Autonomic dysreflexia

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Autonomic dysreflexia
Other namesAutonomic hyperreflexia[1]
SpecialtyNeurology Edit this on Wikidata

Autonomic dysreflexia (AD) is a potential medical emergency classically characterized by uncontrolled hypertension and bradycardia, although tachycardia is known to commonly occur.[2][3][4] AD occurs most often in individuals with spinal cord injuries with lesions at or above the T6 spinal cord level, although it has been reported in patients with lesions as low as T10.[5] Guillain–Barré syndrome may also cause autonomic dysreflexia.[1]

The uncontrolled hypertension in AD may result in mild symptoms, such as sweating above the lesion level, goosebumps, blurred vision, or headache; However, severe hypertension may result in potentially life-threatening complications including seizure, intracranial bleed, or retinal detachment.[2]

AD is triggered by either noxious or non-noxious stimuli, resulting in sympathetic stimulation and hyperactivity.[6] The most common causes include bladder or bowel over-distension, from urinary retention and fecal compaction, respectively.[7] The resulting sympathetic surge transmits through intact peripheral nerves, resulting in systemic vasoconstriction below the level of the spinal cord lesion.[8] The peripheral arterial vasoconstriction and hypertension activates the baroreceptors, resulting in a parasympathetic surge originating in the central nervous system to inhibit the sympathetic outflow; however, the parasympathetic signal is unable to transmit below the level of the spinal cord lesion.[8] This results in bradycardia, vasodilation, flushing, pupillary constriction and nasal stuffiness above the spinal lesion, while there is piloerection, pale and cool skin below the lesion due to the prevailing sympathetic outflow.[8]

Initial treatment involves sitting the patient upright, removing any constrictive clothing (including abdominal binders and support stockings), rechecking blood pressure frequently, and then checking for and removing the inciting issue, which may require urinary catheterization or bowel disimpaction.[2][4] If systolic blood pressure remains elevated (over 150 mm Hg) after initial steps, fast-acting short-duration antihypertensives are considered,[9] while other inciting causes must be investigated for the symptoms to resolve.[2]

Prevention of AD involves educating the patient, family and caregivers of the precipitating cause, if known, and how to avoid it, as well as other triggers.[4] Since bladder and bowel are common causes, prevention involves routine bladder and bowel programs and urological follow-up for cystoscopy/urodynamic studies.[2]

Signs and symptoms[edit]

This condition is distinct and usually episodic, with the people potentially experiencing remarkably high blood pressure, intense headaches, profuse sweating, facial erythema, goosebumps, nasal stuffiness, a "feeling of doom" or apprehension, and blurred vision.[5] An elevation of 20 mm Hg over baseline systolic blood pressure, with a potential source below the neurological level of injury, meets the current definition of dysreflexia.[10]


Autonomic dysreflexia can become chronic and recurrent, often in response to longstanding medical problems like soft tissue pressure injuries or hemorrhoids. Long term therapy may include alpha blockers or calcium channel blockers.[citation needed]

Complications of severe acute hypertension can include seizures, pulmonary edema, myocardial infarction, or cerebral hemorrhage. Additional organs that may be affected include the kidneys and retinas of the eyes.[5]


The first episode of autonomic dysreflexia 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. Early AD tends to be associated with less severe increases in blood pressure.[citation needed]

One common causative factor may be an undetected urinary tract infection. The difficulty in assessing this may be complicated with the usage of indwelling or suprapubic catheters. 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 psychoactive drugs can also lead to urinary retention and constipation thus leading to autonomic dysreflexia when in use over an extended period of time.[citation needed]


Current scientific literature suggests that noxious (painful) stimuli are the primary initiators of AD. (Note: Not all noxious stimuli will cause AD. Some otherwise severe noxious stimuli in unaffected people, e.g. broken bones, may not result in AD, and may in fact even go unnoticed.) 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.[11][12] 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 causative factors include palpation of the bladder and bowel and can also include bladder scan.[citation needed]


Supraspinal vasomotor neurons send projections to the intermediolateral cell column, which is composed of sympathetic preganglionic neurons (SPN) through the T1-L2 segments.[7] The supraspinal neurons act on the SPN and its tonic firing, modulating its action on the peripheral sympathetic chain ganglia and the adrenal medulla.[7] The sympathetic ganglia act directly on the blood vessels they innervate throughout the body, controlling vessel diameter and resistance, while the adrenal medulla indirectly controls the same action through the release of epinephrine and norepinephrine.[7] The descending autonomic pathways, which are responsible for the supraspinal communication with the SPN, are interrupted resulting in decreased sympathetic outflow below the level of the injury.[7] In this circumstance, the SPN is controlled only by spinal influences.[7] The first couple of weeks after a spinal injury, the decreased sympathetic outflow causes reduced blood pressure and sympathetic reflex.[7] Eventually, synaptic reorganization and plasticity of SPN develops into an overly sensitive state, which results in abnormal reflex activation of SPN due to afferent stimuli, such as bowel or bladder distension.[7] Reflex activation results in systemic vasoconstriction below the spinal cord disruption. The peripheral arterial vasoconstriction and hypertension activates the baroreceptors, resulting in a parasympathetic surge originating in the central nervous system, which inhibits the sympathetic outflow; however, the parasympathetic signal is unable to transmit below the level of the spinal cord lesion.[8] This results in vasodilation, flushing, pupillary constriction and nasal stuffiness above the spinal lesion, while there's piloerection, pale and cool skin below the lesion due to the prevailing sympathetic outflow.[8] The reason this issue is much more prominent for lesions at or above the T6 level is because the Splanchnic nerves emerge from the T5 level and below. Loss of brain's control over T6 and below causes splanchnic arteries to reflexively vasoconstrict and since the Splanchnic arteries are the body's largest reservoir for circulating blood, their vasoconstriction dramatically affects the blood pressure of the body.[citation needed]


The symptoms are usually not subtle, although asymptomatic events have been documented. Autonomic dysreflexia differs from autonomic instability, the various 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, spasms (sometimes severe spasms) and erythema (more likely in upper extremities) and may experience 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.[citation needed]


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. Straight 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.[citation needed]

Drug treatment includes the rapidly acting vasodilators, including sublingual or topical nitrates or oral hydralazine or clonidine. Ganglionic blockers are also used to control sympathetic nervous system outflow. Topical nitroglycerin ointment is a convenient and safe treatment—an inch or two can be applied to the chest wall or forehead, and wiped off when blood pressures begin to normalize.[13][9] Autonomic dysreflexia is abolished temporarily by spinal or general anaesthesia. These treatments are used during obstetric delivery of women with autonomic dysreflexia.[citation needed]


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.[citation needed]

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.[citation needed]


  1. ^ a b "Autonomic dysreflexia". Medline. NIH. Retrieved 19 March 2019.
  2. ^ a b c d e Daroff RB, Jankovic J, Mazziotta JC, Pomeroy SL, Bradley WG (2016). Bradley's neurology in clinical practice (Seventh ed.). London. ISBN 978-0-323-28783-8. OCLC 932031625.
  3. ^ Solinsky, Ryan; Kirshblum, Steven C.; Burns, Stephen P. (2018). "Exploring Detailed Characteristics of Autonomic Dysreflexia". The Journal of Spinal Cord Medicine. 41 (5): 549–555. doi:10.1080/10790268.2017.1360434. PMC 6127514. PMID 28784041.
  4. ^ a b c Consortium for Spinal Cord Medicine (2002). "Acute management of autonomic dysreflexia: individuals with spinal cord injury presenting to health-care facilities". The Journal of Spinal Cord Medicine. 25 Suppl 1: S67–88. PMID 12051242.
  5. ^ a b c Vallès M, Benito J, Portell E, Vidal J (December 2005). "Cerebral hemorrhage due to autonomic dysreflexia in a spinal cord injury patient". Spinal Cord. 43 (12): 738–40. doi:10.1038/ PMID 16010281.
  6. ^ Krassioukov A, Warburton DE, Teasell R, Eng JJ (April 2009). "A systematic review of the management of autonomic dysreflexia after spinal cord injury". Archives of Physical Medicine and Rehabilitation. 90 (4): 682–95. doi:10.1016/j.apmr.2008.10.017. PMC 3108991. PMID 19345787.
  7. ^ a b c d e f g h Eldahan KC, Rabchevsky AG (January 2018). "Autonomic dysreflexia after spinal cord injury: Systemic pathophysiology and methods of management". Autonomic Neuroscience. 209: 59–70. doi:10.1016/j.autneu.2017.05.002. PMC 5677594. PMID 28506502.
  8. ^ a b c d e Youmans and Winn neurological surgery. Winn, H. Richard (Seventh ed.). Philadelphia, PA. 30 November 2016. ISBN 9780323287821. OCLC 963181140.{{cite book}}: CS1 maint: others (link)
  9. ^ a b Solinsky, Ryan; Svircev, Jelena N.; James, Jennifer J.; Burns, Stephen P.; Bunnell, Aaron E. (2016). "A retrospective review of safety using a nursing driven protocol for autonomic dysreflexia in patients with spinal cord injuries". The Journal of Spinal Cord Medicine. 39 (6): 713–719. doi:10.1080/10790268.2015.1118186. PMC 5137561. PMID 26838482.
  10. ^ Krassioukov, Andrei; Biering-Sørensen, Fin; Donovan, William; Kennelly, Michael; Kirshblum, Steven; Krogh, Klaus; Alexander, Marca Sipski; Vogel, Lawrence; Wecht, Jill (2012). "International standards to document remaining autonomic function after spinal cord injury". The Journal of Spinal Cord Medicine. 35 (4): 201–210. doi:10.1179/1079026812Z.00000000053. PMC 3425876. PMID 22925746.
  11. ^ Burton AR, Brown R, Macefield VG (October 2008). "Selective activation of muscle and skin nociceptors does not trigger exaggerated sympathetic responses in spinal-injured subjects". Spinal Cord. 46 (10): 660–5. doi:10.1038/sc.2008.33. PMID 18427566.
  12. ^ Marsh DR, Weaver LC (June 2004). "Autonomic dysreflexia, induced by noxious or innocuous stimulation, does not depend on changes in dorsal horn substance p". Journal of Neurotrauma. 21 (6): 817–28. doi:10.1089/0897715041269605. PMID 15253807.
  13. ^ Solinsky, R.; Bunnell, A. E.; Linsenmeyer, T. A.; Svircev, J. N.; Engle, A.; Burns, S. P. (2017). "Pharmacodynamics and effectiveness of topical nitroglycerin at lowering blood pressure during autonomic dysreflexia". Spinal Cord. 55 (10): 911–914. doi:10.1038/sc.2017.58. PMID 28585557.

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