Autonomic dysreflexia

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Autonomic dysreflexia
Other namesAutonomic hyperreflexia
Specialty Physical medicine and rehabilitation, Neurology
CausesBladder distension, urinary tract infection, constipation, skin damage, fractures, etc.
PreventionEducate the patient and caregivers about common triggers
TreatmentRemoval of the noxious stimuli
Prognosis Generally good prognosis with low levels of mortality

Autonomic dysreflexia (AD) is a life-threatening medical emergency characterized by hypertension and cardiac arrhythmias. [1] This condition is sometimes referred to as autonomic hyperreflexia. [2] Most cases of AD occur in individuals with spinal cord injuries. [3] Lesions at or above the T6 spinal cord level are more frequently reported, although there are reports of AD in patients with lesions as low as T10. [4] [5] Guillain–Barré syndrome may also cause autonomic dysreflexia. [6]

Contents

Hypertension in AD may result in mild symptoms, such as sweating above the lesion level, goosebumps, blurred vision, or headache. [7] Severe symptoms may result in life-threatening complications including seizure, intracranial bleeds (stroke), myocardial infarction, and retinal detachment. [8]

Both noxious and non-noxious stimuli can trigger AD. The result is stimulation and hyperactivity of the sympathetic nervous system. [9] The noxious stimuli activate a sympathetic surge that travels through intact peripheral nerves, resulting in systemic vasoconstriction below the level of the spinal cord lesion. [10] The peripheral arterial vasoconstriction and hypertension activates the baroreceptors, resulting in a parasympathetic surge. This surge originates 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 to reduce elevated blood pressure. [10] This can result in bradycardia, tachycardia, vasodilation, flushing, pupillary constriction and nasal stuffiness above the spinal lesion. Piloerection and pale, cool skin occur below the lesion due to the prevailing sympathetic outflow. [10]

The most common causes include bladder or bowel over-distension from urinary retention and fecal compaction. [11] Other causes include pressure sores, extreme temperatures, fractures, undetected painful stimuli (such as a pebble in a shoe), sexual activity, and extreme spinal cord pain. [5]

Treating AD immediately involves removing or correcting the noxious stimuli. This entails sitting the patient upright, removing any constrictive clothing (including abdominal binders and support stockings), and rechecking blood pressure often. [12] The inciting issue may require urinary catheterization or bowel disimpaction. [8] If systolic blood pressure remains elevated (over 150 mm Hg) after these steps, fast-acting short-duration antihypertensives are considered, [13] while other inciting causes must be investigated for the symptoms to resolve. [8]

Educating the patient, family, and caregivers about the avoidance of triggers and the cause, if known, is important in the prevention of AD. [14] Since bladder and bowel are common causes, routine bladder and bowel programs and urological follow-up may help reduce the frequency and severity of attacks. These follow-ups may include cystoscopy/urodynamic studies. [8]

Prognosis of AD is generally good and mortality is rare, given that the trigger is identified and managed.

Signs and symptoms

This condition is distinct and usually episodic. 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. [15]

Common presenting symptoms include: [5]

Complications

Autonomic dysreflexia can become chronic and recurrent. This often occurs in response to longstanding medical problems like soft tissue pressure injuries or hemorrhoids.

Complications of severe acute hypertension can include seizures, pulmonary edema, myocardial infarction, or cerebral hemorrhage. Other organs that may be affected include the kidneys and retinas of the eyes. [4] Long-term therapy to decrease blood pressure may include alpha blockers or calcium channel blockers. [16]

Causes

The first episode of autonomic dysreflexia may occur weeks to years after the spinal cord injury takes place. [5] It may take place anytime after reflexes have returned following spinal shock. [5] Most people at risk develop their first episode within the first year after the injury. [17]

There are many possible triggers of AD in patients who have had spinal cord injuries. The most common causative factor is bladder distention. [18] Other causes include urinary tract infections, urinary retention, blocked catheters, constipation, hemorrhoids or fissures, skin damage, fractures, and sexual intercourse. [5] It is important to note that not all noxious stimuli will cause AD. Some otherwise severe noxious stimuli, e.g. broken bones, may not result in AD, and may in fact even go unnoticed. In the absence of clear triggering factors, recurrent episodes of AD can be important signs that there is an underlying pathology in a patient that has not yet been discovered. [19] [20]

Mechanism

Clinical signs of activation of the sympathetic and parasympathetic nervous systems Parasympathetic and sympathetic.png
Clinical signs of activation of the sympathetic and parasympathetic nervous systems

The autonomic nervous system is comprised of the sympathetic, parasympathetic, and enteric nervous systems. [21] The mechanism of autonomic dysreflexia has to do with the relationship of the sympathetic and parasympathetic systems. [22]

Supraspinal vasomotor neurons send projections to the intermediolateral cell column, which is composed of sympathetic preganglionic neurons (SPN) through the T1-L2 segments of the spinal cord. [11] The supraspinal neurons act on the SPN and its tonic firing by modulating its action on the peripheral sympathetic chain ganglia and the adrenal medulla. [11] The sympathetic ganglia act directly on the blood vessels they innervate throughout the body. This controls vessel diameter and resistance. [21] The adrenal medulla indirectly controls the same action through the release of epinephrine and norepinephrine. [11] [21]

In a patient with a spinal cord lesion, the descending autonomic pathways that are responsible for the supraspinal communication with the SPN are interrupted. [23] This results in decreased sympathetic outflow below the level of the injury. [11] In this circumstance, the SPN is controlled only by spinal influences. [11]

After a spinal injury, the decreased sympathetic outflow causes reduced blood pressure and sympathetic reflex. [11] Eventually, synaptic reorganization and plasticity of the SPN develops into an overly sensitive state. Because of this, there is abnormal reflex activation of SPN due to afferent stimuli. Most commonly, bowel or bladder distension. [11]

Reflex activation then results in systemic vasoconstriction below the spinal cord disruption. This peripheral arterial vasoconstriction and hypertension activates the baroreceptors. There is a resultant parasympathetic surge originating in the central nervous system which inhibits the sympathetic outflow. This parasympathetic signal is unable to transmit below the level of the spinal cord lesion and there is a heightened sympathetic response. [10] [23] This results in vasodilation, flushing, pupillary constriction and nasal stuffiness above the spinal lesion. Below the lesion, piloerection, paleness, and cool skin occur due to the prevailing sympathetic outflow. [10] This issue is much more prominent for lesions at or above the T6 level. This is because the splanchnic nerves emerge from the T5 level and below. [24]

Diagnosis

Autonomic dysreflexia is diagnosed by documenting an increase in systolic blood pressure greater than 20 to 30 mmHg. The associated symptoms vary from life-threatening to asymptomatic. [25]

An essential step to diagnosing AD is careful monitoring of blood pressure and other vital sign changes. Having knowledge of the patient's baseline blood pressure can be helpful in diagnosing AD. [5] Especially in cases of patients with baseline hypotension since the condition may not be recognized unless compared with their baseline levels.

Apart from the increased blood pressure, additional symptoms help differentiate AD from other conditions. These include sweating, spasms, erythema (more likely in upper extremities), headaches, and blurred vision. [5] Older patients with very incomplete spinal cord injuries and systolic hypertension may be experiencing essential hypertension, not autonomic dysreflexia, if they lack additional symptoms. [26]

Differential Diagnoses

Other diagnoses that should be considered due to similar presentation include: [5]

Treatment

Initial management of autonomic dysreflexia includes measuring and monitoring blood pressure and sitting the patient upright to attempt to lower their blood pressure. It is also important to search for and correct the triggering stimuli. [12] Tight clothing and pressure stockings should be removed. Catheterization of the bladder should be performed as well as evaluation for possible urinary tract infection (UTI). Indwelling catheters should be checked for obstruction. Relief of a blocked urinary catheter tube may resolve the problem. A rectal examination can be performed to clear the rectum of any possible stool impaction. If the noxious stimuli cannot be identified or the systolic blood pressure remains above 150 mmHg, then pharmacologic treatment may be needed. [27] In this situation, the aim is to decrease the elevated intracranial pressure until further studies can identify the cause. [28]

Pharmacologic treatment will include antihypertensive medications. Options include sublingual or topical nitrates as well as oral hydralazine or clonidine. Ganglionic blockers can also be used to control sympathetic nervous system outflow. [29] [13] Epidural anesthesia has been demonstrated to be effective in reducing AD in women in labor. However, there is less evidence for its use in reducing AD during general surgical procedures. [30]

If the episode of AD is triggered by bowel or bladder irritants, topical analgesics such as lidocaine and bupivacaine are commonly used. Yet, their effectiveness in reducing AD remains inconclusive. [31] Because bladder distension is a common trigger of AD, botulinum toxin used to treat bladder dysfunction in SCI patients may be effective in reducing attacks. [32] Prophylactic use of medications has also been reported to prevent attacks. Some examples include nifedipine, prazosin, and terazosin. [16]

Patients with AD should have a card or file about their medical history in case they have an episode in public. [33] This will help the individuals responding to the episode manage the situation by looking for common triggers. Patients with history of AD should also carry their medications for easy access in emergency scenarios.

Prognosis

The prognosis of autonomic dysreflexia is generally good, given that the trigger is identified and managed. Attacks can be prevented by recognizing and avoiding triggering stimuli.

Mortality is rare with AD, but morbidities such as stroke, retinal hemorrhage, and pulmonary edema if left untreated can be quite severe. [5] The cause of autonomic dysreflexia itself can be life-threatening. There must be proper investigation and appropriate treatment of the inciting cause to prevent unnecessary morbidity and mortality. [25]

Research directions

Most future work on the topic of autonomic dysreflexia is directed at earlier detection and intervention. Overall, the goal of these research projects involves minimizing complications that result from late detection of autonomic dysreflexia. Some research is aimed at investigating the use of non-invasive sensors to track nerve activity to detect signs of AD. [34] Other work has begun to look at the use of AI for this role, although it has been limited to rat models. [35] Results from a study showed that AI can serve as another non-invasive tool in combination with sensors that track nerve activity. [35] Future work of studies such as these includes using more sensors to track other variables for increasingly accurate results. [35]

Other work revolves around increasing the understanding of the mechanism behind AD. While it is understood that spinal cord injury results in inhibited parasympathetic surges and a heightened sympathetic response that can lead to AD, other details are yet to be defined. [23] It is also understood that the renin-angiotensin system (RAS) plays a significant role in cardiovascular function in addition to the autonomic nervous system (ANS), which includes the sympathetic and parasympathetic systems. [36] What remains to be studied is the degree to which a spinal cord injury affects the relationship between RAS and ANS. [37] It also remains to be determined whether targeting the RAS system can help manage symptoms of AD. [37]

References

  1. ↑ Solinsky R, Kirshblum SC, Burns SP (September 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.
  2. ↑ Lawrence, P.F. (2007). Essentials of Surgical Specialties (3rd ed.). Lippincott Williams & Wilkins. pp. Chapter 1: Anesthesiology. ISBN   978-0781750042.
  3. ↑ Cragg, Jacquelyn; Krassioukov, Andrei (2012-01-10). "Autonomic dysreflexia". Canadian Medical Association Journal. 184 (1): 66. doi:10.1503/cmaj.110859. ISSN   0820-3946. PMC   3255181 . PMID   21989470.
  4. 1 2 3 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): 738–740. doi: 10.1038/sj.sc.3101780 . PMID   16010281.
  5. 1 2 3 4 5 6 7 8 9 10 Allen, Kathrin J.; Leslie, Stephen W. (2025), "Autonomic Dysreflexia", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID   29494041 , retrieved 2025-01-22
  6. ↑ Nguyen, Thy P.; Taylor, Roger S. (2025), "Guillain-Barre Syndrome", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID   30335287 , retrieved 2025-01-22
  7. ↑ Eapen, C.E., Cifu, D.X. (2023). Spinal Cord Injury. Elsevier. pp. Chapter 13. ISBN   978-0-323-83389-9.{{cite book}}: CS1 maint: multiple names: authors list (link)
  8. 1 2 3 4 Daroff RB, Jankovic J, Mazziotta JC, Pomeroy SL, Bradley WG (2016). Bradley's neurology in clinical practice (Seventh ed.). London: Elsevier. ISBN   978-0-323-28783-8. OCLC   932031625.
  9. ↑ 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): 682–695. doi:10.1016/j.apmr.2008.10.017. PMC   3108991 . PMID   19345787.
  10. 1 2 3 4 5 Winn HR, ed. (30 November 2016). Youmans and Winn neurological surgery (Seventh ed.). Philadelphia, PA: Elsevier. ISBN   9780323287821. OCLC   963181140.
  11. 1 2 3 4 5 6 7 8 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.
  12. 1 2 Linsenmeyer, Todd (1997-01-01). "Acute Management of Autonomie Dysreflexia: Adults with Spinal Cord Injury Presenting to Health-Care Facilities". The Journal of Spinal Cord Medicine. 20 (3): 284–309. doi:10.1080/10790268.1997.11719480. ISSN   1079-0268. PMID   27166730.
  13. 1 2 Solinsky R, Svircev JN, James JJ, Burns SP, Bunnell AE (November 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.
  14. ↑ 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 –S88. PMID   12051242.
  15. ↑ Krassioukov A, Biering-Sørensen F, Donovan W, Kennelly M, Kirshblum S, Krogh K, et al. (July 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.
  16. 1 2 Vaidyanathan S, Soni BM, Sett P, Watt JW, Oo T, Bingley J (November 1998). "Pathophysiology of autonomic dysreflexia: long-term treatment with terazosin in adult and paediatric spinal cord injury patients manifesting recurrent dysreflexic episodes". Spinal Cord. 36 (11): 761–770. doi: 10.1038/sj.sc.3100680 . PMID   9848483. S2CID   35222095.
  17. ↑ de Andrade LT, de Araújo EG, Andrade K, de Souza DR, Garcia TR, Chianca TC (February 2013). "[Autonomic dysreflexia and nursing interventions for patients with spinal cord injury]". Revista da Escola de Enfermagem da U S P. 47 (1): 93–100. doi: 10.1590/s0080-62342013000100012 . PMID   23515808.
  18. ↑ Allen KJ, Leslie SW (2022). "Autonomic Dysreflexia". StatPearls. Treasure Island (FL): StatPearls Publishing. PMID   29494041.
  19. ↑ 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): 660–665. doi: 10.1038/sc.2008.33 . PMID   18427566.
  20. ↑ 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): 817–828. doi:10.1089/0897715041269605. PMID   15253807.
  21. 1 2 3 Waxenbaum, Joshua A.; Reddy, Vamsi; Varacallo, Matthew A. (2025), "Anatomy, Autonomic Nervous System", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID   30969667 , retrieved 2025-01-22
  22. ↑ Eldahan, Khalid C.; Rabchevsky, Alexander G. (2018-01-01). "Autonomic dysreflexia after spinal cord injury: Systemic pathophysiology and methods of management". Autonomic Neuroscience: Basic and Clinical. 209: 59–70. doi:10.1016/j.autneu.2017.05.002. ISSN   1566-0702. PMC   5677594 . PMID   28506502.
  23. 1 2 3 Wulf, Mariah J.; Tom, Veronica J. (2023-02-28). "Consequences of spinal cord injury on the sympathetic nervous system". Frontiers in Cellular Neuroscience. 17. doi: 10.3389/fncel.2023.999253 . ISSN   1662-5102. PMC   10011113 . PMID   36925966.
  24. ↑ Sharabi, Alaa F.; Carey, Frederick J. (2025), "Anatomy, Abdomen and Pelvis, Splanchnic Nerves", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID   32809339 , retrieved 2025-01-22
  25. 1 2 Wan D, Krassioukov AV (January 2014). "Life-threatening outcomes associated with autonomic dysreflexia: a clinical review". The Journal of Spinal Cord Medicine. 37 (1): 2–10. doi:10.1179/2045772313Y.0000000098. PMC   4066548 . PMID   24090418.
  26. ↑ Hubli, Michèle; Krassioukov, Andrei V. (May 2014). "Ambulatory Blood Pressure Monitoring in Spinal Cord Injury: Clinical Practicability". Journal of Neurotrauma. 31 (9): 789–797. doi:10.1089/neu.2013.3148. ISSN   0897-7151. PMC   3997095 . PMID   24175653.
  27. ↑ Wan, Darryl; Krassioukov, Andrei V. (January 2014). "Life-threatening outcomes associated with autonomic dysreflexia: A clinical review". The Journal of Spinal Cord Medicine. 37 (1): 2–10. doi:10.1179/2045772313Y.0000000098. ISSN   1079-0268. PMC   4066548 . PMID   24090418.
  28. ↑ Vaidyanathan, Subramanian; Soni, Bakul M.; Mansour, Paul; Oo, Tun (2017-11-02). "Fatal collapse due to autonomic dysreflexia during manual self-evacuation of bowel in a tetraplegic patient living alone: lessons to learn". International Medical Case Reports Journal. 10: 361–365. doi: 10.2147/IMCRJ.S135586 . PMC   5679675 . PMID   29138603.
  29. ↑ Solinsky R, Bunnell AE, Linsenmeyer TA, Svircev JN, Engle A, Burns SP (October 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.
  30. ↑ Petsas, Anna; Drake, Jeremy (2015). "Perioperative management for patients with a chronic spinal cord injury". BJA Education. pp. 123–130. doi:10.1093/bjaceaccp/mku024 . Retrieved 2023-10-26.
  31. ↑ Gray, Katherine; Sheehan, Whitley; McCracken, Laura; Krogh, Klaus; Sachdeva, Rahul; Krassioukov, Andrei V. (12 August 2022). "Are local analgesics effective in reducing autonomic dysreflexia in individuals with spinal cord injury? A systematic review". Spinal Cord. 61 (1): 1–7. doi:10.1038/s41393-022-00840-8. ISSN   1476-5624. PMID   35962043.
  32. ↑ Fougere, Renée J.; Currie, Katharine D.; Nigro, Mark K.; Stothers, Lynn; Rapoport, Daniel; Krassioukov, Andrei V. (2016-09-15). "Reduction in Bladder-Related Autonomic Dysreflexia after OnabotulinumtoxinA Treatment in Spinal Cord Injury". Journal of Neurotrauma. 33 (18): 1651–1657. doi:10.1089/neu.2015.4278. ISSN   0897-7151. PMC   5035837 . PMID   26980078.
  33. ↑ Krassioukov, Andrei; Linsenmeyer, Todd A.; Beck, Lisa A.; Elliott, Stacy; Gorman, Peter; Kirshblum, Steven; Vogel, Lawrence; Wecht, Jill; Clay, Sarah (2021-03-01). "Evaluation and Management of Autonomic Dysreflexia and Other Autonomic Dysfunctions: Preventing the Highs and Lows". Topics in Spinal Cord Injury Rehabilitation. 27 (2): 225–290. doi:10.46292/sci2702-225. ISSN   1082-0744. PMC   8152175 . PMID   34108837.
  34. ↑ Suresh, Shruthi; Everett, Thomas H.; Shi, Riyi; Duerstock, Bradley S. (November 2022). "Automatic Detection and Characterization of Autonomic Dysreflexia Using Multi-Modal Non-Invasive Sensing and Neural Networks". Neurotrauma Reports. 3 (1): 501–510. doi:10.1089/neur.2022.0041. PMC   9718431 . PMID   36479362.
  35. 1 2 3 Pancholi, Sidharth; Everett, Thomas H.; Duerstock, Bradley S. (2024-02-10). "Advancing spinal cord injury care through non-invasive autonomic dysreflexia detection with AI". Scientific Reports. 14 (1): 3439. Bibcode:2024NatSR..14.3439P. doi:10.1038/s41598-024-53718-5. ISSN   2045-2322. PMC   10858945 . PMID   38341453.
  36. ↑ Miller, Amanda J.; Arnold, Amy C. (2019-04-01). "The renin–angiotensin system in cardiovascular autonomic control: recent developments and clinical implications". Clinical Autonomic Research. 29 (2): 231–243. doi:10.1007/s10286-018-0572-5. ISSN   1619-1560. PMC   6461499 . PMID   30413906.
  37. 1 2 Trueblood, Cameron T.; Singh, Anurag; Cusimano, Marissa A.; Hou, Shaoping (October 2024). "Autonomic Dysreflexia in Spinal Cord Injury: Mechanisms and Prospective Therapeutic Targets". The Neuroscientist. 30 (5): 597–611. doi:10.1177/10738584231217455. ISSN   1073-8584. PMC   11166887 . PMID   38084412.

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