American Urological Association - Management of Priapism


Home Guidelines Clinical Guidelines Priapism (2003; Reviewed and Validity Confirmed 2010)

Management of Priapism

Published 2003; Reviewed and Validity Confirmed 2010

Unabridged version of this Guideline [pdf]

Panel Members

Drogo K. Montague, MD, Co-Chairman; Jonathan Jarow, MD, Co-Chairman; Gregory A. Broderick, MD; Roger R. Dmochowski, MD; Jeremy PW Heaton, MD; Tom F. Lue, MD; Ajay Nehra, MD; Ira D. Sharlip, MD


Priapism, a relatively uncommon disorder, is a medical emergency. Although not all forms of priapism require immediate intervention, ischemic priapism is associated with progressive fibrosis of the cavernosal tissues and erectile dysfunction.1, 2 Thus, all patients with priapism should be evaluated emergently in order to intervene as early as possible in those patients with ischemic priapism. The goal of the management of all patients with priapism is to achieve detumescence and preserve erectile function. Unfortunately, some of the treatments aimed at correcting priapism have the potential complication of erectile dysfunction. Therefore, the currently employed treatment modalities for priapism represent a range of options. These options are applied in a step-wise pattern with increasing invasiveness and risk balanced against the likelihood of prolonged ischemia and permanent damage to the corpora cavernosa if treatment is absent or delayed.

Because priapism is rare and usually unpredictable, the literature related to its management is neither voluminous nor rigorous, comprising mostly case reports and small case series rather than controlled trials. As a result, the relative efficacy and safety of different treatments are not clear. The purpose of this guideline is to provide physicians with a consensus of principles and strategies for the management of priapism based on the current state of both clinical practice and the medical literature.

Significant advances in the study of erectile physiology during the 1980s and 1990s have led to a better understanding of the pathophysiology of priapism and its management. For instance, prior to the discovery of pharmacological stimulation of an erection with vasodilators and the subsequent development of tests for penile blood flow, there was little awareness of the difference between ischemic and nonischemic priapism and the role of vasoconstrictor agents (alpha adrenergic sympathomimetics) in the treatment of these disorders. Much of the literature on the management of priapism was published in an era in which the management of patients with priapism was largely empirical and sometimes misguided due to a lack of understanding of erectile physiology. However, even in the absence of effective treatment, it was recognized that, given enough time, ischemic priapism would eventually resolve on its own albeit with possible permanent damage to the penis. The literature reviewed for this guideline straddles both empirical and pathophysiology-based eras and some of the reported positive responses to treatment may reflect the natural course of priapism rather than a true treatment success. In addition, the literature is bereft of follow-up data on patients with priapism.

This document derives from a comprehensive review of the medical literature related to the management of priapism. As noted, deficiencies in this literature made it impossible to develop strict evidence-based guidelines. Most of the recommendations contained herein are based upon expert consensus following review of the literature. Where possible, expert consensus is supplemented with review of limited data. Because the literature review only considered reports of cases in which the duration of erections were longer than four hours, the recommendations made may not apply to erections of shorter duration.

This guideline does not establish a fixed set of rules or define the legal standard of care for the treatment of priapism. Above all, it does not pre-empt physician judgment in individual cases. Variations in patient subpopulations, physician experience and available resources will necessarily influence choice of clinical strategy. Adherence to the recommendations presented in this document cannot assure a successful treatment outcome.

For ease of review, the recommendations are bolded and followed by supporting text. The basis of each recommendation, consensus of the expert Panel with or without data obtained by systematic review of evidence, is noted.

Definitions and Methodology


Priapism is a persistent penile erection that continues hours beyond, or is unrelated to, sexual stimulation. Typically, only the corpora cavernosa are affected. For the purposes of this guideline, the definition is restricted to only erections of greater than four hours duration. Priapism requires prompt evaluation and may require emergency management. Subtypes of priapism include:

  • Ischemic (veno-occlusive, low flow) priapism is a nonsexual, persistent erection characterized by little or no cavernous blood flow and abnormal cavernous blood gases (hypoxic, hypercarbic, and acidotic). The corpora cavernosa are rigid and tender to palpation. Patients typically report pain. A variety of etiologic factors may contribute to the failure of the detumescence mechanism in this condition. Ischemic priapism is an emergency.

    Resolution of ischemic priapism is characterized by the penis returning to a flaccid, nonpainful state. However, in many cases, persistent penile edema, ecchymosis and partial erections can occur and it may mimic unresolved priapism. Resolution of priapism can be verified by measurement of cavernous blood gases or blood flow measurement by color duplex ultrasonography.

  • Nonischemic (arterial, high flow) priapism is a nonsexual, persistent erection caused by unregulated cavernous arterial inflow. Cavernous blood gases are not hypoxic or acidotic. Typically the penis is neither fully rigid nor painful. Antecedent trauma is the most commonly described etiology. Nonischemic priapism does not require emergent treatment.

    Resolution of nonischemic priapism is characterized by a return to a completely flaccid penis.

  • Stuttering (intermittent) priapism is a recurrent form of ischemic priapism in which unwanted painful erections occur repeatedly with intervening periods of detumescence. This historical term identifies a patient whose pattern of recurrent ischemic priapism encourages the clinician to seek options for prevention of future episodes.


The Erectile Dysfunction Guideline Update Panel of the American Urological Association (AUA) was convened in April 2000 at the request of the AUA Board of Directors. The Practice Guidelines Committee of the AUA selected the Erectile Dysfunction Guideline Update Panel Co-Chairmen. The full Panel roster was assembled by invitation to experts in the field.

Literature searches were performed using the MEDLINE database. All searches were restricted to articles written in English and published between 1966 and January 2001, which reported data from human subjects. The search was performed using a group of MeSH headings related to erectile dysfunction. An initial extraction process reviewed the articles and characterized their content in order to retrieve the subset of articles concerning priapism (Appendix 1). Additional relevant articles (e.g. publications prior to 1966) were added at the recommendation of individual Panel members. More detailed data extraction was performed on the articles dealing with priapism (Appendix 2). Of the 217 articles reviewed, 195 were ultimately considered acceptable. The complete list of 217 references is contained in Appendix 3. Reasons for rejecting articles during this stage included inadequate description of methods or definitions, lack of relevant data, or coverage of the same data set in a later publication.

Due to the nature of the disease and the status of the literature, a meta-analysis was deemed inappropriate for this topic. Instead, a series of clinically important and potentially answerable questions was developed (Appendix 4) and the data extracted from the articles were organized to answer these questions. The evidence tables developed from this process focused on three primary outcomes: resolution of the priapism (flaccid penis for at least 24 hours), recurrence of priapism (after 24 hours of flaccidity) and erectile dysfunction. Additional tables detailing side effects were developed for some treatments. These results were then summed to provide crude estimates of treatment effects. The evidence tables were originally arranged to match the questions, but have been reordered by patient characteristics and treatment and included in Appendix 5. A summary of the results, similarly reordered, is included as Appendix 6. Unless otherwise noted, the statistics cited in this document are derived from the evidence tables.

Recommendations were developed either strictly by consensus or by consensus combined with review of the available, limited data. Following review and approval by the entire Panel, the draft guideline was submitted for peer review to 64 urologists and other health care professionals. The Panel made revisions based on peer review comments and the document was submitted to and approved by the Practice Guidelines Committee and the Board of Directors of the AUA.


The diagnosis of priapism is self-evident in the untreated patient. The evaluation of priapism should focus on differentiating ischemic from nonischemic priapism (Table 1). Once this differentiation is made, the appropriate management can be determined and initiated. The evaluation of the patient with priapism has three components: patient history, physical examination and laboratory/radiologic assessment.

Guideline Statement 1

In order to initiate appropriate management, the physician must determine whether the priapism is ischemic or nonischemic.


Ischemic Priapism

Guideline Statement 2

In patients with an underlying disorder, such as sickle cell disease or hematologic malignancy, systemic treatment of the underlying disorder should not be undertaken as the only treatment for ischemic priapism. The ischemic priapism requires intracavernous treatment, and this should be administered concurrently.


Guideline Statement 3

Management of ischemic priapism should progress in a step-wise fashion to achieve resolution as promptly as possible. Initial intervention may utilize therapeutic aspiration (with or without irrigation) or intracavernous injection of sympathomimetics.

No Discussion Available

Guideline Statement 4

If ischemic priapism persists following aspiration/irrigation, intracavernous injection of sympathomimetic drugs should be performed. Repeated sympathomimetic injections should be performed prior to initiating surgical intervention.


Guideline Statement 5

For intracavernous injection of a sympathomimetic agent, the Panel recommends use of phenylephrine because this agent minimizes the risk of cardiovascular side effects that are more common for other sympathomimetic medications.


Guideline Statement 6

For intracavernous injections in adult patients, phenylephrine should be diluted with normal saline to a concentration of 100 to 500 mcg/mL, and 1 mL injections made every 3 to 5 minutes for approximately one hour, before deciding that the treatment will not be successful. Lower concentrations in smaller volumes should be used in children and patients with severe cardiovascular disease.

No Discussion Available

Guideline Statement 7

During and following intracavernous injection of sympathomimetic drugs, the physician should observe patients for subjective symptoms and objective findings consistent with known undesirable effects of these agents: acute hypertension, headache, reflex bradycardia, tachycardia, palpitations, and cardiac arrhythmia. In patients with high cardiovascular risk, blood pressure and electrocardiogram monitoring are recommended.

No Discussion Available

Guideline Statement 8

The use of surgical shunts for the treatment of ischemic priapism should be considered only after a trial of intracavernous injection of sympathomimetics has failed


Guideline Statement 9

A cavernoglanular (corporoglanular) shunt should be the first choice of the shunting procedures because it is the easiest to perform and has the fewest complications. This shunting procedure can be performed with a large biopsy needle (Winter) or a scalpel (Ebbehøj) inserted percutaneously through the glans. It can also be performed by excising a piece of the tunica albuginea at the tip of the corpus cavernosum (Al-Ghorab). Proximal shunting using the Quackels or Grayhack procedures may be warranted if more distal shunting procedures have failed to relieve the priapism.


Guideline Statement 10

Oral systemic therapy is not indicated for the treatment of ischemic priapism.


Nonischemic Priapism

Nonischemic (high-flow) priapism is an uncommon form of priapism caused by unregulated arterial inflow. This condition may follow perineal trauma that results in laceration of the cavernous artery. However, many patients have no apparent underlying cause. Panel summary data found spontaneous resolution to be the outcome of untreated nonischemic priapism in up to 62% of the reported cases with an associated complaint of erectile difficulties in one third of patients.

Rare cases of a high-flow state occurring after resolution of ischemic priapism have been reported 11, but the cause is not understood. Possible mechanisms include the mechanical disruption of arteriolar or sinusoidal anatomy12 and dysregulation of vasorelaxing/vasoconstrictive factors resulting from ischemic damage.13

Guideline Statement 11

In the management of nonischemic priapism, corporal aspiration has only a diagnostic role. Aspiration with or without injection of sympathomimetic agents is not recommended as treatment.


Guideline Statement 12

The initial management of nonischemic priapism should be observation. Immediate invasive interventions (embolization or surgery) can be performed at the request of the patient, but should be preceded by a thorough discussion of chances for spontaneous resolution, risks of treatment-related erectile dysfunction and lack of significant consequences expected from delaying interventions.


Guideline Statement 13

Selective arterial embolization is recommended for the management of nonischemic priapism in patients who request treatment. Autologous clot and absorbable gels, which are non-permanent, are preferable to coils and chemicals, which are permanent, in the interventional radiologic management of nonischemic priapism.


Guideline Statement 14

Surgical management of nonischemic priapism is the option of last resort and should be performed with intraoperative color duplex ultrasonography.


Stuttering Priapism

Patients with ischemic priapism may develop a pattern of recurrence over time that is distinct from persistence or rapid recurrence of a single episode of priapism. This pattern of recurrence, known as stuttering priapism, challenges the clinician to develop a management strategy to prevent future episodes of priapism. Each episode of ischemic priapism in these patients should be managed as described in prior sections of this guideline. While the etiology of the recurrent ischemic priapism is often idiopathic, patients with hematologic abnormalities, such as sickle cell disease, are more prone to developing recurrent (stuttering) priapism.

Guideline Statement 15

The goal of the management of a patient with recurrent (stuttering) priapism is prevention of future episodes while management of each episode should follow the specific treatment recommendations for ischemic priapism.


Guideline Statement 16

A trial of gonadotropin-releasing hormone (GnRH) agonists or antiandrogens may be used in the management of patients with recurrent (stuttering) priapism. Hormonal agents should not be used in patients who have not achieved full sexual maturation and adult stature.


Guideline Statement 17

Intracavernosal self-injection of phenylephrine should be considered in patients who either fail or reject systemic treatment of stuttering priapism.



Clearly, despite the low incidence of priapism and the considerable challenge of providing successful treatment, clinical urology continues to address this potentially emergent condition. While still deficient in many respects, our understanding of the pathophysiology, diagnosis and management of priapism has been advanced by many significant basic and clinical investigative efforts. The published results of clinical studies on priapism have, in particular, made the present document possible.

The review of the clinical literature on priapism has answered some questions and raised new ones. The Panel has made specific recommendations when the weight of consensus and available data was sufficient to support confidence in a particular approach and it has noted when evidence was absent, incomplete, or ambiguous. Certain details of assessment and treatment of priapism are not uniformly reported in the literature. This information is needed to adequately evaluate outcomes, improve practice guidelines and continue the progress to date in the management of priapism.

Recommendations for Future Research:

Clinical studies of priapism should be designed to consider and ultimately report on the following:

  • Documentation of pre-priapism erectile function by retrospective report from the patient, and when possible, also from the partner
  • Time from onset of priapism to initial treatment and time to each subsequent treatment
  • Measurement of sexual function after resolution of priapism
    • Using a standardized instrument for one year
    • Using contemporary validated instruments for assessing quality of life
    • Reporting erection potential as determined by a minimum of subjective reporting within three months of and up to one year after priapism diagnosis and, when not normal, the results of continued evaluation for up to one year
  • Additional treatments used to regain erectile function


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2. Spycher, M. A. and Hauri, D. The ultrastructure of erectile tissue in priapism. J Urol, 135: 142, 1986.

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10. Lowe, F. C. and Jarow, J. P. Placebo-controlled study of oral terbutaline and pseudoephedrine in management of prostaglandin E1-induced prolonged erections. Urology, 42: 51, 1993.

11. Seftel, A. D., Haas, C. A., Brown, S. L., Herbener, T. E., Sands, M., and Lipuma, J. High flow priapism complicating veno-occlusive priapism: pathophysiology of recurrent idiopathic priapism? J Urol, 159: 1300, 1998.

12. Matson, S., Herndon, C. D. A., and Honig, S. C. Pathophysiology of "low flow" priapism: Intermediate phase- evidence of "high flow" defined with duplex ultrasound. Int J Impot Res, 11: S27, 1999.

13. Bastuba, M. D., Saenz de Tejada, I., Dinlenc, C. Z., Sarazen, A., Krane, R. J., and Goldstein, I. Arterial priapism: diagnosis, treatment and long-term followup. J Urol, 151: 1231, 1994.

14. Steers, W. D. and Selby, J. B. Jr. Use of methylene blue and selective embolization of the pudendal artery for high flow priapism refractory to medical and surgical treatments. J Urol, 146: 1361, 1991.

15. Gbadoe, A. D., Assimadi, J. K., and Segbena, Y. A. Short period of administration of diethylstilbestrol in stuttering priapism in sickle cell anemia. Am J Hematol, 69: 297, 2002.

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19. Serjeant, G. R., de Ceulaer, K., and Maude, G. H. Stilboestrol and stuttering priapism in homozygous sickle-cell disease. Lancet, 2: 1274, 1985.

20. Steinberg, J. and Eyre, R. C. Management of recurrent priapism with epinephrine self- injection and gonadotropin-releasing hormone analogue. J Urol, 153: 152, 1995.

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22. Gupta, S., Salimpour, P., Saenz de Tejada, I., Daley, J., Gholami, S., Daller, M., et. al. A possible mechanism for alteration of human erectile function by digoxin: inhibition of corpus cavernosum sodium/potassium adenosine triphosphatase activity. J Urol, 159: 1529, 1998.

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