AUTHOR AND EDITOR INFORMATION

Section 1 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Further Reading
• Multimedia
• References

INTRODUCTION

Section 2 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Further Reading
• Multimedia
• References

Background

Priapism is defined as an abnormal persistent erection of the penis. It is an involuntary prolonged erection unrelated to sexual stimulation and unrelieved by ejaculation. As with many medical emergencies, the saying "time is tissue" holds true for priapism. This condition is a true urologic emergency, and early intervention allows the best chance for functional recovery.

Pathophysiology

The penis is composed of 3 corporeal bodies: 2 corpora cavernosa and 1 corpus spongiosum. Erection is the result of smooth-muscle relaxation and increased arterial flow into the corpora cavernosa, causing engorgement and rigidity (see Image 1).

Engorgement of the corpora cavernosa compresses the venous outflow tracts (ie, subtunical venules), trapping blood within the corpora cavernosa. The major neurotransmitter that controls erection is nitric oxide, which is secreted by the endothelium that lines the corpora cavernosa (see Image 2). These events occur in both normal and pathologic erections. The pathophysiology of priapism involves failure of detumescence and is the result of the underregulation of arterial inflow (ie, high flow) or, more commonly, the failure of venous outflow (ie, low flow). Priapism typically involves engorgement of corpora cavernosa. The corpus spongiosum is typically not engorged.

Priapism must be defined as either a low-flow (ischemic) or a high-flow (nonischemic) type because the causes and treatments for these 2 types are different. Low-flow priapism, which is by far the most common type, is a failure of the detumescence mechanism due to (1) an excessive release of neurotransmitters, (2) blockage of draining venules (eg, mechanical interference in sickle cell crisis, leukemia, or excessive use of intravenous parenteral lipids), (3) paralysis of the intrinsic detumescence mechanism, or (4) prolonged relaxation of the intracavernous smooth muscles (most often caused by the use of exogenous smooth-muscle relaxants such as injectable intracavernosal prostaglandin E1).

Prolonged low-flow priapism leads to a painful ischemic state, which can cause fibrosis of the corporeal smooth muscle and cavernosal artery thrombosis. The degree of ischemia is a function of the number of emissary veins and the duration of occlusion. Light-microscopy studies conducted early on demonstrated that corporeal tissue becomes thickened, edematous, and fibrotic after days of priapism. Further studies with electron microscopy have demonstrated trabecular interstitial edema after 12 hours of priapism and destruction of sinusoidal endothelium, exposure of the basement membrane, and thrombocyte adherence after 24 hours of priapism. At 48 hours, thrombi in the sinusoidal spaces and smooth-muscle cell histopathologic findings varied from necrosis to fibroblastlike cell transformation. Priapism for longer than 24 hours is associated with the likelihood of permanent impotence.

High-flow priapism, in contrast, is the result of uncontrolled arterial inflow from a fistula between the cavernosal artery and the corpus cavernosum. This is generally secondary to blunt or penetrating injury to the penis or perineum. Differentiation between these 2 types of priapism is accomplished by taking a thorough history, performing a careful physical examination, and measuring the oxygen content of blood within the corpora cavernosa by penile blood gas (PBG) analysis (see Workup). The presence of bright red blood during aspiration is a helpful but not pathognomonic finding of high-flow priapism.

Frequency

United States

The frequency of priapism depends on the population being considered. The combination of intracavernosal agents and other drugs is the cause of approximately 21-80% of all adult priapism. Agents used to treat erectile dysfunction are common causes of adult priapism in the Western world. The overall rate of priapism in persons using these agents ranges from 0.05-6%. This group tends to be better educated about the risk of priapism; therefore, they seek treatment earlier. At other centers, sickle cell disease (SCD) and sickle cell trait predominate as the cause of adult priapism. The rate of priapism in adults with SCD is as high as 89%. Approximately two thirds of all pediatric patients who have priapism also have SCD. The rate of priapism among children with SCD is as high as 27%.

Mortality/Morbidity

• Priapism is painful at onset. Corporeal fibrosis due to persistent priapism can result in deep-tissue infections of the penis.
• The major chronic morbidity associated with all types of priapism is persistent erectile dysfunction and impotence.
• The duration of symptoms is the most important factor affecting outcome. A recent Scandinavian study reported that 92% of patients with priapism for less than 24 hours remained potent, while only 22% of patients with priapism that lasted longer than 7 days remained potent.¹

Race

• Priapism is common in African Americans with SCD.

Sex

• Priapism occurs exclusively in males.

Age

• Priapism can occur in males of any age group, with peaks at age 5-10 years and 20-50 years.
• Among patients with SCD, the prevalence is higher in men aged 19-21 years.

CLINICAL

Section 3 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Further Reading
• Multimedia
• References

History

Patients with priapism report a persistent erection. The symptoms depend on the type of priapism and the duration of engorgement.

• Low-flow, ischemic-type priapism is generally painful, although the pain may disappear with prolonged priapism.
• High-flow, nonischemic priapism is generally not painful. This type of priapism is associated with blunt or penetrating injury to the perineum. It may manifest in an episodic manner.
• Aspects of history are as follows:  
• • Erection: Duration of longer than 4 hours is consistent with priapism.
  • Duration of pain
  • Similar prior episodes
  • Genitourinary (GU) trauma
  • Medical history (eg, sickle cell disease [SCD]): Onset occurs during sleep, when relative oxygenation decreases.
  • Medication and/or recreational drug use, especially the antidepressant trazodone, intracavernosal injections of prostaglandin E1 used to treat impotence, and illicit cocaine injection into the penis
  • History of malignancy (prostate cancer)
  • Penile prosthesis: The permanent erection that occurs with some penile prostheses may mimic priapism.
  • Recent urologic surgery
• Aspects of history in high-flow priapism are as follows:
• • Not painful
  • May be sexually active
  • Straddle injury usually the initiating event
  • Chronic recurrent presentation
  • Generally not caused by medication
• Aspects of history of low-flow priapism are as follows:
• • Painful
  • Inactive sexually and without desire
  • No history of trauma
  • Usually presents to emergency department (ED) within hours
  • Associated with substance abuse or vasoactive penile injections
  • Rarely caused by leukemia, fat embolism, acute spinal cord injury, or (extremely rare) cancer metastases to the corporeal bodies

Physical

Obvious erection is the key physical finding in any case of priapism. Penile priapism generally involves only the paired corpora cavernosa, with the glans and corpora spongiosum remaining flaccid or softly distended without rigidity. Careful physical examination may reveal specific causal factors. Remember that no single pathology excludes all others; therefore, a thorough history and physical examination should address the patient as a whole.

• Aspects of the physical examination are as follows:
• • Penile color, rigidity, and sensation (soft glans vs firm glans)
  • Penile discharge, lesions, or both
  • Evidence of local trauma
  • Presence of prosthetic devices: Hardware malfunction may cause pseudopriapism.
  • Regional lymphadenopathy (ie, metastatic disease)
  • Rectal tone: High spinal cord lesions or stenosis may cause priapism.
• Aspects of the physical examination consistent with high-flow priapism are as follows:
• • Adequate arterial flow
  • Well-oxygenated corpora
  • Evidence of trauma
• Aspects of the physical examination consistent with low-flow priapism are as follows:
• • Rigid erection
  • Ischemic corpora as indicated by dark blood upon corporeal aspiration
  • No evidence of trauma

Causes

Priapism can result from idiopathic or secondary causes. In the United States, the most common cause of priapism in the adult population involves agents used to treat erectile dysfunction. The most common cause of priapism in the pediatric population is SCD. Internationally, the most common cause is idiopathic.

• Uncommonly, both low- and high-flow priapism are idiopathic in nature.
• Secondary causes of low-flow priapism are as follows:  
• • Thromboembolic/hypercoagulable states
  • • Sickle cell anemia - Polycythemia
    • Thalassemia
    • Total parenteral nutrition
    • Fabry disease
    • Dialysis
    • Vasculitis
    • Fat embolism (after multiple long-bone fractures or after iatrogenic intravenous lipids as part of total parenteral nutrition)
  • Neurogenic disease
  • • Spinal cord stenosis (ie, trauma to the medulla)
    • Autonomic neuropathy and cauda equina compression
  • Neoplastic disease (metastatic to the penis or obstructive to venous outflow)
  • • Prostate cancer and GU (highest risk) bladder cancer
    • Hematological (leukemia)
    • Renal carcinoma
    • Melanoma
  • Pharmacologic causes
  • • Intracavernosal agents - Papaverine, phentolamine, prostaglandin E1
    • Intraurethral pellets (ie, medicated urethral system for erection with intracavernosal prostaglandin E1)
    • Antihypertensives - Ganglion-blocking agents (eg, guanethidine), arterial vasodilators (eg, hydralazine), alpha-antagonists (eg, prazosin), calcium channel blockers
    • Psychotropics - Phenothiazine, butyrophenones, hypnotics (eg, mesoridazine, perphenazine), trazodone, selective serotonin reuptake inhibitors (eg, fluoxetine, sertraline)²
    • Anticoagulants - Heparin, warfarin
    • Recreational drugs - Cocaine, marijuana, ethanol
    • Hormones - Gonadotropin-releasing hormone (GnRH), tamoxifen, testosterone
    • Herbal medicine - Ginkgo biloba with concurrent use of antipsychotic agents³
    • Miscellaneous medications - Metoclopramide, omeprazole, penile injection of cocaine, epidural infusion of morphine and bupivacaine⁴
• Secondary causes of high-flow priapism are as follows:
• • GU trauma
  • • Straddle injury
    • Intracavernous injections with direct cavernosal artery injury
  • Drugs - Cocaine
• Other causes of priapism (rare) are as follows:
• • Amyloidosis (massive amyloid infiltration)
  • Gout (one case report)
  • Carbon monoxide poisoning
  • Malaria
  • Black widow spider venom
  • Asplenia

DIFFERENTIALS

Section 4 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Further Reading
• Multimedia
• References

Other Problems to be Considered

The diagnosis of priapism is straightforward, depending on the physical findings. Pathologic states associated with priapism give rise to the differential diagnosis. Some of the major considerations are as follows:

Intracavernosal agents used to treat impotence
Oral agents used to treat impotence
Sickle cell disease (SCD)
GU trauma
Medications
Cocaine
Spinal stenosis
High spinal cord injury

WORKUP

Section 5 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Further Reading
• Multimedia
• References

Lab Studies

• Complete blood cell count: This is performed to determine if the patient has anemia, leukocytosis, or thrombocytosis.
• Plasma thromboplastin or activated partial thromboplastin time: Priapism may require surgical intervention if medical treatment fails.
• Blood type and hold: Exchange transfusion may be necessary to treat underlying sickle cell disease (SCD).
• PBG measurement  
• • Test results allow differentiation between high- and low-flow priapism.
  • Low-flow PBG findings may include a pH of less than 7.0, a PCO₂ of greater than 60 mm Hg, and a PO₂ of less than 30 mm Hg. Variation depends on duration.
  • High-flow PBG findings should reflect normal arterial values.

Imaging Studies

• Perform penile duplex Doppler ultrasonography to help identify and locate a fistula in patients with high-flow priapism.
• Perform pelvic angiography to help confirm the fistula location, followed by embolization in patients with high-flow priapism.
• Perform chest radiography or CT scanning if the history is consistent with a malignant or metastatic condition.

Other Tests

• Perform an ECG if the patient is older than 55 years, has a history of cardiac disease, or is a possible surgical candidate.

TREATMENT

Section 6 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Further Reading
• Multimedia
• References

Medical Care

All cases of priapism require prompt consultation with a GU medicine specialist. When treating priapism in the ED, physicians must first differentiate between the high- and low-flow varieties. With appropriate training and protocols, ED personnel may begin treatment with saline irrigation and injection of alpha-agonist drugs such as phenylephrine.

• High-flow priapism  
• • A painless erection with PBG findings that approximate normal arterial values differentiates high-flow priapism from the low-flow variety. Blunt or penetrating trauma to the penis or perineum causes this condition.
  • Treatment focuses on identification and obliteration of secondary fistulas. Penile duplex ultrasonography with angiographic confirmation helps to identify the location of general fistulae; this can be followed by selective arterial embolization, using autologous blood clot, gelatin sponge, microcoils, or chemicals.^{5, 6, 7}              
  • Surgical intervention may be necessary.
• Sickle cell disease
• • Treatment of sickle cell disease (SCD) deserves special mention.
  • Key steps in the management of SCD-associated priapism include oxygenation, analgesics (eg, intravenous morphine), hydration, alkalization, and exchange transfusions to increase the hematocrit value to greater than 30% and to decrease the hemoglobin-S value to less than 30%. Although conservative management has commonly been advocated in the literature, several studies have questioned the efficacy, and most experts advocate emergent surgical decompression when conservative management fails.
• Low-flow ischemic priapism  
• • Most priapism cases are the low-flow ischemic type. Treatment should progress in a stepwise fashion, involving supportive care and the identification and treatment of reversible causes.
  • Management of recurrent priapism should focus on prevention of future episodes, while management of each episode should follow the specific treatment recomendations.⁷
  • A trial of GnRH agonist or antiandrogens may be used to manage recurrent priapism but should be avoided in patients who have not fully matured sexually.⁷
  • Some experts recommend oral pseudoephedrine or oral beta-agonists such as terbutaline, especially in patients using vasoactive agents to treat erectile dysfunction.  A review of the literature did not reveal support for its efficacy; however, a theoretical benefit may be gained based on its alpha-agonist properties.
  • Intracavernosal phenylephrine (Neo-Synephrine) is the drug of choice and first-line treatment of low-flow priapism because the drug has almost pure alpha-agonist effects and minimal beta activity. In short-term priapism (<6 h), especially for drug-induced priapism, intracavernosal injection of phenylephrine alone may result in detumescence. Use a mixture of 1 ampule of phenylephrine (1 mL:1000 mcg) and dilute it with an additional 9 mL of normal saline. Using a 29-gauge needle, inject 0.3-0.5 mL into the corpora cavernosa, waiting 10-15 minutes between injections. Vital signs should be monitored, and compression should be applied to the area of injection to help prevent hematoma formation.
  • The next step in the treatment of low-flow priapism is aspiration of the corpora cavernosa followed by saline irrigation and, if necessary, injection of an alpha-adrenergic agonist (eg, phenylephrine). Placement of a penile nerve block with a long-acting local anesthetic such as bupivacaine (Sensorcaine) without epinephrine increases patient comfort and improves patient cooperation with the sometimes-painful penile aspiration procedure.
  • Aspiration is best performed by placing a large-bore intravenous catheter (ie, 16- to 18-gauge) into the lateral aspect of the corpus cavernosum. An alternate approach is through the glans penis, but this approach generally is not necessary because of the efficacy of the lateral approach. A unilateral approach is adequate because of the vascular channels between the 2 corpora cavernosa. Local lidocaine or a penile ring block may be used for anesthesia. Aspiration may be difficult because of the sludging of blood within the corpus cavernosum. Saline irrigation and repeated aspirations may improve flow dynamics.
  • If the aforementioned interventions are unsuccessful, a diluted solution of phenylephrine may be used for irrigation. A diluted solution can be infused 10-20 mL at a time. If unable to irrigate with the diluted solution, straight intracorporeal injection of 200- to 500-mcg aliquots may be administered, taking care to not exceed a maximum dose of 1500 mcg. Compression must be applied. If phenylephrine is not available, epinephrine can be used. However, epinephrine has more adverse effects and is considered second-line treatment.
  • If medical treatment fails, the condition warrants surgical intervention.

Surgical Care

• A transglanular to corpus cavernosal scalpel or needle-core biopsy (Ebbehoj or Winter technique) is the first reasonable approach for refractory cases (see Image 3). A unilateral shunt is often effective. Bilateral shunts are used only if necessary (usually apparent after 10 min).
• The El-Ghorab procedure is a more aggressive open surgical cavernosal shunt and is indicated if the Winter shunt fails.
• Quackel shunts (see Image 4) are cavernosal-spongiosum shunts (unilateral or bilateral) and are performed via a perineal approach. Such shunts are rarely effective if a more distal shunt has already failed (eg, El-Ghorab procedure) because thrombosis of the corpora is usually already present.
• A Grayhack shunt (see Image 5) is a cavernosal-saphenous vein shunt (rarely necessary or indicated).

Consultations

• Urologist
• Cardiologist (for patients with cardiac disease or hypertension)
• Hematologist (priapism as a complication of SCD)

MEDICATION

Section 7 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Further Reading
• Multimedia
• References

The goals of pharmacotherapy are to reduce morbidity and to restore sexual function.

Drug Category: Adrenergic agonists

Primary benefit in treatment of priapism is vasoconstrictive properties.

FOLLOW-UP

Section 8 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Further Reading
• Multimedia
• References

Further Inpatient Care

• Patients with priapism that is not responsive to treatment in the ED or those who have priapism of uncertain etiology should see a urologist for further treatment and workup.

Complications

• Erectile dysfunction
• Impotence
• Infection (secondary to trauma or possibly as a result of treatment)

Prognosis

• Prognosis depends on the duration of symptoms, the patient's age, and the underlying pathology. The time to treatment is the single most important factor affecting outcome.

Patient Education

• Education is the best way to avoid undesirable outcomes.
• • Any high-risk patient, especially a person using oral or intracavernosal agents for the treatment of impotence, must understand that a persistent erection and the need for prompt medical attention are possibilities.
  • Patients presenting with priapism deserve special counseling, beginning with the first episode of priapism.
  • A patient must understand that a poor outcome is possible despite appropriate and timely management.
• For excellent patient education resources, visit eMedicine's Erectile Dysfunction Center. Also, see eMedicine's patient education articles Impotence/Erectile Dysfunction and Erectile Dysfunction FAQs.

MISCELLANEOUS

Section 9 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Further Reading
• Multimedia
• References

Medical/Legal Pitfalls

• The potential medical and legal pitfalls deserve special attention in the treatment of priapism. Meticulous documentation is essential and helps protect the physician from future litigation by a patient who may be upset by a poor outcome despite appropriate management and careful counseling at the time of treatment. Prompt treatment and referral to a urologist, as necessary, is encouraged. At least 50% of patients with priapism have persistent impotence, either because of the priapism event or its treatment, and legal liability exposure is higher than that seen in many other urologic diseases.

FURTHER READING

Section 10 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Further Reading
• Multimedia
• References

For more information, see Medscape’s Erectile Dysfunction Resource Center.

MULTIMEDIA

Section 11 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Further Reading
• Multimedia
• References

Media file 1:  Priapism. Corporeal relaxation causes external pressure on the emissary veins exiting the tunica albuginea, trapping blood in the penis and causing erection.
	View Full Size Image
Media type:  Image

Media file 2:  Priapism. Sexual stimulation causes the release of nitric oxide (NO) via stimulation of nonadrenergic noncholinergic neurons. NO-activated intracellular guanylate cyclase, converting guanosine triphosphate (GTP) to cyclic guanosine monophosphate (cGMP), causes relaxation of cavernosal arteries and increased penile blood flow, resulting in erection.
	View Full Size Image
Media type:  Image

Media file 3:  Priapism. Winter shunt placed by biopsy needle, usually under local anesthetic.
	View Full Size Image
Media type:  Image

Media file 4:  Priapism. Proximal cavernosal-spongiosum shunt (Quackel shunt) surgically connects the proximal corpora cavernosa to the corpora spongiosum.
	View Full Size Image
Media type:  Image

Media file 5:  Priapism. Proximal cavernosal-saphenous shunt (Grayhack shunt) surgically connects the proximal corpora cavernosum to the saphenous vein.
	View Full Size Image
Media type:  Image

REFERENCES

Section 12 of 12

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Further Reading
• Multimedia
• References

1. Kulmala RV, Lehtonen TA, Tammela TL. Preservation of potency after treatment for priapism. Scand J Urol Nephrol. Aug 1996;30(4):313-6. [Medline].
2. Casiano H, Globerman D, Enns MW. Recurrent priapism during treatment with clozapine, quetiapine and haloperidol. J Psychopharmacol. Nov 2007;21(8):898-9. [Medline].
3. Lin YY, Chu SJ, Tsai SH. Association between priapism and concurrent use of risperidone and Ginkgo biloba. Mayo Clin Proc. Oct 2007;82(10):1289-90. [Medline].
4. Ruan X, Couch JP, Shah RV, Liu H, Wang F, and Chiravuri S. Priapism - A Rare Complication Following Continuous Epidural Morphine and Bupivacaine Infusion. Pain Physician. Sep 2007;10(5):707-711. [Medline].
5. Kim KR, Shin JH, Song HY, Ko GY, Yoon HK, Sung KB, et al. Treatment of high-flow priapism with superselective transcatheter embolization in 27 patients: a multicenter study. J Vasc Interv Radiol. Oct 2007;18(10):1222-6. [Medline].
6. Hellstrom WJ, Derosa A, Lang E. The use of transcatheter superselective embolization to treat high flow priapism (arteriocavernosal fistula) caused by straddle injury. J Urol. Sep 2007;178(3 Pt 1):1059. [Medline].
7. American Urological Association, Inc.: 2003. Guideline on the management of priapism. Available at http://www.auanet.org/guidelines/main_reports/priapism/online.pdf.
8. Agrawal DK, Jha S, Verma A, Tripathi AK, Singh BN. Priapism, complicating chronic myeloid leukemia--a case report. Indian J Cancer. Mar 1991;28(1):51-2. [Medline].
9. Atala A, Amin M, Harty JI, Liu YK, Keeling MM. Priapism associated with asplenic state. Urology. Oct 1992;40(4):371-3. [Medline].
10. Baba H, Furusawa N, Tanaka Y, Imura S, Tomita K. Intermittent priapism associated with lumbar spinal stenosis. Int Orthop. Jun 1994;18(3):150-3. [Medline].
11. Banos JE, Bosch F, Farre M. Drug-induced priapism. Its aetiology, incidence and treatment. Med Toxicol Adverse Drug Exp. Jan-Feb 1989;4(1):46-58. [Medline].
12. Baruchel S, Rees J, Bernstein ML, Goodyer P. Relief of sickle cell priapism by hydralazine. Report of a case. Am J Pediatr Hematol Oncol. Feb 1993;15(1):115-6. [Medline].
13. Bastuba MD, Saenz de Tejada I, Dinlenc CZ, Sarazen A, Krane RJ, Goldstein I. Arterial priapism: diagnosis, treatment and long-term followup. J Urol. May 1994;151(5):1231-7. [Medline].
14. Bochinski DJ, Deng DY, Lue TF. Management of Priapism. AUA Update Series. 2004;23:Lesson 3.
15. Bos SD, Buys GA. Treatment of priapism with ethyl chloride spray after failed intracavernous injection with adrenaline. Br J Urol. Nov 1994;74(5):677-8. [Medline].
16. Dogra PN, Wadhwa SN, Mehta VK. Vivax malaria causing priapism. J Assoc Physicians India. Jul 1991;39(7):571-2. [Medline].
17. Dore F, Bonfigli S, Pardini S, Pirozzi F, Longinotti M. Priapism in thalassemia intermedia. Haematologica. Nov-Dec 1991;76(6):523. [Medline].
18. Dutertre JP, Soutif D, Jonville AP, Cadenne M, Valat JP, Autret E. Sexual disturbances during omeprazole therapy. Lancet. Oct 19 1991;338(8773):1022. [Medline].
19. Ekström B, Olsson AM. Priapism in patients treated with total parenteral nutrition. Br J Urol. Feb 1987;59(2):170-1. [Medline].
20. Fernando IN, Tobias JS. Priapism in patient on tamoxifen. Lancet. Feb 25 1989;1(8635):436. [Medline].
21. Flanagan NG, Jain A, Ridway JC. Priapism in myeloma. Clin Lab Haematol. 1987;9(2):209-10. [Medline].
22. Fowler JE Jr, Koshy M, Strub M, Chinn SK. Priapism associated with the sickle cell hemoglobinopathies: prevalence, natural history and sequelae. J Urol. Jan 1991;145(1):65-8. [Medline].
23. Gupta S, Moreland RB, Munarriz R, Daley J, Goldstein I, Saenz de Tejada I. Possible role of Na(+)-K(+)-ATPase in the regulation of human corpus cavernosum smooth muscle contractility by nitric oxide. Br J Pharmacol. Oct 1995;116(4):2201-6. [Medline].
24. Hamre MR, Harmon EP, Kirkpatrick DV, Stern MJ, Humbert JR. Priapism as a complication of sickle cell disease. J Urol. Jan 1991;145(1):1-5. [Medline].
25. Hauri D, Spycher M, Brühlmann W. Erection and priapism: a new physiopathological concept. Urol Int. 1983;38(3):138-45. [Medline].
26. Hidalgo Ovejero AM, Garcia Mata S, Sauras Herranz MA, Maravi Petri E, Martinez Grande M. Intermittent priapism in spinal stenosis. Acta Orthop Belg. 1991;57(2):192-4. [Medline].
27. Jiva T, Anwer S. Priapism associated with chronic cocaine abuse. Arch Intern Med. Aug 8 1994;154(15):1770. [Medline].
28. Keoghane SR, Sullivan ME, Miller MA. The aetiology, pathogenesis and management of priapism. BJU Int. Jul 2002;90(2):149-54. [Medline].
29. Kim N, Azadzoi KM, Goldstein I, Saenz de Tejada I. A nitric oxide-like factor mediates nonadrenergic-noncholinergic neurogenic relaxation of penile corpus cavernosum smooth muscle. J Clin Invest. Jul 1991;88(1):112-8. [Medline].
30. Lee M, Cannon B, Sharifi R. Chart for preparation of dilutions of alpha-adrenergic agonists for intracavernous use in treatment of priapism. J Urol. Apr 1995;153(4):1182-3. [Medline].
31. Levine JF, Saenz de Tejada I, Payton TR, Goldstein I. Recurrent prolonged erections and priapism as a sequela of priapism: pathophysiology and management. J Urol. Apr 1991;145(4):764-7. [Medline].
32. Levine LA, Guss SP. Gonadotropin-releasing hormone analogues in the treatment of sickle cell anemia-associated priapism. J Urol. Aug 1993;150(2 Pt 1):475-7. [Medline].
33. Lue TF. Physiology of erection and pathophysiology of impotence. In: Walsh PC, Retik AB, Stamey TA, Vaughan ED, eds. Campbell's Urology. 6^th ed. Philadelphia, Pa: WB Saunders; 1992:702.
34. Lue TF. Physiology of penile erection and pathophysiology of erectile dysfunction and priapism. In: Walsh PC, Retik AB, eds. Campbell's Urology. 8^th ed. Philadelphia, Pa: WB Saunders; 2002:1591-618.
35. Melman A, Christ GJ, Hirsch MS. Anatomy and physiology of the penis. In: Bennett AH, ed. Impotence: Diagnosis and Management of Erectile Dysfunction. Philadelphia, Pa: WB Saunders; 1994:18-30.
36. Papadopoulos I, Kelâmi A. Priapus and priapism. From mythology to medicine. Urology. Oct 1988;32(4):385-6. [Medline].
37. Parrillo SJ, Manfrey S. Idiopathic priapism treated with inhalation of amyl nitrite. Ann Emerg Med. Apr 1983;12(4):226-7. [Medline].
38. Ruch W, Jenny P. Priapism following testosterone administration for delayed male puberty. Am J Med. Feb 1989;86(2):256. [Medline].
39. Saenz de Tejada I, Ware JC, Blanco R, Pittard JT, Nadig PW, Azadzoi KM, et al. Pathophysiology of prolonged penile erection associated with trazodone use. J Urol. Jan 1991;145(1):60-4. [Medline].
40. Stackl W, Mee SL. Priapism. In: Krane RJ, Siroky MB, Firzpatrick JM, eds. Clinical Urology. Philadelphia, Pa: Lippincott, Williams & Wilkins; 1994:1245-58.
41. Steers WD, Selby JB Jr. Use of methylene blue and selective embolization of the pudendal artery for high flow priapism refractory to medical and surgical treatments. J Urol. Nov 1991;146(5):1361-3. [Medline].
42. Stothers L, Ritchie B. Priapism in the newborn. Can J Surg. Jun 1992;35(3):325-6. [Medline].
43. Velek M, Stanford GK, Marco L. Priapism associated with concurrent use of thioridazine and metoclopramide. Am J Psychiatry. Jun 1987;144(6):827-8. [Medline].
44. Vilke GM, Harrigan RA, Ufberg JW, Chan TC. Emergency evaluation and treatment of priapism. J Emerg Med. Apr 2004;26(3):325-9. [Medline].
45. Winter CC, McDowell G. Experience with 105 patients with priapism: update review of all aspects. J Urol. Nov 1988;140(5):980-3. [Medline].

Article Last Updated: Mar 3, 2008