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Autonomic dysreflexia (AD) in spinal cord injury (SCI) is a potentially life-threatening syndrome which results from a response to stimuli below the neurologic level of injury (NLI) resulting in a sympathetic nervous system response below the level of injury, leading to a sudden increase in systolic blood pressure of 20 to 40 mmHg, with compensatory parasympathetic activity above the level of injury.1


Any stimulus below the level of injury may cause AD, but the most common are bladder or bowel distention or irritation.1,2 Bladder issues are by far the most common culprit with 75% of incidents precipitated by bladder-related concerns.3

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/orgasm.4

Gastrointestinal causes include bowel distention or impaction, acute abdomen (including appendicitis and cholecystitis), GERD, gastric ulcers, and anal fissures.1

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

Procedures, such as urodynamics, cystoscopy, vibratory stimulation, electroejaculation, and functional electrical stimulation, can also potentially precipitate AD.2,3,5

Epidemiology including risk factors and primary prevention

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

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

AD typically occurs in people with NLI at T6 or higher, although it has been reported with NLI as low as T10.6

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

The focus of prevention of AD has been on educating patients to recognize its signs and symptoms and removing or avoiding triggering factors. One of the most important AD management strategies is to help a patient acquire a consistent and reliable method of bladder drainage, given the predominance of bladder distension and irritation as the underlying trigger of AD.

AD triggered by labor and delivery can be prevented by using 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.1


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

AD begins with a noxious sensory input from peripheral nerves below the level of injury that 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 which leads to an increase in arterial blood pressure and a potential hypertensive crisis.

The brain senses the increase in blood pressure through the baroreceptors in the carotid bodies. It responds by increasing parasympathetic output via the vagus nerve causing bradycardia which is unable to fully compensate for the increase in blood pressure. Additionally, the brain attempts to reduce the sympathetic response and engage the parasympathetic response, but these impulses do not pass below the level of injury, thus resulting in the classic presentation of AD with predominantly parasympathetic activity above the NLI and predominantly sympathetic activity below the NLI.1

The development of AD is correlated with aberrant sprouting of 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 usually presents for the first time between 6 and 12 months after an acute SCI.6 However, Krassioukov et al reported a 5.7% incidence of early-onset AD within the first month after injury in cervical SCI.8

Specific secondary or associated conditions and complications

Seizures, intracerebral hemorrhage, subarachnoid hemorrhage, and myocardial infarction are potential complications.1 There has been a case report of neurogenic pulmonary edema associated with AD.9

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

Essentials of Assessment


Symptoms of AD vary and are characterized by a mixture of parasympathetically-mediated symptoms such as flushing, nasal congestion, upper body sweating, and sympathetically-mediated symptoms such as headache, piloerection, and feelings of apprehension or anxiety1

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

Patients may be asymptomatic, a phenomenon often referred to as “silent” AD.

Physical examination

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 described in the classical presentation of AD, particularly if the injury is caudal to the 4th thoracic spinal segment but is not always present. 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 should be considered 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 fractures, nephrolithiasis, or cholelithiasis.

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.10

Rehabilitation Management and Treatments

Available or current treatment guidelines

The Consortium for Spinal Cord Medicine has published clinical practice guidelines titled Evaluation and Management of Autonomic Dysreflexia and other Autonomic Dysfunctions: Preventing the Highs and Lows.4 It provides an algorithm as a summary of its 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 clothing and/or devices also help with blood pooling and removal of possible triggers.
  • If BP is still elevated, evaluate the urinary system.
    • Catheterize the patient if an indwelling urinary catheter is not in place. Instill 2% 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 for fecal impaction. Urinary and bowel causes comprise 85% of the causes of AD. To treat fecal impaction, use a generous amount of numbing agent (e.g., lidocaine or dibucaine) 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 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, captopril 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.11

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

Coordination of care

Patients with SCI at risk for AD should 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 to recognize it and follow a basic treatment protocol. Providers should also document any episodes of AD with the precipitating cause and treatment so that future providers are able to have this information available to guide treatment.

If a pregnant woman with a SCI at or above T6 presents with signs or symptoms of AD, consider coordinating care with an obstetric healthcare provider.

Additionally, literature has been developed to help educate non-physiatrists who may not be familiar with AD about its presentation and management.12 Likewise, physiatrists should engage primary care providers and emergency room practitioners to help them recognize and address this condition.

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/Emerging and Unique 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.

Additionally, while the classically taught presentation includes bradycardia as a sign based on understood pathophysiology, current research finds that this sign may not appear as often as previously thought. Solinsky et al found in a study of 78 patients with 445 episodes of AD relative tachycardia in 68% of cases, 31.8% of cases without change heart rate by greater than 10 beats per minute, and only 1 episode (0.3% of cases) with relative bradycardia.15

Typically, AD is thought to be a rare occurrence, however recent work has started to reveal that AD may have greater prevalence than previously expected. In one such study, patients were found to have anywhere from 0-41 AD events with 24-hour ambulatory monitoring and 0-135 potential AD events based on a patient questionnaire.16

As reviewed by Eldahan et al., many novel approaches for management of AD are emerging from studies of immunomodulation and metabolic processes underlying AD.17

Gaps in the Evidence-Based Knowledge

Given the improvement in recognizing and treating AD and a growing knowledge of previously unrecognized “silent” AD, it will be important to establish 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.10


  1. Sabharwal S. Cardiovascular Dysfunction in Spinal Cord Disorders. In: Kirshblum SC, Lin V, eds. Spinal Cord Medicine: Third Edition. New York: Demos Medical; 2018:212-224.
  2. Krassioukov A, Warburton DE, Teasell R, Eng JJ. A systematic review of the management of autonomic dysreflexia after spinal cord  injury. Arch Phys Med Rehabil. 2009;90(4):682-695. doi:10.1016/j.apmr.2008.10.017
  3. Sabharwal S. Cardiovascular and autonomic consequences: Overview. In: Essentials of Spinal Cord Medicine. 1st ed. Demos Medical; 2013.
  4. Consortium for Spinal Cord Medicine. Evaluation and Management of Autonomic Dysreflexia and Other Autonomic Dysfunctions: Preventing the Highs and Lows. 2nd ed. Washington DC: Paralyzed Veterans of America; 2020.
  5. 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):869-877. doi:10.1038/sc.2012.83
  6. Liu N, Zhou M, Biering-Sørensen F, Krassioukov A V. Iatrogenic urological triggers of autonomic dysreflexia: a systematic review. Spinal Cord. 2015;53(7):500-509. doi:10.1038/sc.2015.39
  7. Liu N, Fougere R, Zhou M-W, Nigro MK, Krassioukov A V. Autonomic dysreflexia severity during urodynamics and cystoscopy in individuals  with spinal cord injury. Spinal Cord. 2013;51(11):863-867. doi:10.1038/sc.2013.113
  8. Krassioukov A V, Furlan JC, Fehlings MG. Autonomic dysreflexia in acute spinal cord injury: an under-recognized clinical  entity. J Neurotrauma. 2003;20(8):707-716. doi:10.1089/089771503767869944
  9. 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):423-425. doi:10.1038/sc.2008.152
  10. 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):201-210. doi:10.1179/1079026812Z.00000000053
  11. 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;39(6):713-719. doi:10.1080/10790268.2015.1118186
  12. 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;58(8):831-835.
  13. Gee CM, West CR, Krassioukov A V. Boosting in Elite Athletes with Spinal Cord Injury: A Critical Review of  Physiology and Testing Procedures. Sports Med. 2015;45(8):1133-1142. doi:10.1007/s40279-015-0340-9
  14. Mazzeo F, Santamaria S, Iavarone A. “Boosting” in Paralympic athletes with spinal cord injury: doping without drugs. Funct Neurol. 2015;30(2):91-98. doi:10.11138/fneur/2015.30.2.091
  15. Solinsky R, Kirshblum SC, Burns SP. Exploring detailed characteristics of autonomic dysreflexia. J Spinal Cord Med. 2018;41(5):549-555. doi:10.1080/10790268.2017.1360434
  16. Hubli M, Gee CM, Krassioukov A V. Refined assessment of blood pressure instability after spinal cord injury. Am J Hypertens. 2015;28(2):173-181. doi:10.1093/ajh/hpu122
  17. Eldahan KC, Rabchevsky AG. Autonomic dysreflexia after spinal cord injury: Systemic pathophysiology and  methods of management. Auton Neurosci. 2018;209:59-70. doi:10.1016/j.autneu.2017.05.002

Original Version of the Topic:

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

Previous Revision(s) of the Topic:

Jennifer Yang, MD, Umu-Kulthum Al-Maawy, DO, MPH. Autonomic Dysreflexia in Spinal Cord Injury. 4/6/2016

Sameer Siddiqui, MD, Donna Huang, MD. Autonomic Dysreflexia in Spinal Cord Injury. 12/15/2020

Author Disclosures

Sameer Siddiqui, MD
Nothing to Disclose

Donna Huang, MD
Nothing to Disclose