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Autonomic dysreflexia (AD) in spinal cord injury (SCI) is a potentially life-threatening syndrome characterized by an exaggerated response of the autonomic nervous system to a stimulus originating below the level of injury, resulting in a sudden increase in blood pressure.


Any stimulus below the level of injury may cause AD, the most common being bladder or bowel distention or irritation.1,2

Genitourinary causes include bladder or urethral distention, detrusor sphincter dyssynergia, urinary tract infections, nephrolithiasis, epididymitis, testicular torsion, vaginal dilation (including labor), penile stimulation, and intercourse.3

Gastrointestinal causes include bowel distention or impaction, acute abdomen (including appendicitis and cholecystitis), GERD, gastric ulcers, and anal fissures1

Other causes include ingrown toenails, pressure ulcers, sunburn, DVT and fractures.2

Procedures like urodynamics4,5 cystoscopy,4,5 vibratory stimulation, electroejaculation, and functional electrical stimulation.2

Epidemiology including risk factors and primary prevention

AD typically occurs in people with neurologic level of injury (NLI) at T6 or higher, although it has been reported with NLI as low as T10.6

The incidence of AD reported in the literature ranges from 48% to 85% depending on the characteristics of the SCI population being studied.6

Individuals with higher NLI have a higher risk of more severe cardiovascular complications.

AD is more common in persons with in complete tetraplegia (25%) as compared to incomplete tetraplegia.7

The focus of prevention of AD has been on educating patients to recognize its signs and symptoms and removing triggering factors related to the bladder. Most important is to help a patient acquire a consistent and reliable method of bladder drainage and prevention of bladder over-distention.

AD triggered by labor and delivery can be prevented by the use of spinal or epidural anesthesia.1

Although most common in the setting of traumatic SCI, AD has been reported in non-traumatic SCI such as in patients with multiple sclerosis.8


AD results from loss of supraspinal control of the sympathetic nervous system. During an episode of AD, sympathetic activity predominates below while parasympathetic activity predominates above the level of injury.

AD begins with a strong sensory input from peripheral nerves below the level of injury, ascends through the spinothalamic tract and posterior columns of the spinal cord. This stimulus incites a reflex sympathetic response from the adjacent preganglionic sympathetic neurons located in the intermediolateral cell column below the level of injury. This sympathetic surge ultimately leads to widespread vasoconstriction below the level of injury, most significantly in the splanchnic vasculature. There is an increase in peripheral arterial blood pressure, potentially leading to hypertensive crisis.

The brain responds in two ways to the increase in blood pressure:

  • The brainstem attempts to reduce blood pressure via the intact vagal nerve, causing bradycardia mediated by parasympathetic input. Bradycardia in itself is ineffective in reducing blood pressure against the powerful vasoconstriction in the splanchnic vasculature.
  • The brain sends descending inhibitory impulses down the spinal cord, but these do not reach most of the sympathetic outflow due to the SCI. This results in a parasympathetic response above the level of injury, including dilation of blood vessels in the brain, but not an overall reduction in blood pressure.

The development of AD is correlated with aberrant sprouting of peptidergic afferent fibers into the spinal cord and denervation hypersensitivity of adrenergic receptors below the injury.

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

AD does not routinely present acutely following SCI, but Krassioukov et al. reported a 5.7% incidence of early-onset AD within the first month after injury in cervical SCI.9

AD usually presents for the first time between 6 and 12 months after an acute SCI.6

Specific secondary or associated conditions and complications

Seizures, intracerebral hemorrhage, subarachnoid hemorrhage, and myocardial infarction are potential complications.6 There has been a case report of neurogenic pulmonary edema associated with AD.10

Numerous pathologic arrhythmias such as premature ventricular contractions and second degree AV block have been reported.



Symptoms vary but often include a combination of: headache, flushing and profuse sweating above the NLI, nasal congestion, blurry vision, and anxiety.

The headache is usually pounding and in the frontal and occipital areas.

Patients may be asymptomatic.

Physical examination

Physical findings are due to sympathetically mediated effects below and parasympathetically mediated effects above the NLI, although sacral parasympathetic stimulation can occur as well. The most common finding is an increase in blood pressure of 20 to 40 mmHg or higher above baseline for adults, and 15 mm Hg or higher in adolescents and children.

Bradycardia is a classic presentation, particularly if the injury is caudal to the 4th thoracic spinal segment, but this is not always the case. Tachycardia can also occur

Mydriasis may occur if the NLI is above T1.

Penile erection and seminal fluid emission may occur due to sacral parasympathetic stimulation.

Pallor and piloerection occur below the NLI.

Laboratory studies

Laboratory studies are not commonly used to evaluate AD, and they are obtained only after the most common etiologies are ruled out (bladder distention and bowel impaction).

The choice of laboratory studies depends on the clinical evaluation. A complete blood count (CBC) may be needed if a urinary tract infection (UTI) is suspected as the etiology.


Imaging studies can be used to evaluate AD, but only after the most common etiologies (bladder distention and bowel impaction) have been ruled out. Imaging studies are chosen based on clinical findings.

Plain x-rays may be used to screen for factures, nephrolithiasis, or gallstones.

Lower extremity ultrasound may be used to screen for DVT.

Supplemental assessment tools

Currently no assessment tools specific for evaluating AD are available.

The International Spinal Cord Society and American Spinal Injury Association have jointly developed an autonomic standards assessment form, which includes a section on the autonomic control of blood pressure.11


Available or current treatment guidelines

The Consortium for Spinal Cord Medicine has published clinical practice guidelines titled Acute Management of Autonomic Dysreflexia: Adults with Spinal Cord Injury Presenting to Health-Care Facilities.2 It provides an algorithm as a summary of its 24 treatment recommendations. There is also a consumer version of this guideline.

At different disease stages

The most basic tenet of treatment for AD is rapid recognition of its signs and symptoms and subsequent prompt removal of the precipitating factor.

Blood pressure (BP) monitoring is most important. Once symptoms of AD are identified, the patient’s BP must be checked immediately. During an acute episode, the BP should be monitored every few minutes. Once the BP is normalized, it should be monitored for at least 2 hours after the episode to ensure that AD does not recur.

The following steps are recommended for the initial evaluation of AD :

If the BP is elevated and the patient is supine, sit the patient up and loosen any restrictive clothing or devices. This takes advantage of an orthostatic decrease in BP; in the upright position, blood pools in the LE and viscera due to the loss of resistance due to SCI. Loosening of tight fitting devices also help with blood pooling and removal possible triggers.

If BP is still elevated, evaluate the urinary system.

  • Catheterize the patient if an indwelling urinary catheter is not in place. Use 2 percent lidocaine jelly into the urethra and wait several minutes before inserting the catheter.
  • If the individual has an indwelling catheter, check for kinks or obstructions. For blocked catheters, gently irrigate the bladder with a small amount of body temperature fluid such as normal saline. If the catheter is not draining and the blood pressure is still elevated, remove and replace the catheter, instilling 2% lidocaine jelly into the urethra before doing so. Avoid tapping on or manually compressing the bladder.

If the BP continues to be elevated, evaluate the bowels for fecal impaction. Urinary and bowel causes comprise 85% of the causes of AD. To treat fecal impaction, use a generous amount of 2% lidocaine on a gloved finger for digital stimulation. Gently remove any stool present.

If the BP is above 150 mm Hg, consider pharmacologic management with an antihypertensive agent that has a rapid onset and short duration of action, in order to reduce the BP prior to checking for fecal impaction.

If the BP remains elevated, consider admitting the patient to a hospital for pharmacologic treatment of BP and evaluation for other causes of the AD.

Pharmacologic treatment

There are no studies determining the most effective pharmacologic agent to use to treat AD.

The most commonly used agents are nitrates and nifedipine.1

  • Apply 1 inch of 2% nitroglycerin ointment onto the skin above the NLI. This can be easily wiped off in case the patient develops hypotension. Nitrates are contraindicated in patients taking cGMP-phosphodiesterase type 5 inhibitors.
  • Nifedipine should be used with caution in patients who cannot tolerate a hypotensive episode with reflex tachycardia, such as elderly patients with coronary artery disease.

Other agents that have been used include: hydralazine, mecamylamine, diazoxide, phenoxybenzamine, beta-blockers, terazosin, prazosin, captropril prostaglandin E2 and sildenafil.1

A nursing-driven protocol utilizing conservative measures, nitroglycerin paste and oral hydralazine achieved target blood pressure with a high success rate and low incidence of adverse events.12

Insufficient evidence exists for phenazopyridine for AD due to cystitis, magnesium for AD due to labor or life-threating AD in the ICU, and dizoxide for acute AD .1

Coordination of care

Patients with SCI at risk for AD can carry a wallet-sized information card and provide it to emergency, urgent care and other healthcare providers. This card can help providers not familiar with AD recognize it and follow a basic treatment protocol.

If a pregnant women with a spinal cord injury at or above T6 presents with signs or symptoms of AD, consider coordinating care with an obstetric healthcare provider.

Patient & family education

Patients and families should be educated on the signs and symptoms of AD during rehabilitation by a healthcare provider.

Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills

Always consider AD in the evaluation of elevated BP or a headache in an SCI individual.

Athletes with SCI may engage in the practice of boosting. The athlete incites AD in order to improve cardiac output and in turn, athletic performance.13 In addition to the health risks, boosting can lead to disqualification from competition.14


Cutting edge concepts and practice

There are ongoing efforts to establish more objective criteria (for example using urodynamics or measuring sympathetic skin responses) to establish presence and severity of AD.


Gaps in the evidence-based knowledge

Given the improvement in recognizing and treating AD, it will be important to establish current incidence and prevalence rates. When more objective criteria are developed for diagnosing AD, new and established treatments can be evaluated and compared more rigorously. The recent autonomic standards assessment form may be useful in such studies.11


  1. Krassioukov A, Warburton DE, Teasell R, Eng JJ, Spinal Cord Injury Rehabilitation Evidence Research Team. A systematic review of the management of autonomic dysreflexia after spinal cord injury. Arch Phys Med Rehabil. 2009;90(4):682-95.
  2. Paralyzed Veterans of America/Consortium for Spinal Cord Medicine. Acute management of autonomic dysfunction: adults with spinal cord injury presenting to health-care facilities, 2nd Washington, DC: Paralyzed Veterans of America (PVA); 2001 Jul. [138 references].
  3. Courtois F, Rodrigue X, Côté I, et al. Sexual function and autonomic dysreflexia in men with spinal cord injuries: how should we treat?. Spinal Cord. 2012;50(12):869-77.
  4. Liu N, Zhou M, Biering-sørensen F, Krassioukov AV. Iatrogenic urological triggers of autonomic dysreflexia: a systematic review. Spinal Cord. 2015;53(7):500-9.
  5. Liu N, Fougere R, Zhou MW, Nigro MK, Krassioukov AV. Autonomic dysreflexia severity during urodynamics and cystoscopy in individuals with spinal cord injury. Spinal Cord. 2013;51(11):863-7.
  6. Garstang, SV, Walker H. Cardiovascular and Autonomic Dysfunctions after Spinal Cord Injury. In: Kirshblum S. and Campagnolo DI, eds. Spinal Cord Medicine, 2ndPhiladelphia, PA: Wolters Kluwer Health/Lippincott Williams & Wilkins; 2011.
  7. Helkowski WM, Dittuno JF Jr, Boninger M. Autonomic dysreflexia: incidence in persons with neurologically complete and incomplete tetraplegia. J Spinal Cord Med 2003; 26(3) 244-247.
  8. Kulcu DG, Akbas B, Citci B, Cihangiroglu M. Autonomic dysreflexia in a man with multiple sclerosis. J Spinal Cord Med. 2009;32(2):198-203.
  9. Krassioukov AV, Furlan JC, Fehlings MG. Autonomic dysreflexia in acute spina cord injury: an under-recognized clinical entity. J. Neurotrauma 2003; 20(8):707-716
  10. Calder KB, Estores IM, Krassioukov A. Autonomic dysreflexia and associated acute neurogenic pulmonary edema in a patient with spinal cord injury: a case report and review of the literature. Spinal Cord. 2009;47(5):423-5.
  11. Krassioukov A, Biering-sørensen F, Donovan W, et al. International standards to document remaining autonomic function after spinal cord injury.  J Spinal Cord Med.     2012;35(4):201-10.
  12. Solinsky R, Svircev JN, James JJ, Burns SP, Bunnell AE. A retrospective review of safety using a nursing driven protocol for autonomic dysreflexia in patients with spinal cord injuries. J Spinal Cord Med. 2016.
  13. Gee CM, West CR, Krassioukov AV. Boosting in Elite Athletes with Spinal Cord Injury: A Critical Review of Physiology and Testing Procedures. Sports Med. 2015;45(8):1133-42.
  14. Mazzeo F, Santamaria S, Iavarone A. “Boosting” in Paralympic athletes with spinal cord injury: doping without drugs. Funct Neurol. 2015; 1-8.
  15. Karlsson AK.Autonomic dysreflexia. Spinal Cord. 1999;37:383-391.

Original Version of the Topic:

Scott Campea, MD. Autonomic Dysreflexia in Spinal Cord Injury. Publication Date: 2011/11/10.

Author Disclosures

Jennifer Yang, MD
Nothing to Disclose

Umu-Kulthum Al-Maawy, DO, MPH
Nothing to Disclose