Karlsson, 1999). Causes The most common causes of autonomic hyperreflexia in patients with spinal cord injury are loss of bowel and bladder function, resulting in impaction in the case of the bowels and distention in case of the bladder. These are generally found in patients with a spinal cord injury above the T6 (6th Thoracic Vertebral) level, but can occur in patients with a transection as low as T10 (10th Thoracic Vertebral) level. When a painful stimulus occurs, as when voiding is interrupted or a bowel obstruction occurs, nerve impulses are sent to the brain via the spinal cord. [2] However, in spinal cord transection, these impulses are unable to travel past the injury. This results in a spinal cord reflex to the autonomic nervous system in response to pain. In patients with spinal cord transection, types of stimulation that are tolerated by healthy people create an excessive response from the person's nervous system. Other causes include medication side effects and various disease processes. The use of stimulants such as cocaine and amphetamines which can result in urinary retention, and the use of CNS depressants and other psychotropic and psychoactive drugs can also lead to urinary retention and constipation thus leading to autonomic dysreflexia when in use over an extended period of time.Guillain-Barre syndrome a demyelinating disease that can result in peripheral paralysis can progress to encompass autonomic functions leading to a loss of normal respiratory, bladder and bowel function, thus resulting in autonomic dysreflexia. Severe head trauma, and other brain injuries [3] can instigate autonomic dysreflexia at the Central Nervous System by interfering with the reception of the signal that brings the urge to void the bladder and bowels and with the volutary abiliity to micturate and defecate. Other causal theories for Autonomic Dysreflexia include Noxious Stimuli or painful stimuli arising from the peripheral sensory neurons. These stimuli are interrupted in their journey to the brain due to a transection of the spine result in a paradoxical stimulation of autonomic pathways of the Autonomic Nervous System .

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YAutonomic dysreflexia

Autonomic dysreflexia, "AD" also known as "autonomic hyperreflexia or Hyperreflexia, is a potentially life

threatening condition which can be considered amedical emergency requiring immediate attention. AD

occurs most often in spinal cord-injured individuals with spinal lesions above the (T6) spinal cord level.

Acute AD is a reaction of the autonomic (involuntary) nervous system to overstimulation. It is characterised

by severe paroxysmal hypertension (episodic high blood pressure) associated with throbbing headaches,

profuse sweating, nasal stuffiness, flushing of the skin above the level of the lesion, bradycardia,

apprehension and anxiety, which is sometimes accompanied by cognitive

impairment.[1]

The sympathetic discharge that occurs is usually in association with spinal cord injury (SCI)

or disease (e.g. multiple sclerosis). AD is believed to be triggered by afferent stimuli (nerve signals that

send messages back to the spinal cord and brain) which originate below the level of the spinal cord lesion.

It is believed that these afferent stimuli trigger and maintain an increase in blood pressure via a

sympathetically mediated vasoconstriction in muscle, skin and splanchnic (gut) vascular beds (Karlsson,

1999).

Causes

The most common causes of autonomic hyperreflexia in patients with spinal cord injury are loss of bowel

and bladder function, resulting in impaction in the case of the bowels and distention in case of the bladder.

These are generally found in patients with a spinal cord injury above the T6 (6th Thoracic Vertebral) level,

but can occur in patients with a transection as low as T10 (10th Thoracic Vertebral) level. When a painful

stimulus occurs, as when voiding is interrupted or a bowel obstruction occurs, nerve impulses are sent to

the brain via the spinal cord.[2]

However, in spinal cord transection, these impulses are unable to travel past

the injury. This results in a spinal cord reflex to the autonomic nervous system in response to pain. In

patients with spinal cord transection, types of stimulation that are tolerated by healthy people create an

excessive response from the person's nervous system.

Other causes include medication side effects and various disease processes. The use of stimulants such

as cocaine and amphetamines which can result in urinary retention, and the use of CNS depressants and

other psychotropic and psychoactive drugs can also lead to urinary retention and constipation thus leading

to autonomic dysreflexia when in use over an extended period of time.Guillain-Barre syndrome a

demyelinating disease that can result in peripheral paralysis can progress to encompass autonomic

functions leading to a loss of normal respiratory, bladder and bowel function, thus resulting in autonomic

dysreflexia. Severe head trauma, and other brain injuries[3]

can instigate autonomic dysreflexia at

the Central Nervous System by interfering with the reception of the signal that brings the urge to void the

bladder and bowels and with the volutary abiliity to micturate and defecate. Other causal theories for

Autonomic Dysreflexia include Noxious Stimuli or painful stimuli arising from the peripheral sensory

neurons. These stimuli are interrupted in their journey to the brain due to a transection of the spine result in

a paradoxical stimulation of autonomic pathways of the Autonomic Nervous System.

Controversy Over Peripherally Noxious Causes of Autonomic Dysreflexia

Current scientific literature suggests that noxious (painful) stimuli are the primary initiators of AD. However,

different studies have found that activation of pain receptors in muscle and skin below the lesion in spinal

cord injured individuals did not trigger AD.[4][5]

These studies suggests that not all noxious stimuli are

reliable triggers of AD, and because non-noxious stimuli can also trigger AD, attribution of an episode of

AD to noxious stimuli may cause clinicians to overlook underlying non-noxious triggers. As a result, non-

noxious trigger factors remain undetected, prolonging an episode of AD. They concluded that when

deducing the potential causes of AD it is important to consider non-noxious sources of stimulation in

addition to noxious triggers. Current Assessment of Autonomic Dysreflexia in patients with known causitive

factors include palpation of the bladder and bowel and can also include bladder scan.

Diagnosis

The diagnosis is usually not subtle, although asymptomatic events have been documented. Autonomic

dysreflexia differs from autonomic instability, a term used to describe the variety of modest cardiac and

neurological changes that accompany a spinal cord injury, including bradycardia, orthostatic hypotension,

and ambient temperature intolerance. In autonomic dysreflexia, patients will experience hypertension,

sweating, and erythema (more likely in upper extremities) and may suffer from headaches and blurred

vision. Mortality is rare with AD, but morbidity such as stroke, retinal hemorrhage and pulmonary edema if

left untreated can be quite severe. Older patients with very incomplete spinal cord injuries and

systolic hypertension without symptoms are usually experiencing essential hypertension, not autonomic

dysreflexia. Aggressive treatment of these elderly patients with rapidly acting antihypertensive medications

can have disastrous results.

Onset

The risk is greatest with cervical spinal cord lesions and is rare with lesions below T6 Thoracic vertebrae. It

has rarely been reported in spinal cord lesions as low as T10. The first episode may occur weeks to years

after spinal cord injury takes place, but most people at risk (80%) develop their first episode within the first

year after injury.

Symptoms

This condition is distinct and usually episodic, with the patient experiencing remarkably high blood pressure

(often with systolic readings over 200 mm. Hg), intense headaches, profuse sweating, facialerythema,

goosebumps, nasal stuffiness, and a "feeling of doom". An elevation of 40 mm. Hg. over baseline systolic

should be suspicious for dysreflexia.

Treatment

Proper treatment of autonomic dysreflexia involves administration of anti-hypertensives along with

immediate determination and removal of the triggering stimuli. Often, sitting the patient up and dangling

legs over the bedside can reduce blood pressures below dangerous levels and provide partial symptom

relief. Tight clothing and stockings should be removed. Catheterization of the bladder, or relief of a blocked

urinary catheter tube may resolve the problem. The rectum should be cleared of stool impaction, using

anaesthetic lubricating jelly. If the noxious precipitating trigger cannot be identified, drug treatment is

needed to decrease elevating intracranial pressure until further studies can identify the cause.

Drug treatment includes the rapidly acting vasodilators, including sublingual nitrates or oral clonidine.

Topical nitropaste is a convenient and safe treatment—an inch or two can be applied to the chest wall, and

wiped off when blood pressures begin to normalize. Autonomic dysreflexia is abolished temporarily

by spinal or general anaesthesia. These treatment are used during obstetric delivery of a woman with

autonomic dysreflexia.

Complications

Autonomic dysreflexia can become chronic and recurrent, often in response to longstanding medical

problems like soft tissue ulcers or hemorrhoids. Long term therapy may include alpha blockers orcalcium

channel blockers.

Complications of severe acute hypertension can include seizures, pulmonary edema, myocardial

infarction or cerebral hemorrhage.

Prognosis

The cause of autonomic dysreflexia itself can be life threatening, and must also be completely investigated

and treated appropriately to prevent unnecessary morbidity and mortality.

The Consortium for Spinal Cord Medicine has developed evidence-based clinical practice guidelines for the

management of autonomic dysreflexia in adults, children, and pregnant women. There is also a consumer

version of this guideline.

Autonomic Dysreflexia in Spinal Cord Injury Introduction

Background

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. (See image below and Image 1.)

(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.

Pathophysiology

This phenomenon occurs after the phase of spinal shock in which reflexes return. Individuals with

injury above the major splanchnic outflow may develop autonomic dysreflexia (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.1 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. This reflex

action cannot compensate for severe vasoconstriction, explained by the Poiseuille formula, where

pressure in a tube is affected to the fourth power by change in radius (vasoconstriction) and only

linearly by 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 have 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.2

Frequency

United States

Reported prevalence rates vary, 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. Autonomic

dysreflexia (AD) occurs during labor in approximately two thirds of pregnant women with SCI above

the level of T6. The occurrence of AD increases as the patient evolves out of spinal shock. With the

return of sacral reflexes, the possibility of AD increases.3

Mortality/Morbidity

Morbidity related to autonomic dysreflexia is associated with hypertension, which can cause

retinal/cerebral hemorrhage, myocardial infarction, or seizures. Mortality is rare.

Sex

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

phenomenon.

Age

No specific relationship has been documented between autonomic dysreflexia and age.

Clinical

History

The patient with autonomic dysreflexia 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

A patient with autonomic dysreflexia (AD) may have 1 or more of the following findings on physical

examination:

A sudden significant rise in systolic and diastolic blood pressures, usually associated with

bradycardia, can appear. The 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.

Profuse sweating above the level of lesion, especially in the face, neck, and shoulders, may

be noted, but it rarely occurs below the level of the lesion because of sympathetic cholinergic

activity.

Goose bumps above, or possibly below, the level of the lesion may be observed.

Flushing of the skin above the level of the lesion, especially in the face, neck, and shoulders,

frequently is noted.

The patient may report blurred vision.

Spots may appear in the patient's visual fields.

Nasal congestion is common.

No symptoms may be observed, despite elevated blood pressure.

Causes

Episodes of autonomic dysreflexia (AD) can be triggered by many potential causes.4 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 distension

Urinary tract infection

Cystoscopy

Urodynamics

Detrusor-sphincter dyssynergia5

Epididymitis or scrotal compression

Bowel distension

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

Heterotopic bone

Fractures or other trauma

Surgical or diagnostic procedures

Pain

More on Autonomic Dysreflexia in Spinal Cord Injury

Overview: Autonomic Dysreflexia in Spinal Cord Injury

Differential Diagnoses & Workup: Autonomic Dysreflexia in Spinal Cord Injury

Treatment & Medication: Autonomic Dysreflexia in Spinal Cord Injury

Follow-up: Autonomic Dysreflexia in Spinal Cord Injury

Multimedia: Autonomic Dysreflexia in Spinal Cord Injury

References

Further Reading

Differential Diagnoses

Other Problems to Be Considered

Essential hypertension

Pheochromocytoma

Treatment

Rehabilitation Program

Physical Therapy

Physical therapists who treat SCI patients need to have a good understanding of autonomic

dysreflexia (AD) and be familiar with the signs and symptoms of this potentially life-threatening

condition.3When 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).4

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 respond quickly if the condition develops during a therapy

session.3 The occupational therapist performs extensive training in the performance of activities of

daily living with patients who have sustained SCI. Activities of daily living include proper bowel and

bladder management, which can help prevent 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.

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 care of individuals with SCI, the speech therapist must be familiar with the

manifestations of this potential life-threatening complication.3

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 and know how to respond appropriately if

the patient develops symptoms during a recreational therapy session.3

Medical Issues/Complications

Complications associated with autonomic dysreflexia result directly from sustained, severe peripheral

hypertension and include retinal/cerebral hemorrhage, myocardial infarction, and seizures.

Consultations

If the cause of the autonomic dysreflexia 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 ICU monitoring and

treatment of the hypertension.

Medication

Check the patient's blood pressure. If 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 they have stabilized; blood pressures can fluctuate quickly during an AD

episode from impaired autonomic regulation. Survey the person for instigating causes, beginning with

the urinary system, the most common cause of autonomic dysreflexia (AD).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 of the indwelling catheter.

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.

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 administration, not sublingual. Other agents used are mecamylamine, diazoxide, and

phenoxybenzamine.

Use antihypertensives with extreme caution in older persons or 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 ER for monitoring, maintenance of pharmacologic control of blood

pressure, and investigation of other possible causes of the AD.

Document the episode.

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.5 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.

Antihypertensives

Antihypertensive agents with rapid onset and short duration are administered while the causes of

autonomic dysreflexia (AD) are investigated if BP is at or above 150 mm Hg systolic. Patients who

have experienced episodes of AD are treated with antihypertensives prior to procedures known to

cause their AD episodes.

Nifedipine (Procardia)

Calcium ion influx inhibitor (slow-channel blocker or calcium ion antagonist); inhibits transmembrane

influx of calcium ions into cardiac and smooth muscle. Reduces arterial pressure at rest and at a

given level of exercise by dilating peripheral arterioles and reducing the total peripheral resistance

(afterload).

Dosing

Interactions

Contraindications

Precautions

Adult

10 mg cap PO initially; bite and swallow

Pediatric

Not recommended

Nitroglycerine (Depo-Nit, Nitrostat, Nitrol, Nitro-Bid)

Principal pharmacologic action of nitroglycerin is relaxation of vascular smooth muscle, producing

vasodilator effect on both peripheral arteries and veins with more prominent effects on the latter.

Dilation of postcapillary vessels, including large veins, promotes peripheral pooling of blood and

decreases venous return to the heart, thereby reducing left ventricular end-diastolic pressure

(preload). Arteriolar relaxation reduces systemic vascular resistance and arterial pressure (after-load).

Dosing

Interactions

Contraindications

Precautions

Adult

0.4 mg per metered spray for SL use or 2% nitroglycerine ointment

Start with 0.5-in strip to chest wall and titrate as necessary; alternatively, 0.15-0.6 mg tab SL or 5

mcg/min IV

Pediatric

Not established

Phenoxybenzamine hydrochloride (Dibenzyline)

Long-acting, adrenergic, alpha-receptor blocking agent that can produce and maintain chemical

sympathectomy by oral administration; increases blood flow to skin, mucosae, and abdominal viscera

and lowers supine and erect blood pressures.

No effect on parasympathetic system.

Dosing

Interactions

Contraindications

Precautions

Adult

Adjust dose to fit needs of each patient

Slowly increase dose until desired effect obtained or side effects from blockade problematic

Observe patient on each level before instituting increase

Dosage should provide symptomatic relief and/or objective improvement, but not to where side effects

from blockage are troublesome

Initially, administer 10 mg of Dibenzyline (phenoxybenzamine hydrochloride) PO bid; increase dose

qod, usually to 20-40 mg 2 or 3 times/d, until an optimal dosage is obtained, as judged by blood

pressure control

Pediatric

Not established

Mecamylamine (Inversine)

Potent oral secondary amine, antihypertensive agent, and ganglion blocker.

Produces smooth and predictable reduction of blood pressure with small oral dose.

Antihypertensive effect predominantly orthostatic, but supine blood pressure also significantly

reduced.

Used for management of moderately severe-to-severe essential hypertension and in uncomplicated

cases of malignant hypertension.

Dosing

Interactions

Contraindications

Precautions

Adult

2.5 mg PO prn

Pediatric

Not established

Diazoxide (Hyperstat)

Nondiuretic benzothiadiazine antihypertensive agent; achieves prompt reduction of blood pressure by

relaxing smooth muscle in peripheral arterioles; cardiac output increases as blood pressure is

reduced.

Dosing

Interactions

Contraindications

Precautions

Adult

1-3 mg/kg IV to maximum dose of 150 mg in single injection; repeat at 5-15 min intervals until

reduction of BP is satisfactory (eg, diastolic pressure <100 mm Hg)

Pediatric

Administer as in adults

Follow-up

Deterrence

Good bladder and bowel care (ie, preventing fecal impaction, bladder distention) are mainstays in

preventing episodes of autonomic dysreflexia.

Patient Education

All medical professionals should educate the patient and family members or caregivers about this

potentially life-threatening complication of SCI.3

Miscellaneous

Medicolegal Pitfalls

Failure to have a high index of suspicion and recognize autonomic dysreflexia quickly could present

medical and legal problems for the physician. For example, a physician who assumes that headache

and anxiety in a person with complete C6 tetraplegia is a manifestation of depression, without

checking vital signs, is at medical/legal risk.

Media file 1: (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.