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Priapism

Priapism is a persistent penile erection lasting more than 4 hours in the absence of sexual stimulation and not relieved by ejaculation or orgasm.[1][2] It is classified by pathophysiology into three subtypes — ischemic (low-flow, veno-occlusive), non-ischemic (high-flow, arterial), and stuttering (recurrent ischemic) — each with fundamentally different management pathways. Ischemic priapism accounts for roughly 95% of cases and is a urologic emergency: beyond 4 hours, progressive ischemia, acidosis, smooth-muscle injury, and fibrosis destroy corporal tissue, and longer duration reduces the chance of erectile recovery. Medical detumescence can still succeed after 24–36 hours; duration alone does not mandate a particular operation.[3][4]

Management is governed by the 2021 AUA/SMSNA Guideline on Acute Ischemic Priapism and the 2022 AUA/SMSNA Guideline on Recurrent Ischemic, Sickle-Cell, and Non-Ischemic Priapism.[2][3]

Classification and Pathophysiology​

Ischemic (low-flow, veno-occlusive) priapism​

Venous outflow obstruction → blood stasis in the corpora cavernosa → progressive hypoxia, hypercapnia, acidosis, and eventually smooth-muscle necrosis and fibrosis. The corpora are rigid and painful; the glans is soft (spongiosum is not involved).[1]

Corporal blood gas:

ParameterIschemicNormal arterial
pO₂<30 mmHg>90 mmHg
pCO₂>60 mmHg<40 mmHg
pH<7.25~7.40
ColorDark, deoxygenatedBright red

Non-ischemic (high-flow, arterial) priapism​

Uncontrolled arterial inflow via an arteriocavernosal fistula, usually after blunt perineal or penile trauma (straddle injury, saddle trauma). The corpora remain oxygenated; the erection is partial and non-painful. This is not a surgical emergency — observation is first-line.[1][4]

Stuttering (recurrent ischemic) priapism​

Repeated self-limited ischemic episodes, typically <3 hours each, with intervening detumescence. Pathophysiologically ischemic and a risk factor for prolonged ischemic events.[3][5]

Molecular mechanisms (ischemic)​

  • Dysregulation of the NO–cGMP–PDE5 pathway — chronic hypoxia reduces endothelial NO and alters PDE5 set-point
  • Rho-Rho kinase pathway dysregulation
  • Adenosine accumulation — signals through A2B receptor to drive fibrosis[6]
  • Oxidative stress and reactive-oxygen-species injury
  • In sickle-cell disease: intravascular hemolysis → impaired NO bioavailability → exaggerated corpus cavernosum relaxation and sickling in the corpora during nocturnal tumescence[7][8]

Epidemiology and Etiology​

CauseComment
Sickle cell diseaseImportant cause, especially in children; lifetime prevalence estimates vary and may approach half of men with SCD. Do not interpret age at first event among affected men as cumulative risk for all men with SCD[5][9]
Intracavernosal injection therapyMajor cause — papaverine, phentolamine, PGE1 (alprostadil); can account for >50% of cases in some series[10]
MedicationsAntidepressants (e.g., trazodone) and antipsychotics (e.g., chlorpromazine, risperidone), α-blockers, anticoagulants, recreational cocaine
Hematologic disordersThalassemia, polycythemia vera, multiple myeloma, CML/CLL
MalignancyMetastatic infiltration of corpora (rare but reported — bladder, prostate, renal primaries)
NeurologicSpinal cord injury (especially cervical), autonomic dysreflexia
IdiopathicSignificant proportion of adult cases
TraumaPerineal/straddle injury — non-ischemic (high-flow) priapism specifically

Initial Evaluation​

History​

  • Duration of erection (drives the urgency of intervention)
  • Preceding sexual activity, perineal trauma, recreational drugs, new medications
  • Prior priapism episodes (stuttering pattern)
  • Known sickle-cell, thalassemia, leukemia
  • Current ICI use and agent

Physical examination​

  • Ischemic: rigid corpora, soft glans, painful
  • Non-ischemic: partially tumescent, non-painful, may have perineal ecchymosis
  • Examine perineum and genitalia for evidence of recent trauma

Corporal blood gas​

The gold-standard diagnostic. A 19–21 gauge needle is placed laterally into the corpus cavernosum (avoiding the dorsal neurovascular bundle at 12 o'clock and the urethra at 6 o'clock). Aspirate; color is the first clue. Send for gas analysis. Obtain a corporal blood gas in the initial assessment when subtype is uncertain; aspiration is also therapeutic. A clinically clear presentation should receive prompt treatment without avoidable diagnostic delay.[1][4]

Imaging​

  • Color Doppler ultrasound (CDUS) — used when blood gas is equivocal or when non-ischemic is suspected. Ischemic: absent or minimal cavernosal arterial flow. Non-ischemic: high arterial flow, often with visible arteriocavernosal fistula.[11][12]
  • MRI — useful in delayed presentations (>36–48 hours) to assess extent of cavernosal necrosis and fibrosis; informs early-implant decision
  • CT/MR angiography — defines pudendal arterial anatomy for selective embolization in non-ischemic priapism

Management — Ischemic Priapism (the Acute Emergency)​

The AUA/SMSNA algorithm is stepwise and time-pressured — each step is attempted and, if unsuccessful, escalated quickly.[2]

First-line treatment — aspiration plus phenylephrine​

Laterally into the corpus cavernosum; aspirate 20–30 mL of dark blood. Combine aspiration with intracavernosal phenylephrine, with or without saline irrigation, for acute ischemic priapism. Aspiration-only steps should not create unnecessary treatment delays.

Intracavernosal phenylephrine within first-line treatment​

Phenylephrine is the α-agonist of choice because of α1 selectivity and avoidance of β-mediated cardiac stimulation; hypertension and other serious cardiovascular effects remain possible.[13]

  • Use a verified dilute preparation, ideally pharmacy-prepared, with independent concentration/dose checks and BP/heart-rate monitoring.
  • AUA Appendix A: 100–500 micrograms in 1 mL normal saline, intracavernosally at least 5 minutes apart. Stop injections for blood-pressure changes; select a single protocol and escalate according to response.[25]
  • EAU adult regimen: 200 micrograms intracavernosally every 3–5 minutes, maximum 1 mg within one hour. At 200 micrograms/mL, each dose is 1 mL. Different institutional/AUA-based regimens exist; avoid mixing a concentration from one protocol with a volume from another.[24]
  • Children and significant cardiovascular disease: reduce dose and individualize under specialist supervision; a universal pediatric 100-microgram dose/500-microgram ceiling is not established by these guidelines.
  • EAU advises avoiding sympathomimetics in malignant/poorly controlled hypertension and with MAO inhibitors. Monitor during administration and for adverse effects afterward; stop/escalate for cardiovascular intolerance.[24]

Repeat aspiration and irrigation within first-line treatment​

Corporal saline irrigation and re-aspiration may accompany phenylephrine to clear stagnant blood and coagulum. These are components of combined first-line treatment. AUA advises definitive treatment when repeated attempts over about one hour fail, with earlier escalation appropriate for prolonged ischemia or poor response. Do not restart an additional hour of irrigation after an unsuccessful injection protocol.[25]

Surgical shunting — for persistent ischemia despite first-line treatment​

The shunt creates a communication between the rigid corpus cavernosum and either the glans or the corpus spongiosum, allowing stasis blood to drain.

For detailed operative technique comparisons, see Priapism Shunts & Decompression.

Distal shunts (attempted first):

ShuntTechnique
WinterPercutaneous large-bore biopsy needle (Tru-Cut) through the glans into the distal corpus cavernosum, creating a fistula
EbbehojStab incision with a scalpel through the glans into the distal corpus cavernosum
T-shuntT-shaped scalpel incision distally through the glans into corpus cavernosum (variant of Ebbehoj)
Al-GhorabOpen excision of distal tunica albuginea through a glanular incision; no shunt has established universal comparative superiority

Historical proximal/venous shunts: evidence is limited and morbidity can be substantial; these are not an automatic next step after distal failure.

Tunneling and alternative decompression​

Tunneling extends the distal shunt by passing a dilator (Hegar or Mecholl) proximally through the cavernosum from the shunt site to disrupt ischemic coagulum along the entire length of the corpus. AUA allows tunneling for persistent ischemia after distal shunting; comparative evidence is limited:[2]

  • Burnett snake technique — Al-Ghorab shunt + retrograde corporal tunneling with a 7/8 Hegar dilator
  • Penoscrotal decompression (PSD) — glans-sparing proximal corporal decompression through penoscrotal or proximal shaft corporotomies; increasingly used as salvage after failed distal shunts and as an alternative primary surgical strategy for prolonged ischemic priapism[14][18][19][20]

Step 5b — Penoscrotal decompression (PSD)​

PSD treats prolonged ischemic priapism as a corporal compartment syndrome. Instead of creating a corporoglanular fistula through the glans, PSD opens the proximal corpora, evacuates stagnant blood and clot directly, irrigates the corporal bodies, and closes the corporotomies. This can spare the glans and avoid some distal-shunt complications while preserving the option for later elective penile prosthesis placement if erectile function does not recover.[18][19]

When to consider PSD:

ScenarioRole of PSD
Failed aspiration / irrigation / phenylephrineSurgical decompression option when medical detumescence fails
Failed distal shunt or failed corporoglanular tunnelingSalvage strategy that bypasses the glans and directly clears proximal corporal clot
Prolonged ischemic priapism, especially >36–48 hAlternative to glans-based shunting in centers familiar with the technique; counsel that erectile recovery remains time-dependent
PSD failure or very late presentation with nonviable corporaConfirm persistent ischemia and discuss prosthesis timing or symptom-focused management through shared decision-making

Technique options:

ApproachExposureTechnical notes
Original penoscrotal approachLongitudinal or transverse incision at the penoscrotal junction; familiar to implant surgeonsExpose ventrolateral tunica, protect urethra with a Foley catheter, perform 2–3 cm longitudinal corporotomy, evacuate dark blood and clot, irrigate to clear return, repeat contralaterally, close tunica with absorbable suture[18][19]
Modified proximal shaft approachProximal penile shaft incision or degloving exposure, analogous to penile fracture repairMay make bilateral corporal exposure faster and more familiar for general urologists comfortable with fracture exploration; evacuation, irrigation, and tunical closure are otherwise the same[20]

Operative pearls:

  • Place a Foley catheter before dissection so the urethra / corpus spongiosum can be palpated and protected.
  • Put corporotomies on the ventrolateral corporal surface, away from the dorsal neurovascular bundle and away from the urethra.
  • Evacuate aggressively but deliberately: prolonged cases often contain viscous, gelatinous, or organized clot that will not drain through a small distal shunt.
  • Laterality evidence is observational. In a 25-patient series, recurrence occurred after 2/10 unilateral versus 0/15 primary bilateral procedures. A 26-patient later series also favored bilateral decompression; these small, selected comparisons do not establish a universal mandate.[19][20]
  • Apply a light compressive dressing after closure; monitor for recurrent rigidity, hematoma, skin issues, and early pain relief.

Step 6 — Early penile prosthesis implantation​

AUA states that a prosthesis may be considered for untreated ischemic priapism >36 hours or failure of shunting ± tunneling. EAU recommends discussing implantation after delayed presentation (>48 hours) or failed injection/distal-shunt therapy.[2][3][24]

  • Erectile recovery becomes unlikely with prolonged confirmed ischemia, but “zero after 36 hours” is too absolute. Verify the duration, including any intervening detumescence.
  • Early implantation can avoid later dense fibrosis and length loss, but carries infection/erosion risks. EAU advises delaying implantation after a shunt to reduce those risks.
  • Discuss early versus delayed placement, device choice and the patient's goals. A malleable device can later be exchanged for an inflatable implant; neither implantation nor one device type is mandatory.[15][24]

See penile implants — revision scenarios for the cavernotome toolkit and Carter-Trost technique used in the fibrosed corpus.

Special Considerations — Sickle Cell Disease​

The 2022 AUA/SMSNA guideline is explicit:[3]

  • Do not delay urologic intervention for exchange transfusion. Exchange transfusion does not terminate priapism faster than standard urologic management and delays effective intervention by 6+ hours — an interval during which ischemic injury progresses.
  • Simple transfusion to Hb 9–10 g/dL is reasonable before general anesthesia if surgical shunting is needed, to reduce sickling risk intraoperatively.
  • ASPEN syndrome (association of sickle cell, priapism, exchange, and neurologic events) has been described after rapid exchange transfusion — another argument against reflexive exchange.

Chronic prevention in SCD​

After an acute episode resolves, prevention of recurrence is the main goal:

  • Hydroxyurea — established SCD therapy; benefit specifically preventing recurrent priapism remains incompletely established
  • Scheduled monthly transfusion programs in selected patients
  • Pseudoephedrine at bedtime (limited evidence)
  • PDE5 inhibitors — low-dose daily sildenafil has been used with the paradoxical rationale of restoring PDE5 regulatory tone; evidence is limited but mechanism is biologically plausible[5]
  • GnRH analogues / antiandrogens — specialist options with limited evidence; counsel about libido, erectile function, fertility and effects on sexual maturation

Management — Non-Ischemic (High-Flow) Priapism​

Not an emergency. Management pathway:[1][3]

  1. Observation + conservative measures — ice packs, compression, avoidance of stimulation
  2. ~60% of high-flow priapism resolves spontaneously over weeks
  3. Selective arterial embolization — if the patient desires treatment or conservative measures fail
    • Temporary agents include autologous clot and absorbable gelatin sponge (Gelfoam); material choice depends on anatomy, prior treatment and interventional expertise
    • Permanent agents include coils and some particles/glues. Counsel about recurrence and ED; comparative estimates are limited by selection and technique
  4. Surgical ligation — rarely needed; reserved for embolization failures

Management — Stuttering / Recurrent Ischemic Priapism​

Acute episode: treat exactly as acute ischemic priapism (aspiration + phenylephrine).

Preventive strategies (the 2022 AUA/SMSNA guideline frames these as "may offer" options given limited evidence):[3]

  • At-home phenylephrine self-injection — for episodes not yet meeting 4-hour threshold; patient must be thoroughly trained and aware of hypertensive-crisis risk
  • Daily low-dose PDE5 inhibitor — an off-label preventive option with limited evidence; begin only while flaccid, not to treat an acute episode
  • α-agonist agents (pseudoephedrine, etilefrine where available)
  • Ketoconazole — off-label specialist option; requires attention to hepatotoxicity, adrenal suppression and drug interactions
  • GnRH analogues / antiandrogens — limited-evidence options with fertility and sexual-function consequences; avoid before sexual maturation
  • Hydroxyurea / chronic transfusion for SCD-associated stuttering

PIN trial (2025): In 64 men with sickle-cell anemia, this phase 2 feasibility trial did not establish added preventive benefit from tadalafil over placebo when both groups received hydroxyurea (between-group p = 0.654; median follow-up 10 months). It was designed around recruitment, retention and adherence; improvement from each group’s baseline does not establish hydroxyurea efficacy or treatment equivalence. Discuss prevention individually with hematology and sexual-medicine specialists.[26]

Outcomes​

Duration is the dominant predictor of ED​

DurationRisk of ED
<12 hoursLow
12–24 hoursModerate
24–36 hoursHigh
>36 hoursHigh risk; OR 61.3 was reported in a single-center retrospective series of 186 cases, not a universal risk estimate[10]
>48 hoursRecovery is less likely; the cited 43% figure applies to all 35 followed patients in a mixed-duration cohort, not the >48-hour subgroup[16]

Other predictors​

  • In the 35-patient follow-up cohort, complete detumescence was the only significant predictor in multivariable analysis; this is not a universally validated prediction model[16]
  • Degree of fibrosis on MRI — heterogeneous low-signal areas from hemosiderin and fibrosis correlate with ED severity
  • In a single-county-hospital study of 334 ischemic-priapism encounters, phenylephrine and/or aspiration resolved 78%; some episodes >36 hours still responded[17]
  • In that same cohort, shunting occurred in 10%, with lower rates for SCD (2.2%) than other etiologies (15.2%)[17]

Long-term complications​

  • Erectile dysfunction — the dominant long-term morbidity
  • Penile fibrosis — progressive, adenosine-A2B-driven; detected in 20/35 (57%) of a followed mixed-duration cohort, more often after episodes >48 hours[6][16]
  • Penile shortening — especially with delayed prosthesis implantation
  • Acquired penile curvature
  • Psychological distress and relationship-impacting sexual dysfunction[5]

Prolonged Priapism (≥ 24 hours) — the Operative Window​

Prolonged ischemia increases the likelihood of failed medical treatment and later ED, but 24 hours is not an automatic surgical cutoff. Treat promptly and escalate according to response, confirmed perfusion and the patient's goals.[2][17][24]

Distal shunts alone have limited durability in prolonged cases because the ischemic coagulum spans the entire corporal length. Success of traditional distal shunting falls as duration passes 36–48 hours, and glans-based shunts can be limited by recurrent occlusion, urethral injury, cavernosospongiosal fistula, and the inability to clear proximal clot.[14][18][23]

Where PSD fits​

PSD is a glans-sparing proximal decompression option after failed medical treatment, including selected cases before or after distal shunting. Its place depends on presentation and expertise; it is not a mandatory step before prosthesis discussion.[24]

Evidence anchorFindings
Fuchs 2018Initial PSD series: 6/6 achieved detumescence and immediate pain relief; acute malleable prosthesis comparators had high revision / extrusion burden in ischemic tissue[18]
Baumgarten 202025 patients/27 PSD procedures; recurrence 2/10 unilateral versus 0/15 primary bilateral. Spontaneous penetrative erections were reported by 9/15 with documented sexual follow-up, not 60% of all treated patients[19]
Basile 2025Two-center retrospective series, 26 patients: immediate detumescence 96%, pain relief 92%, composite success 18/26 (69%), complications 2/26. Sexual outcomes sometimes included subsequent prosthesis use[20]
VanDyke 2023/2024 surgeon surveyAmong high-volume male-genital surgeons who had performed both procedures, PSD was perceived as more effective than corporoglanular tunneling (47.3% vs 18.7% rating "very or extremely effective"), although tunneling remains more widely performed[21]

Practical approach:

  1. Prompt aspiration/irrigation plus phenylephrine, with cardiovascular monitoring.
  2. If ischemia persists, distal shunting ± tunneling; EAU also permits PSD as an alternative first surgical option with a weak recommendation.[24]
  3. After a shunt, persistent tumescence may reflect reperfusion rather than ongoing ischemia: reassess with corporal blood gas or Doppler before repeat surgery.[2]
  4. Discuss prosthesis options for prolonged confirmed ischemia or refractory disease, including the effect of recent shunting on timing and complication risk.

PSD vs acute prosthesis​

PSD avoids implanting hardware into swollen, ischemically injured tissue and keeps later inflatable penile prosthesis placement available under more controlled conditions. That is its major appeal. Its limitation is equally important: decompression may relieve pain and rigidity without restoring erectile function if smooth-muscle necrosis has already occurred.

Early penile prosthesis remains appropriate when the presentation is very late, corporal viability is doubtful, the patient prioritizes length preservation over native erectile recovery, or PSD / shunting fails. The EAU systematic review found prosthesis reliably resolves priapism but carries nontrivial complication risk, while post-shunting reviews emphasize that evidence after failed shunting remains retrospective and center-dependent.[22][23]

The choice between decompression, early implant and later implant is individualized. PSD evidence remains based on small retrospective cohorts, and a surgeon-preference survey cannot establish superiority or predict recovery for an individual patient.[18][19][20][21]

Videos​

Priapism — technique demonstration
Ischemic priapism management
Priapism management — operative video
Surgical approach and shunt technique

External video references:

  • Penoscrotal decompression of refractory ischemic priapism — surgical technique — Videos in Sexual Medicine (vjsm.info): Residents Corner
  • Penoscrotal decompression — a better method for priapism management — Videos in Sexual Medicine (vjsm.info): Full video

See Also​

References​

1. Pang KH, Alnajjar HM, Lal A, Muneer A. An update on mechanisms and treatment options for priapism. Nat Rev Urol. 2025. doi:10.1038/s41585-025-01069-9

2. Bivalacqua TJ, Allen BK, Brock G, et al. Acute ischemic priapism: an AUA/SMSNA guideline. J Urol. 2021;206(5):1114–1121. doi:10.1097/JU.0000000000002236

3. Bivalacqua TJ, Allen BK, Brock GB, et al. The diagnosis and management of recurrent ischemic priapism, priapism in sickle cell patients, and non-ischemic priapism: an AUA/SMSNA guideline. J Urol. 2022;208(1):43–52. doi:10.1097/JU.0000000000002767

4. Ericson C, Baird B, Broderick GA. Management of priapism: 2021 update. Urol Clin North Am. 2021;48(4):565–576. doi:10.1016/j.ucl.2021.07.003

5. Idris IM, Burnett AL, DeBaun MR. Epidemiology and treatment of priapism in sickle cell disease. Hematology Am Soc Hematol Educ Program. 2022;2022(1):450–458. doi:10.1182/hematology.2022000380

6. Wen J, Jiang X, Dai Y, et al. Increased adenosine contributes to penile fibrosis, a dangerous feature of priapism, via A2B adenosine receptor signaling. FASEB J. 2010;24(3):740–9. doi:10.1096/fj.09-144147

7. Pereira DA, Calmasini FB, Costa FF, Burnett AL, Silva FH. Nitric oxide resistance in priapism associated with sickle cell disease: mechanisms, therapeutic challenges, and future directions. J Pharmacol Exp Ther. 2024;390(2):203–212. doi:10.1124/jpet.123.001962

8. Iacopucci APM, da Silva Pereira P, Pereira DA, et al. Intravascular hemolysis leads to exaggerated corpus cavernosum relaxation: implication for priapism in sickle cell disease. FASEB J. 2022;36(10):e22535. doi:10.1096/fj.202200867R

9. Chinegwundoh FI, Smith S, Anie KA. Treatments for priapism in boys and men with sickle cell disease. Cochrane Database Syst Rev. 2020;4:CD004198. doi:10.1002/14651858.CD004198.pub4

10. Borrell JA, Bettencourt A, Furtado TP, et al. Risk factors, diagnosis, and long-term erectile dysfunction outcomes in priapism: a retrospective analysis of 186 cases from a single institution. Int J Impot Res. 2026;38(1):23–29. doi:10.1038/s41443-025-01076-9

11. von Stempel C, Walkden M, Kirkham A. Review of the role of imaging in the diagnosis of priapism. Int J Impot Res. 2024. doi:10.1038/s41443-024-00928-0

12. McHugh K, Gibbons RC. Point-of-care ultrasound diagnosis of high flow priapism. J Emerg Med. 2022;62(2):207–209. doi:10.1016/j.jemermed.2021.07.037

13. Graham BA, Abdulla W, Jack C, Mitchell RA, Hellstrom WJG. An overview of emergency pharmacotherapy for priapism. Expert Opin Pharmacother. 2022;23(12):1371–1380. doi:10.1080/14656566.2022.2099271

14. Lumbiganon S, Moukhtar Hammad MA, Azad B, Yafi FA. A narrative review of initial treatment for ischemic priapism. Int J Impot Res. 2024. doi:10.1038/s41443-024-00951-1

15. Yassin M, Chen R, Ager M, Desouky E, Minhas S. Penile implants in low flow priapism. Int J Impot Res. 2023;35(7):651–663. doi:10.1038/s41443-023-00787-1

16. El-Bahnasawy MS, Dawood A, Farouk A. Low-flow priapism: risk factors for erectile dysfunction. BJU Int. 2002;89(3):285–90. doi:10.1046/j.1464-4096.2001.01510.x

17. Masterson TA, Parmar M, Tradewell MB, et al. Using artificial intelligence to predict surgical shunts in men with ischemic priapism. J Urol. 2020;204(5):1033–1038. doi:10.1097/JU.0000000000001183

18. Fuchs JS, Shakir N, McKibben MJ, et al. Penoscrotal decompression-promising new treatment paradigm for refractory ischemic priapism. J Sex Med. 2018;15(5):797–802. doi:10.1016/j.jsxm.2018.02.010

19. Baumgarten AS, VanDyke ME, Yi YA, et al. Favourable multi-institutional experience with penoscrotal decompression for prolonged ischaemic priapism. BJU Int. 2020;126(4):441–446. doi:10.1111/bju.15127

20. Basile G, Ralph D, Wardak S, Sangster P, Christopher N, Lee WG. Penoscrotal decompression should be considered for prolonged ischaemic priapism. J Sex Med. 2025;22(11):2072–2078. doi:10.1093/jsxmed/qdaf229

21. VanDyke ME, Smith WJ, Holland LC, et al. Current opinions on the management of prolonged ischemic priapism: does penoscrotal decompression outperform corporoglanular tunneling? Int J Impot Res. 2024;36(1):62–67. doi:10.1038/s41443-023-00808-z

22. Milenkovic U, Cocci A, Veeratterapillay R, et al. Surgical and minimally invasive treatment of ischaemic and non-ischaemic priapism: a systematic review by the EAU Sexual and Reproductive Health Guidelines Panel. Int J Impot Res. 2024;36(1):36–49. doi:10.1038/s41443-022-00604-1

23. Schifano N, Capogrosso P, Baldini S, et al. Current evidence on the management of ischaemic priapism post-shunting: a narrative review. Int J Impot Res. 2025. doi:10.1038/s41443-025-01078-7

24. European Association of Urology. Sexual and Reproductive Health Guidelines: Priapism. 2026. Guideline.

25. AUA/SMSNA. The Diagnosis and Management of Priapism. 2022. Appendix A: phenylephrine dosing and administration. Full guideline.

26. Idris IM, Yusuf AA, Ismail II, et al. A controlled trial for preventing priapism in sickle cell anemia: hydroxyurea plus placebo vs hydroxyurea plus tadalafil. Blood. 2025;145(26). doi:10.1182/blood.2024027898.