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Autonomic Dysreflexia

Autonomic dysreflexia (AD) is a potentially life-threatening syndrome of uncontrolled sympathetic discharge triggered by noxious or non-noxious stimuli below the level of a spinal-cord injury (SCI), most commonly arising at or above the T6 level. It manifests as acute, severe hypertension with reflex compensatory parasympathetic activation above the lesion (headache, flushing, sweating; heart rate may fall or rise). The dominant trigger across SCI series is urinary (bladder distension, catheter blockage, urinary tract infection, or urologic procedures).[1][2][3]

For the broader NLUTD framework see the Neurogenic Lower Urinary Tract Dysfunction section. For urodynamics in this population see Urodynamics. For the surgical interventions that depend on AD-aware perioperative management see Sacral Neuromodulation, Intradetrusor OnabotulinumtoxinA, and Augmentation Cystoplasty.

Definition and Epidemiology​

The ASIA/ISCoS International Standards to Document Autonomic Function Following SCI (2021 second edition) describe AD as a systolic blood-pressure rise of more than 20 mmHg above baseline after noxious or non-noxious stimulation below the neurologic injury level, most commonly in people with SCI at or above T6.[20] The Consortium for Spinal Cord Medicine/PVA guideline (2.1) and the EAU Neuro-Urology guideline (2026) use the same threshold. Resting systolic pressure after high SCI is often only 90–110 mmHg, so a reading that looks normal in an able-bodied patient (for example 130 mmHg) can already be AD. Know the patient's baseline.[4][6][14]

ParameterDetail
Prevalence in T6 and above SCICommon. Signs of AD appeared during urodynamics in 13/22 tetraplegic patients (59%; 91% with complete lesions, 27% with incomplete lesions) and in none of the paraplegic patients in one series;[5] 63% of a T6-and-above outpatient cohort had a systolic rise > 20 mmHg during urodynamics;[9] 62/121 (51%) people injured at age 13 or younger with SCI at or above T6 had documented AD in one pediatric-onset cohort[12]
Onset after injuryIn one tetraplegia cohort, first documented AD episodes appeared 1–6 months after injury; AD has also been reported within days after acute high SCI. Incomplete injuries remain at risk.[2][3]
Lesion-level thresholdT6 and above — splanchnic sympathetic outflow (T5–L2) split off from supraspinal control
Below T6AD is rare and generally less severe; isolated reports in T7–T10 lesions
Trigger distributionBladder > bowel > cutaneous / pressure ulcer / fracture / DVT / labor (in one pediatric-onset series, urologic 75%, bowel impaction 18%)[12]

Pathophysiology​

The pathophysiologic substrate is a disconnection of supraspinal inhibitory control from the sympathetic outflow that supplies the splanchnic vasculature (T5–L2). When a noxious stimulus enters the cord below the lesion, it triggers a massive, unopposed sympathetic discharge. Above the lesion, baroreceptor activation drives a parasympathetic counter-response, but the parasympathetic limb cannot cross the lesion to inhibit the runaway sympathetic outflow below.[1][3]

Below the lesionAbove the lesion
Massive sympathetic discharge → vasoconstriction, severe hypertensionCompensatory parasympathetic activation
Pale, cool skin; piloerectionBaroreflex bradycardia is the classic finding, but among 400 episodes with heart-rate data (from 445 total) in 78 hospitalized men with chronic SCI, relative tachycardia occurred in 272 (68%) and relative bradycardia in one (0.3%)[8]
Splanchnic vasoconstrictionFlushing, sweating, blurred vision, nasal congestion
Pounding headache (the cardinal symptom)

Afferent input from bladder and bowel distension or manipulation can activate the sympathetic reflex below the lesion.[3][6]

Clinical Presentation​

The classic syndrome combines acute hypertension (often 20–40 mmHg above the SCI baseline of about 90–110 mmHg systolic) with a pounding headache and a constellation of vasomotor and autonomic symptoms above and below the lesion.[1][6]

Above the lesion​

  • Pounding or throbbing headache is a common manifestation of symptomatic AD.[6]
  • Flushing, profuse sweating (especially face, neck, upper torso)
  • Nasal congestion
  • Blurred vision, mydriasis
  • Anxiety, sense of impending doom
  • Heart-rate change. Bradycardia or tachycardia may accompany AD; neither a heart-rate change nor headache is required for diagnosis.[6]

Below the lesion​

  • Pale, cool, dry skin with piloerection ("goosebumps")
  • Spasticity exacerbation

Severity spectrum​

  • Asymptomatic AD ("silent AD"). Measurable BP elevation without symptoms. In a yearly urodynamic evaluation of 45 men with complete SCI above T6, 15 of 35 with hypertension during voiding reported no AD symptoms.[7]
  • Symptomatic AD. The classic syndrome above
  • Severe AD. Hypertensive episodes can cause intracerebral hemorrhage, hypertensive encephalopathy, seizures, retinal hemorrhage, myocardial ischemia, pulmonary edema, and death.[1][6]

Common Triggers​

The dominant trigger categories, most common first (bladder and bowel account for most episodes):[1][2][3]

CategorySpecific triggers
UrinaryBladder distension (kinked catheter, blocked supra-pubic tube, retention from CIC overdue), UTI, bladder stones, urodynamics, cystoscopy, intradetrusor botulinum-toxin injection, ESWL, urethral catheterization, prostate stimulation / vibrostimulation for sperm retrieval
BowelFecal impaction, flatulence, anal fissure, hemorrhoids, digital rectal exam, enema, anorectal procedure
CutaneousPressure ulcer, ingrown toenail, burns, tight clothing
Skeletal / orthopedicLong-bone fracture, heterotopic ossification
VascularDVT, thrombophlebitis
ReproductiveLabor / delivery, menstrual cramps, ejaculation, vibrostimulation, electroejaculation
PharmacologicMisoprostol; sympathomimetics; abrupt withdrawal of clonidine or baclofen

In a retrospective within-person series of 21 SCI patients with AD during both procedures, mean systolic BP rise was 67.1 ± 33.8 mmHg during cystoscopy versus 51.8 ± 21.8 mmHg during urodynamics (P = .039), despite lower cystoscopy fill volume (150 versus 500 mL). The authors proposed that urethral, prostatic or outlet stimulation may contribute to the difference; monitor and prepare to treat during either procedure.[16]

Acute Management​

The Consortium for Spinal Cord Medicine/PVA guideline guides acute care:[6]

1. Position upright​

  • Sit the patient up immediately and lower the legs. Blood pools below the lesion and BP falls. Monitor BP and pulse every 1–2 minutes until stabilized.[6]
  • Loosen tight clothing or constrictive devices (binders, abdominal binders, support stockings).

2. Identify and remove the trigger — bladder first​

Because urinary triggers dominate, check the bladder first. Avoid the Credé maneuver and suprapubic tapping, which can exacerbate AD.[6]

Catheter statusAction
No indwelling catheterCatheterize promptly. At systolic BP ≥150 mmHg, consider a rapid-onset, short-duration antihypertensive before catheterization without delaying needed drainage. Instill 2% lidocaine jelly if immediately available, wait about 5 minutes if feasible, and monitor BP during drainage.[6]
Indwelling catheter presentCheck the full system for kinks, clots, sediment, an overfilled bag, and catheter position; correct problems promptly. If BP remains elevated, irrigate gently with 10–15 mL body-temperature saline (5–10 mL if under age 2); stop if fluid does not drain. Remove and replace a blocked catheter. If removal or replacement is difficult, consider lidocaine jelly, pharmacologic BP treatment and emergency urology consultation; for a man with a history of difficult passage, consider a coudé catheter.[6]
Suprapubic tubeSame — confirm patency; replace if blocked
CIC schedule overdueCatheterize immediately

Persistent hypertension requires assessment for bowel and other triggers. Before rectal examination or disimpaction, consider antihypertensive treatment if systolic BP remains ≥150 mmHg and use topical anesthetic; stop if AD worsens.[6]

3. Pharmacologic BP reduction​

At ≥150 mmHg systolic in adults, consider rapid-onset, short-duration medication before catheter manipulation; do not wait for all triggers to be removed:[6]

AgentDoseNotes
Nitroglycerin 2% ointment (nitropaste)0.5–2 inches (1.25–5 cm), thin layer on clean hairless skin of the chest or backFirst-line in the CPG appendix; wipe it off after treating the trigger when systolic BP is <20 mmHg above baseline. Avoid with severe anemia or increased intracranial pressure.[6] Not available in some countries; for prophylaxis before cystoscopy or sperm retrieval when ointment is unavailable, the CPG gives nitroglycerin spray 400 mcg, one spray every 5–10 minutes, up to three sprays in 30 minutes
Nifedipine immediate-release10 mg orally, capsule swallowed (or punctured and swallowed)The CPG advises against sublingual use: absorption is variable and little faster than swallowing. Can cause a significant BP drop. Avoid in older adults and in coronary disease
Captopril25 mg sublingualAlternative when nitrates are unavailable or contraindicated; onset within about 15 minutes. Avoid in renal failure; the hypotensive effect may last longer in renal impairment. Contraindicated in pregnancy.[6]
Hydralazine10–20 mg orally (CPG appendix)Onset 20–30 minutes; a parenteral form is used in monitored hospital settings
Clonidine0.1–0.2 mg orally (sublingual clonidine is also named in Rec 2.13)Slower onset (30–60 minutes)

The CPG (Rec 2.13) names nitropaste, nifedipine, hydralazine or sublingual clonidine as rapid-onset, short-duration options. Expect the drug to keep acting after the trigger is cleared, so watch for hypotension.[6]

Ask about recent PDE5 inhibitor use before giving a nitrate. The PVA guideline lists 24 hours after sildenafil or vardenafil and 48 hours after tadalafil; Princeton IV also advises at least 24 hours after avanafil because of severe hypotension risk.[6][24] Use captopril or another non-nitrate agent instead. Headache and flushing from a PDE5 inhibitor can mimic AD, so check the BP before treating. The EAU guideline likewise counsels that patients using on-demand nitrates for AD must not take PDE5 inhibitors.[6][14]

4. Continuous BP and HR monitoring​

  • BP and HR every 1–2 minutes during the acute episode (Rec 2.7); after treating the trigger and elevated BP, monitor for symptomatic hypotension every 2–5 minutes until BP is stable (Rec 2.30).[6]
  • Once resolved, continue monitoring for at least 2 hours in a clinic or inpatient setting to detect recurrent AD or hypotension (Rec 2.31).
  • If AD does not resolve after the bladder and bowel are cleared, look for other triggers (skin, fracture, DVT) and send the patient to an emergency department.[6]

Prevention in Urologic Practice​

Bladder stimuli are the most common AD triggers.[6] For patients at risk for AD, EAU 2026 strongly recommends BP and heart-rate monitoring during urodynamics and other invasive procedures.[14]

The 2021 AUA/SUFU NLUTD guideline states three Clinical Principles for testing: patients at risk for AD must be hemodynamically monitored during urodynamics and cystoscopic procedures (statement 9); if AD develops, the study is terminated, the bladder is drained immediately and monitoring continues (statement 10); and AD that persists after drainage is treated pharmacologically and/or care is escalated (statement 11).[15]

Routine outpatient procedures​

ProcedureAD-prevention strategy
CICPatient education on schedule adherence; technique; lidocaine jelly
Indwelling catheter exchangesPre-procedure lidocaine; monitor during drainage and exchange
CystoscopyCheck preprocedure BP; if >20 mmHg above baseline, evaluate and treat AD and consider rescheduling if it persists (CPG 4.2–4.3). Instill 2% lidocaine jelly at least 3–5 minutes beforehand (CPG 4.4); consider pharmacologic prophylaxis (4.5); BP at least every 2 minutes; treat UTI and ensure a recent bowel program first (4.1)[6][7]
UrodynamicsConfirm the rectal ampulla is empty before testing. When assessing the BP response, do not give prophylactic antihypertensives; keep rescue medication available. Monitor BP at least every 2 minutes, more often if AD develops (CPG 4.7).[6][14] If AD develops, AUA/SUFU Statement 10 requires immediate study termination, bladder drainage and continued hemodynamic monitoring. PVA Recommendations 4.8–4.9 (Level V; Strength C) instead advise drainage, then pharmacologic treatment if needed, and stopping the procedure and sitting the patient up if AD remains uncontrolled.[15][6] Higher AD risk with cervical injury, DSD, poor compliance and > 2 years since injury. Document AD susceptibility on the report[6][9]
Intradetrusor BoNT-AFor cystoscopic injections in patients at risk for AD, monitor hemodynamics continuously and keep a rapid-onset antihypertensive available. PVA advises considering prophylactic medication before cystoscopy in patients prone to or with recent AD; for known AD, its rationale suggests 0.5–1 inch nitropaste 4–6 minutes before instrumentation after checking PDE5 inhibitor use.[6][15]
ESWL / cystolitholapaxyAnesthesia / sedation with continuous BP monitoring; postprocedural hypertension surveillance
Vibrostimulation / electroejaculation for fertilityBP every minute (CPG 4.6). The CPG suggests nifedipine 10 mg bite-and-chew for sperm retrieval only in men familiar with its effects or monitored in clinic. The cited 10-man electroejaculation series used sublingual nifedipine starting at 20 mg 15 minutes before stimulation, with later dose adjustments to 10 or 30 mg; the unweighted average of the 10 patient-level mean peak systolic BPs was 168 mmHg with pretreatment versus 196 mmHg without it; 0/56 treated versus 8/25 untreated trials were aborted. One man had transient hypotension at 20 mg. The EAU guideline strongly recommends counselling men with SCI at or above T6 and fertility clinics about AD[6][10][14]

Surgical procedures​

SettingConsiderations
Sacral neuromodulationAUA/SUFU 2021 advises against offering SNM to NLUTD patients with SCI or spina bifida .[22] EAU 2026 recommends considering SNM in selected neurological patients , while noting uncertainty about disease-specific candidacy.[14] If SNM is planned for a patient with SCI at or above T6, discuss AD precautions with anesthesia beforehand; consider intraoperative arterial-line BP monitoring.
Augmentation cystoplastySignificant AD risk during bladder mobilization and distension; arterial-line monitoring; regional vs general anesthesia decision driven by AD susceptibility and respiratory function
Bladder neck reconstruction / closureIn patients susceptible to AD, plan BP monitoring with anesthesia; during an AD episode, the guideline calls for frequent BP checks and considers continuous monitoring ideal when available.[6]
Renal stone surgeryPCNL / ureteroscopy positioning effects; intraoperative AD reported during ureteric manipulation

Long-term prevention​

  • Optimize bladder management. Use CIC when the patient cannot empty effectively and catheterization is appropriate after shared decision-making[14]; treat urodynamically proven NDO with antimuscarinics or, when they are ineffective, intradetrusor BoNT-A; use β3-agonists for neurogenic overactive-bladder symptoms when appropriate[14]; consider augmentation cystoplasty for refractory NDO when otherwise indicated; evidence is insufficient to determine whether augmentation prevents AD[14][18]
  • Evaluate and treat symptomatic UTI. Bacteriuria alone does not establish a UTI; symptomatic UTI is a recognized urinary AD trigger[6]
  • Bowel program. Prevent fecal impaction with scheduled bowel care
  • Skin surveillance. Pressure-ulcer prevention
  • Patient and caregiver education. Teach patients and caregivers to recognize an abrupt blood-pressure rise above baseline, including episodes without headache or other symptoms, and to follow the home algorithm.[6][7]

Special Populations​

Pregnancy and labor​

AD can complicate labor in SCI women and is a recognized cause of intracerebral hemorrhage in this population. The CPG recommends anesthesia even when labor is painless: spinal or epidural anesthesia is the most reliable way to prevent AD in women with SCI at T6 and above (Rec 5.5), planned with an anesthesiologist before labor begins (5.2). Regional anesthesia blocks the afferent limb of the reflex. AD can occur antepartum, intrapartum and postpartum and can interfere with uteroplacental blood flow; multidisciplinary care includes counseling that breastfeeding, breast engorgement and mastitis may trigger postpartum AD.[6] Hypertension in pregnancy needs differentiation from preeclampsia.[6][11][21]

Pediatric SCI​

AD presents similarly in children but baseline BP is lower; the PVA recognition threshold is a systolic rise greater than 15 mmHg above baseline. Pharmacologic treatment thresholds are age-specific: about 120 mmHg in young children, 130 mmHg at 6–12 years and 140 mmHg in adolescents.[6] Infants and preschool children may show only subtle signs; headache and piloerection are uncommon at age 5 years or younger.[12] Lumbosacral myelomeningocele is most common, but AD may occur with thoracic myelomeningocele or brainstem anomalies. Assess neurologic level and prior AD episodes before urologic procedures.[6][17]

Athletes — "boosting"​

A doping-related concern: some Paralympic athletes have intentionally induced AD ("boosting") to improve performance through the secondary BP / cardiac-output effect. The IPC prohibits the practice given the cerebrovascular risk, and detected attempts lead to disqualification.[13]

Differential Diagnosis​

In a patient with SCI susceptible to AD, acute hypertension should prompt evaluation for AD and other causes:[6]

  • Pre-existing essential hypertension. Sustained hypertension on repeated resting or ambulatory measurements may favor this diagnosis after AD evaluation; an acute rise from baseline warrants AD assessment even without headache.[23][6]
  • Hypertensive emergency. Usually no clear noxious trigger
  • Pulmonary embolism. Hypoxia and tachycardia; tachycardia does not exclude AD
  • Acute coronary syndrome. Chest discomfort if sensation preserved
  • Sepsis. Fever, tachycardia, hypotension trajectory
  • Substance / sympathomimetic ingestion

Complications and Outcomes​

Untreated severe AD carries serious morbidity:

ComplicationMechanism
Intracerebral hemorrhageAcute hypertensive cerebrovascular event
Hypertensive encephalopathy / seizuresCerebral autoregulation failure
Retinal hemorrhageMicrovascular rupture
Pulmonary edemaAcute LV afterload mismatch
Myocardial ischemia / infarctionCoronary supply-demand mismatch
DeathA possible consequence of unrecognized or poorly managed AD[6]

Recognition, positioning, bladder drainage and pharmacologic treatment when needed guide acute care; after AD resolves, continue monitoring for recurrent hypertension and treatment-related hypotension.[6] The cumulative cardiovascular toll of recurrent AD over a lifetime is the more chronic concern, driving the long-term-prevention emphasis on bladder optimization.[1][3]

Key Takeaways​

  1. AD is a urologic disease in functional terms; the bladder is the most common trigger. Check it first in any AD episode.
  2. Recognize the blood-pressure rise. In a patient with SCI at or above T6, a systolic rise >20 mmHg above baseline can be AD even without headache or other symptoms; seek a noxious or non-noxious trigger, beginning with the bladder.[4][6][7]
  3. Sit upright, monitor, and check the bladder promptly; consider medication before instrumentation when BP is high.
  4. Lidocaine jelly before urethral instrumentation is a simple, low-cost measure suggested by the CPG when immediately available. Evidence for prevention strategies overall is mostly observational; a 2023 systematic review found mixed lidocaine effects across four randomized and two quasi-experimental studies, so its ability to prevent AD remains uncertain.[1][6][19]
  5. Nitrates are contraindicated shortly after PDE5 inhibitors (24 hours for sildenafil or vardenafil, 48 hours for tadalafil); use an alternative agent.[6]
  6. Document AD susceptibility on every urodynamics, cystoscopy, and operative report; the next provider needs to know.
  7. Long-term prevention centers on bladder and trigger management. Maintain dependable drainage and treat NDO and symptomatic UTI; consider augmentation for otherwise indicated refractory NDO with an unestablished effect on AD.[14][18]

See Also​

References​

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. doi:10.1016/j.apmr.2008.10.017

2. Helkowski WM, Ditunno JF Jr, Boninger M. Autonomic dysreflexia: incidence in persons with neurologically complete and incomplete tetraplegia. J Spinal Cord Med. 2003;26(3):244–7. doi:10.1080/10790268.2003.11753691

3. 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

4. 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. doi:10.1179/1079026812Z.00000000053

5. Curt A, Nitsche B, Rodic B, Schurch B, Dietz V. Assessment of autonomic dysreflexia in patients with spinal cord injury. J Neurol Neurosurg Psychiatry. 1997;62(5):473–7. doi:10.1136/jnnp.62.5.473

6. Krassioukov A, Linsenmeyer TA, Beck LA, et al. Evaluation and Management of Autonomic Dysreflexia and Other Autonomic Dysfunctions: Preventing the Highs and Lows. J Spinal Cord Med. 2021;44(4):631-683 (Consortium for Spinal Cord Medicine/PVA clinical practice guideline; PVA-hosted copy). doi:10.1080/10790268.2021.1925058

7. Linsenmeyer TA, Campagnolo DI, Chou IH. Silent autonomic dysreflexia during voiding in men with spinal cord injuries. J Urol. 1996;155(2):519–22. doi:10.1016/s0022-5347(01)66438-3. PMID 8558650

8. Solinsky R, Kirshblum SC, Burns SP. Exploring detailed characteristics of autonomic dysreflexia. J Spinal Cord Med. 2018;41(5):549–55. doi:10.1080/10790268.2017.1360434

9. Liu N, Zhou MW, Biering-Sørensen F, Krassioukov AV. Cardiovascular response during urodynamics in individuals with spinal cord injury. Spinal Cord. 2017;55(3):279–84. doi:10.1038/sc.2016.110

10. Steinberger RE, Ohl DA, Bennett CJ, McCabe M, Wang SC. Nifedipine pretreatment for autonomic dysreflexia during electroejaculation. Urology. 1990;36(3):228–31. doi:10.1016/0090-4295(90)80261-k

11. ACOG Committee on Obstetric Practice. ACOG Committee Opinion: obstetric management of patients with spinal cord injuries. Obstet Gynecol. 2002;100(3):625–7. doi:10.1016/s0029-7844(02)02261-5

12. Hickey KJ, Vogel LC, Willis KM, Anderson CJ. Prevalence and etiology of autonomic dysreflexia in children with spinal cord injuries. J Spinal Cord Med. 2004;27 Suppl 1:S54–60. doi:10.1080/10790268.2004.11753786

13. Mazzeo F, Santamaria S, Iavarone A. "Boosting" in Paralympic athletes with spinal cord injury: doping without drugs. Funct Neurol. 2015;30(2):91–8. doi:10.11138/fneur/2015.30.2.091

14. European Association of Urology. EAU Guidelines on Neuro-Urology. Limited update, March 2026: section 3.3.6.a (autonomic dysreflexia) and sexual-function recommendations. uroweb.org/guidelines/neuro-urology

15. Ginsberg DA, Boone TB, Cameron AP, et al. "The AUA/SUFU Guideline on Adult Neurogenic Lower Urinary Tract Dysfunction: Diagnosis and Evaluation." J Urol. 2021;206(5):1097–1105. doi:10.1097/JU.0000000000002235

16. Liu N, Fougere R, Zhou MW, et al. "Autonomic dysreflexia severity during urodynamics and cystoscopy in individuals with spinal cord injury." Spinal Cord. 2013;51(11):863–7. doi:10.1038/sc.2013.113

17. Hartigan S, Walsh B. "Perioperative management of patients with spina bifida." BJA Educ. 2024;24(6):203–209. doi:10.1016/j.bjae.2024.02.004

18. Le BT, Denys P, Joussain C. "Treating neurogenic detrusor overactivity in order to manage autonomic dysreflexia - A systematic review." Auton Neurosci. 2026;267:103454. doi:10.1016/j.autneu.2026.103454

19. Gray K, Sheehan W, McCracken L, Krogh K, Sachdeva R, Krassioukov AV. "Are local analgesics effective in reducing autonomic dysreflexia in individuals with spinal cord injury? A systematic review." Spinal Cord. 2023;61(1):1–7. doi:10.1038/s41393-022-00840-8

20. Wecht JM, Krassioukov AV, Alexander M, et al. "International Standards to document Autonomic Function following SCI (ISAFSCI): Second Edition." Top Spinal Cord Inj Rehabil. 2021;27(2):23–49. doi:10.46292/sci2702-23

21. American College of Obstetricians and Gynecologists. "Obstetric Management of Patients with Spinal Cord Injuries: ACOG Committee Opinion, Number 808." Obstet Gynecol. 2020;135(5):e230–e236. doi:10.1097/AOG.0000000000003842

22. Ginsberg DA, Boone TB, Cameron AP, et al. "The AUA/SUFU Guideline on Adult Neurogenic Lower Urinary Tract Dysfunction: Treatment and Follow-up." J Urol. 2021;206(5):1106–1113. doi:10.1097/JU.0000000000002239

23. Smith L, Weber G. "Differentiating essential hypertension from autonomic dysreflexia: a case report." Spinal Cord Ser Cases. 2023;9(1):51. doi:10.1038/s41394-023-00607-0

24. Kloner RA, Burnett AL, Miner M, et al. "Princeton IV consensus guidelines: PDE5 inhibitors and cardiac health." J Sex Med. 2024;21(2):90–116. doi:10.1093/jsxmed/qdad163