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Priapism Management — Pharmacologic Agents

Ischemic priapism requires urgent treatment. This is the drug reference; use the clinical priapism page for diagnosis and the shunts and decompression page for operative decisions. AUA/SMSNA 2022 recommends intracavernosal phenylephrine with corporal aspiration, with or without irrigation, as first-line therapy before operative intervention .[1]

Ischemic versus non-ischemic priapism​

Priapism is an erection that persists for hours beyond, or is unrelated to, sexual stimulation. Ischemic (low-flow) priapism has little or no cavernous blood flow and hypoxic, hypercarbic, acidotic corporal blood gas. It is a medical emergency, and delay risks cavernosal fibrosis and erectile dysfunction. Non-ischemic (high-flow) priapism is usually arterial, often after perineal or penile trauma. AUA/SMSNA 2022 advises initial observation for confirmed non-ischemic priapism, which is not an emergency . It calls for corporal blood gas at initial presentation , with penile duplex Doppler available when the subtype remains indeterminate .[10] Treat according to the subtype and ischemia, as recurrent ischemic episodes can last less than four hours.[10][3][1]

Depending on patient goals, resources and clinician experience, treatment may be intracavernosal phenylephrine alone, aspiration with or without irrigation, distal shunting, or non-emergent prosthesis placement.[10][1]

Phenylephrine​

Phenylephrine activates α₁ receptors, contracting cavernosal smooth muscle to promote detumescence. Its relative lack of β activity favors it over mixed sympathomimetics; cardiovascular and neurologic complications remain possible.[2][1]

Adult intracavernosal regimen​

SourceRegimenImportant distinction
AUA/SMSNA 2022, Appendix A 100–500 micrograms in 1 mL normal saline, at intervals at least 5 minutes apart, for up to 1 hourPrefer pharmacy-prepared syringes. Stop injections for blood-pressure changes; persistent ischemia requires escalation, sometimes sooner with prolonged presentation.[1]
EAU 2026200 micrograms every 3–5 minutes; maximum 1 mg within 1 hourConcentration 100–500 micrograms/mL in normal saline. Lower doses in children or severe cardiovascular disease.[2]

Check the amount and final concentration before injection. The AUA preparation contains 100–500 micrograms/mL; concentrated stock vials are not the ready-to-inject preparation. Intracavernosal administration for priapism is off-label.[1] Pediatric dosing needs a specialist protocol rather than extrapolation from an adult syringe.

Appendix B's sample aspiration and irrigation cycle allows 3–5 minutes before repetition; Appendix A's phenylephrine dosing instruction specifies at least 5 minutes between doses.[1]

AUA/SMSNA 2022 calls for blood pressure and heart rate monitoring during phenylephrine treatment ; its discussion also advises monitoring afterward.[1] EAU additionally specifies checks every 15 minutes for 1 hour afterward. Hypertension, reflex bradycardia, tachycardia, palpitations and sporadic subarachnoid hemorrhage have been reported. EAU (panel opinion) regards sympathomimetics as contraindicated in malignant or poorly controlled hypertension and with concurrent monoamine oxidase inhibitors, and its algorithm also lists cerebrovascular disease; AUA describes cautious, lower-dose titration with monitoring for MAOI users. Resolve this guideline difference with specialist assessment in the monitored emergency setting.[1][2]

Technique​

Severe penile pain may warrant a dorsal, circumferential or shaft penile block before corporal aspiration and injection.[2] Aspiration and injection can use the same access. A 19-gauge butterfly needle is a common teaching variant. AUA/SMSNA Appendix B describes a sample aspiration protocol using a 16–18-gauge butterfly needle connected to a 30–60-mL Luer-lock syringe, without ranking needles or techniques.[1]

  1. Insert the needle into the lateral corpus cavernosum near the penile base, at about 3 or 9 o'clock, avoiding the dorsal neurovascular bundle and the ventral urethra.[1]
  2. Aspirate dark, deoxygenated blood. Typical ischemic corporal blood gas values are pO₂ below 30 mmHg, pCO₂ above 60 mmHg and pH below 7.25.[23][1]
  3. Irrigate with normal saline until bright-red blood returns, if it does not return with aspiration alone.
  4. Inject phenylephrine as above, then compress the corpora for about a minute.
  5. Repeat at the chosen interval with blood pressure and pulse monitoring during and after treatment.[1]

Muruve and Hosking treated 9 patients with 0.5 mg phenylephrine in 2 mL saline without aspiration or irrigation (8 detumesced after 1–6 injections), and concluded that routine aspiration was not necessary.[14] In the EAU review of non-sickle-cell-disease ischemic priapism, injection combined with aspiration, with or without irrigation, was successful in 70–100% of cases, versus 0–100% for sympathomimetic injection alone.[15] AUA/SMSNA 2022 recommends intracavernosal phenylephrine with corporal aspiration, with or without irrigation, as first-line therapy . EAU 2026 recommends aspiration and washout first for other ischemic episodes, adding a sympathomimetic if priapism persists ; after intracavernosal vasoactive injection, it recommends a sympathomimetic first .[1][2]

Efficacy and hemodynamic safety​

The first three rows report detumescence and hemodynamic observations from retrospective phenylephrine cohorts without comparative efficacy or cardiovascular safety testing. The fourth row is a systematic review including retrospective studies, prospective single-arm studies and randomized trials.[11][12][13][15]

StudyPopulationResult
Sidhu 201874 encounters (62% drug-induced); median phenylephrine dose 1,000 micrograms53/58 (91%) of those receiving phenylephrine detumesced at the bedside; small statistically significant falls in heart rate (−4.2/min) and blood pressure (−1.8/−5.4 mmHg); no adverse events[11]
Scarberry 2022123 patients; 97 received phenylephrine62/97 (63.9%) resolved without surgery. Resolution tracked duration (mean 8.8 h in those who resolved vs 57.3 h in those who did not). Resolution did not differ significantly between lower- and higher-dose groups (median 500 versus 2,000 micrograms per hour). 21 patients (17.1%) were judged at hemodynamic risk, and phenylephrine was stopped for hemodynamic change in 4[12]
Ridyard 201658 patients, 136 encounters; high-concentration phenylephrine, doses reported up to 12 mgNonsurgical detumescence in 86% of patients (94% counting repeat visits); all patients presenting within 36 hours resolved nonsurgically; no reported phenylephrine-related complications or associated symptoms in this series[13]
EAU systematic review 2024Non-sickle-cell-disease ischemic priapism; 41 retrospective studies, 3 prospective single-arm studies and 3 RCTsLonger time to resolution was associated with more erectile dysfunction at follow-up (30–70%), especially beyond 24 hours[15]

Hemodynamic effects may be under-reported, so document baseline and repeat blood pressure and pulse.[12] AUA/SMSNA identifies intracavernosal phenylephrine as the preferred agent, citing its efficacy and alpha-1 selectivity, which may limit cardiovascular effects.[24][1] Epinephrine and norepinephrine, which also act on β receptors, have been used historically and are largely replaced by phenylephrine for that reason.[24] Reported sympathomimetic side effects include angina and headache; case reports describe severe complications including subarachnoid hemorrhage and myocardial infarction with cardiogenic shock, although AUA notes that causation is uncertain in some reports.[23][24][1]

Avoid delays in definitive care​

  • EAU 2026 asks that management start as early as possible (within four to six hours) and follow a stepwise sequence : aspiration and washout until fresh red blood returns; a sympathomimetic injection if priapism persists; repeat both before any surgery . Distal shunting is the first surgical step , with peno-scrotal decompression as an alternative first-line option . Sympathomimetic injection replaces aspiration as the first step when priapism follows an intracavernosal vasoactive injection .[2]
  • Aspiration and phenylephrine are complementary. AUA Appendix A advises proceeding to definitive treatment when an erection persists despite repeated injections and aspiration or irrigation for approximately 1 hour; presentation beyond 36 hours may warrant earlier escalation.[1]
  • AUA/SMSNA recommends a distal corporoglanular shunt, with or without tunneling, after phenylephrine and aspiration fail . Consider tunneling if ischemia persists after a distal shunt . Evidence is inadequate to quantify the benefit of proximal shunting after distal-shunt failure . Persistent tumescence after shunting requires corporal blood gas or color duplex Doppler before repeat surgery .[1]
  • AUA/SMSNA advises counseling that erectile-function recovery is unlikely after an ischemic episode lasting more than 36 hours .[1] It permits consideration of a prosthesis in untreated ischemia lasting more than 36 hours or disease refractory to shunting, with or without tunneling , with discussion of early versus delayed placement .[1] EAU 2026 recommends prosthesis discussion after more than 48 hours of ischemia or disease refractory to injection therapy and distal shunting , describes implantation within the first three weeks as optimal when a prosthesis is chosen, and advises further delay after a shunt for wound healing and lower infection or erosion risk .[1][2]

Prolonged erection after an ED injection​

An erection lasting 4 hours or more requires immediate medical assessment. AUA/SMSNA 2022 instructs patients receiving ICI teaching or an in-office induced erection to return to the office or emergency department for an erection lasting more than 4 hours .[3] For post-injection erections lasting 4 hours or less that require intervention, it names intracavernosal phenylephrine as initial treatment , and recommends phenylephrine when conservative management fails .[1][3] Rigidity, duration and the injected agent guide treatment of earlier erections; partial erections do not necessarily count toward the four-hour criterion. Oral pseudoephedrine or terbutaline must not delay effective treatment; evidence for oral rescue is inconsistent. Avoid ice or cold exposure in sickle cell disease.[3][1]

In one placebo-controlled trial of 75 patients with prostaglandin E1-induced prolonged erections, detumescence occurred in 36% with terbutaline, 28% with pseudoephedrine and 12% with placebo; only terbutaline was significantly better than placebo.[16] The EAU review likewise rates oral β₂-agonists as mildly to moderately effective, and ice packs, exercise, cold enemas and ejaculation as less effective (1–55%).[15] Terbutaline can cause tremor, tachycardia and palpitations. EAU 2026 reports success of 30–60% in three placebo-controlled trials of injection-induced priapism and lists 5 mg orally for an erection lasting over 2.5 hours after an intracavernosal injection; use it cautiously with coronary disease, fluid overload, edema or hypokalemia.[2]

The prescribing injection service should provide a clear rescue or contact plan during ICI training. Home phenylephrine is reserved for selected patients with recurrent ischemic priapism who have specific training and an individualized plan. It aborts episodes; it does not prevent them.[3]

Recurrent ischemic (“stuttering”) priapism​

AUA/SMSNA 2022 advises informing patients that optimal prevention strategies are unknown , and that hormonal regulators may impair fertility and sexual function .[3] Balance episode burden, underlying disease, sexual function, fertility and adverse effects with the patient. EAU advises avoiding hormonal suppression before sexual maturation. EAU 2026 recommends managing each acute episode as ischemic priapism . Its weak recommendations cover hormonal therapy (GnRH agonists or antagonists) or antiandrogens for frequent relapses; digoxin, alpha-adrenergic agonists, baclofen, gabapentin or terbutaline only for frequent, uncontrolled relapses; and interim home sympathomimetic injection for acute episodes.[2] It notes little efficacy from oral baclofen, and describes digoxin at 0.25–0.5 mg daily in idiopathic cases.[2][3]

PDE5 inhibitors and the major randomized evidence​

Daily sildenafil or tadalafil has been used off-label for prevention; AUA/SMSNA describes conflicting efficacy, with observational reports suggesting fewer or shorter episodes.[3] The rationale is that in sickle cell disease and idiopathic recurrent priapism, reduced nitric oxide bioavailability and PDE5 dysregulation impair the mechanism that terminates an erection, and continuous low-level PDE5 inhibition is proposed to recondition that regulation.[17][25] The principle is regimented daily dosing, not on-demand use; Burnett's randomized trial gave sildenafil 50 mg daily, unrelated to sleep or sexual activity.[4] Start during a flaccid interval, not as treatment for an acute erection.[2]

EvidenceWhat it establishes
Burnett 2006: 7 patients (4 sickle cell, 3 idiopathic), retrospectiveSildenafil or tadalafil off-label: recurrences alleviated or resolved in 6/7; erectile function unchanged in 6 and improved in 1; no limiting adverse effects. Feasibility data only.[17]
Burnett 2014: 13 patients with sickle cell diseaseSildenafil 50 mg daily for 8 weeks did not improve the primary outcome versus placebo in the blinded phase. Improvement in 5/8 during open treatment was uncontrolled.[4]
Hou and Burnett 2021: 24 evaluable patients, retrospective (12 idiopathic, 11 sickle cell)Median 3 months of regimented PDE5 inhibitor: emergency department visits fell 4.4-fold, 22/24 (92%) reported improvement and 9 reported resolution. Among 17 who relapsed after stopping, priapism duration and frequency increased. Uncontrolled, short follow-up.[18]
Cochrane 2020: 3 trials, 102 participantsEvidence for preventing sickle-cell-associated episodes was low or very low certainty. Sildenafil may have little or no effect; etilefrine, ephedrine and stilboestrol remained uncertain. The review predates PIN.[5]
PIN, Idris 2025: 64 men with sickle cell anemiaHydroxyurea plus placebo versus hydroxyurea plus tadalafil: 2.5 versus 3.02 priapism events per participant-month (usual-care-to-tadalafil IRR 0.8, 95% CI 0.3–1.9), with no significant difference. This phase 2 feasibility trial had a median 10-month follow-up.[6]

See PDE5 inhibitors for contraindications and interactions.[6]

Ketoconazole with glucocorticoid replacement​

This is off-label specialist treatment, supported by small uncontrolled series. Hoeh and Levine reported on-treatment resolution in 16/17 patients; the absence of a comparison group prevents ranking it above other options.[7] AUA/SMSNA includes ketoconazole with prednisone among reported preventive approaches, with caution about liver toxicity and frequent liver-function testing.[7][3]

The authors' current regimen, described as their own, is ketoconazole 200 mg three times daily with prednisone 5 mg daily for 2 weeks, then ketoconazole 200 mg nightly for 6 months.[7] They stop at 6 months because most patients did not need to resume. On treatment, 16/17 had complete resolution and none needed an emergency visit for priapism; one patient stopped after 4 days because of nausea and vomiting.[7] Among the 14 men who discontinued ketoconazole (mean post-treatment follow-up 36.7 months), 11/14 (78.6%) still had partial or complete resolution, and 4/14 (29%) reported no further episodes.[7] An earlier series of 8 patients titrated ketoconazole and prednisone to a testosterone of about 200 ng/dL, with monthly review; mean testosterone fell from 468 to 275 ng/dL, and mean IIEF-5 was 24.8.[19]

Oral ketoconazole has boxed warnings for serious or fatal liver injury and QT prolongation, including life-threatening arrhythmias with interacting drugs.[8] It is contraindicated in acute or chronic liver disease. Check baseline liver tests and medication interactions, advise against alcohol and avoid other hepatotoxic drugs when possible; the US label calls for weekly ALT throughout treatment, with interruption if ALT exceeds the upper limit of normal, reaches 30% above baseline, or liver-injury symptoms develop.[8] The series' 600 mg/day ketoconazole induction exceeds the US tablet label's 400 mg/day recommended maximum for approved fungal indications; the label notes reduced adrenal corticosteroid secretion at 400 mg/day or higher and warns of adrenal insufficiency.[7][8] Suppressing testosterone also requires fertility and sexual-function counseling.[8]

Etilefrine​

Oral etilefrine, a mixed α- and β-adrenergic agonist[2], has been used mainly outside the United States. EAU 2026 quotes oral doses of 5–10 mg daily with response up to 72%, which differs from the dose range in the Okpala report below; a randomized trial found no difference between etilefrine and ephedrine.[2] In Okpala's series of 17 adults with sickle cell disease and one with sickle cell trait, 13/18 (72%) had a good response to etilefrine 50–100 mg daily; none developed hypertension or sexual dysfunction during 1–48 months of follow-up.[20] Virag combined preventive oral etilefrine with self-administered intracavernosal etilefrine for episodes lasting over 1 hour: in 6 patients, all were protected from acute episodes and 4 needed no injections.[21] Both are small uncontrolled series, and the Cochrane review rates the randomized etilefrine and ephedrine evidence as very low certainty.[5]

Other preventive approaches​

Pseudoephedrine, baclofen, dutasteride and androgen-suppressing agents have limited evidence. Ephedrine and etilefrine were compared with placebo in a Cochrane-included trial, with very low certainty of benefit. Drug selection and monitoring remain individualized; hormonal treatment may be unacceptable when fertility is a priority.[3][5]

Reported case-series dosing for the named 5-alpha-reductase inhibitors and antiandrogens: finasteride tapered from 5 to 3 to 1 mg daily over 120 days in 35 patients with sickle cell disease, and 1 mg daily in four patients or 1 mg twice daily in one patient in a separate five-patient pediatric sickle-cell series;[26][27] dutasteride 0.5 mg daily, tapered after response;[28] and low-dose bicalutamide, described as controlling recurrent priapism in a three-patient series (two with sickle cell disease and one with spinal cord injury) without major side effects reported.[29] A separate case report described tapering bicalutamide to weekly and then every-other-week dosing after daily sildenafil was added; earlier chronic bicalutamide had caused gynecomastia requiring mastectomy, reduced libido, and erectile dysfunction.[30] The mechanism of 5-alpha-reductase inhibitors in recurrent priapism is unclear. Central androgen ablation with intramuscular leuprolide acetate should seldom be used and only after informed discussion of its short- and long-term hormonal side effects, given the fertility and sexual-function trade-offs above.[29]

Sickle cell disease​

Coordinate with hematology. AUA/SMSNA advises against delaying standard acute ischemic priapism treatment for disease-specific systemic interventions and against exchange transfusion as primary treatment . Its discussion suggests considering simple packed-red-cell transfusion to a hemoglobin of 9–10 g/dL before general anesthesia if operative shunting is required; this is not an exchange-transfusion target or an automatic order for every episode. Longer-term hydroxyurea or transfusion decisions belong with the patient and hematologist.[3]

In PIN, both arms took hydroxyurea and priapism rates fell by 58.3% (usual care) and 66.3% (tadalafil) from prerandomization rates in a post hoc pre-post comparison.[6] Disease-modifying therapy decisions belong with the patient's hematologist for overall sickle cell disease care.[3][6] Among 40 trial participants with semen samples at baseline, trial exit and 3 months after stopping hydroxyurea, median sperm concentration, motility and normal morphology fell during treatment and returned to pretreatment levels after stopping; counsel men about fertility.[6]

Historical alternatives: methylene blue and mixed sympathomimetics​

Methylene blue inhibits guanylate cyclase and so blocks the nitric oxide-cGMP relaxation pathway. In Martínez Portillo's series, corporal blood was aspirated before a reported 5 mL methylene-blue injection; the dye was left for 5 minutes, aspirated, and followed by 5 minutes of penile compression.[9] The reported volume does not specify a drug dose.[9] Transient burning and blue discoloration of the penis are the main side effects.[9] A 2001 methylene-blue series included 12 patients: 10 had injection-induced erections and all resolved with methylene blue after aspiration; the two others (leukemia-associated and idiopathic high-flow) did not respond and needed phenylephrine and pudendal embolization respectively. In deHoll's 11-patient mixed-treatment series, 67% of methylene-blue recipients had immediate detumescence; all patients with injection- or trazodone-induced priapism responded.[22] EAU 2026 lists methylene blue (50–100 mg intracavernosally, left 5 minutes, then aspirated with 5 minutes of compression) as supported only by small retrospective series in short-term pharmacologically induced priapism; it should not delay established emergency treatment.[2] For its separate hemolysis and serotonergic interaction risks, see methylene blue.[2][9]

Treatment sequence at a glance​

SituationSequence
Acute ischemic priapismCorporal aspiration with or without irrigation and blood gas; intracavernosal phenylephrine with blood pressure and pulse monitoring; reassess after an unsuccessful cycle and escalate to a distal shunt (with tunneling if needed); prosthesis in selected prolonged or refractory cases.[10][1]
Prolonged erection after an ED injectionAssess duration, rigidity and the injected agent. AUA/SMSNA uses phenylephrine as initial treatment when intervention is needed at 4 hours or less; erections beyond 4 hours follow the acute ischemic pathway. EAU lists oral terbutaline for selected earlier injection-induced erections; oral treatment must not delay detumescence when urgent treatment is needed.[3][16][2]
Recurrent ischemic priapismTreat each acute episode as above; individualize prevention (regimented PDE5 inhibitor, ketoconazole with glucocorticoid, or other agents) with fertility counseling; consider selected home phenylephrine rescue; in sickle cell disease, coordinate hydroxyurea and other disease-modifying decisions with hematology.[3][6]

See Also​


References​

1. AUA/SMSNA. The Diagnosis and Management of Priapism (2022): acute ischemic recommendations and Appendices A–B. Official guideline.

2. EAU. Guidelines on Sexual and Reproductive Health, Limited Update March 2026, section 10 (priapism), Table 10.4 and sections 10.1.4 and 10.2.1.c. Current chapter.

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;208:43–52. doi:10.1097/JU.0000000000002767.

4. Burnett AL, Anele UA, Trueheart IN, Strouse JJ, Casella JF. Randomized controlled trial of sildenafil for preventing recurrent ischemic priapism in sickle cell disease. Am J Med. 2014;127:664–668. doi:10.1016/j.amjmed.2014.03.019.

5. 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.

6. 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;145:3101–3112. doi:10.1182/blood.2024027898.

7. Hoeh MP, Levine LA. Prevention of recurrent ischemic priapism with ketoconazole: evolution of a treatment protocol and patient outcomes. J Sex Med. 2014;11:197–204. doi:10.1111/jsm.12359.

8. Ketoconazole tablets. US prescribing information: boxed warning, contraindications, hepatotoxicity, adrenal insufficiency and interactions. DailyMed.

9. Martínez Portillo F, Hoang-Boehm J, Weiss J, Alken P, Jünemann K. Methylene blue as a successful treatment alternative for pharmacologically induced priapism. Eur Urol. 2001;39:20–23. doi:10.1159/000052407.

10. 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.

11. Sidhu AS, Wayne GF, Kim BJ, et al. The hemodynamic effects of intracavernosal phenylephrine for the treatment of ischemic priapism. J Sex Med. 2018;15:990–996. doi:10.1016/j.jsxm.2018.05.012.

12. Scarberry K, Deebel NA, Dutta R, et al. Safety and efficacy of phenylephrine administration for the treatment of ischemic priapism: an opportunity for quality improvement in periprocedural safety assessment. Urology. 2022;169:115–119. doi:10.1016/j.urology.2022.08.011.

13. Ridyard DG, Phillips EA, Vincent W, Munarriz R. Use of high-dose phenylephrine in the treatment of ischemic priapism: five-year experience at a single institution. J Sex Med. 2016;13:1704–1707. doi:10.1016/j.jsxm.2016.09.010.

14. Muruve N, Hosking DH. Intracorporeal phenylephrine in the treatment of priapism. J Urol. 1996;155:141–143. doi:10.1016/s0022-5347(01)66575-3. PMID 7490814.

15. Capogrosso P, Dimitropolous K, Russo GI, et al. Conservative and medical treatments of non-sickle cell disease-related ischemic priapism: a systematic review by the EAU Sexual and Reproductive Health Panel. Int J Impot Res. 2024;36:6–19. doi:10.1038/s41443-022-00592-2.

16. Lowe FC, Jarow JP. Placebo-controlled study of oral terbutaline and pseudoephedrine in management of prostaglandin E1-induced prolonged erections. Urology. 1993;42:51–53. doi:10.1016/0090-4295(93)90338-b.

17. Burnett AL, Bivalacqua TJ, Champion HC, Musicki B. Feasibility of the use of phosphodiesterase type 5 inhibitors in a pharmacologic prevention program for recurrent priapism. J Sex Med. 2006;3:1077–1084. doi:10.1111/j.1743-6109.2006.00333.x.

18. Hou LT, Burnett AL. Regimented phosphodiesterase type 5 inhibitor use reduces emergency department visits for recurrent ischemic priapism. J Urol. 2021;205:545–553. doi:10.1097/JU.0000000000001365.

19. Abern MR, Levine LA. Ketoconazole and prednisone to prevent recurrent ischemic priapism. J Urol. 2009;182:1401–1406. doi:10.1016/j.juro.2009.06.040.

20. Okpala I, Westerdale N, Jegede T, Cheung B. Etilefrine for the prevention of priapism in adult sickle cell disease. Br J Haematol. 2002;118:918–921. doi:10.1046/j.1365-2141.2002.03691.x.

21. Virag R, Bachir D, Lee K, Galacteros F. Preventive treatment of priapism in sickle cell disease with oral and self-administered intracavernous injection of etilefrine. Urology. 1996;47:777–781. doi:10.1016/s0090-4295(96)00027-1.

22. deHoll JD, Shin PA, Angle JF, Steers WD. Alternative approaches to the management of priapism. Int J Impot Res. 1998;10:11–14. doi:10.1038/sj.ijir.3900308.

23. Broderick GA, Kadioglu A, Bivalacqua TJ, et al. Priapism: pathogenesis, epidemiology, and management. J Sex Med. 2010;7:476–500. doi:10.1111/j.1743-6109.2009.01625.x.

24. Bobo GA, Almajed W, Conlon J, et al. An overview of emergency pharmacotherapy for priapism. Expert Opin Pharmacother. 2022;23:1371–1380. doi:10.1080/14656566.2022.2099271.

25. 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;390:203–212. doi:10.1124/jpet.123.001962.

26. Rachid-Filho D, Cavalcanti AG, Favorito LA, Costa WS, Sampaio FJ. Treatment of recurrent priapism in sickle cell anemia with finasteride: a new approach. Urology. 2009;74(5):1054–1057. doi:10.1016/j.urology.2009.04.071.

27. Barroso U Jr, Marques TC, Novaes HF. Finasteride for recurrent priapism in children and adolescents: a report on 5 cases. Int Braz J Urol. 2012;38(5):682–686. doi:10.1590/s1677-55382012000500014.

28. Baker RC, Bergeson RL, Yi YA, Ward EE, Morey AF. Dutasteride in the long-term management of stuttering priapism. Transl Androl Urol. 2020;9(1):87–92. doi:10.21037/tau.2019.07.15.

29. Dahm P, Rao DS, Donatucci CF. Antiandrogens in the treatment of priapism. Urology. 2002;59:138. doi:10.1016/s0090-4295(01)01492-3.

30. Pierorazio PM, Bivalacqua TJ, Burnett AL. "Daily phosphodiesterase type 5 inhibitor therapy as rescue for recurrent ischemic priapism after failed androgen ablation." J Androl. 2011;32(4):371–374. doi:10.2164/jandrol.110.011890