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Continuing Education Activity

Priapism is a disorder in which the penis maintains a prolonged erection in the absence of appropriate stimulation. Three broad categories exist for this disease: ischemic, nonischemic, and recurrent ischemic. Ischemic causes of priapism are a true emergency and require prompt intervention to prevent damage to the penis, which can progress to erectile dysfunction and permanent impotence. Emergent management of this disease is directed toward achieving detumescence. This activity reviews the pathophysiology of priapism and highlights the role of the interprofessional team in its management.


  • Review the presentation of priapism.
  • Describe the pathophysiology of priapism.
  • Summarize the treatment for priapism.
  • Review the importance of improving care coordination among interprofessional team members to improve patient outcomes affected by priapism.


Priapism is a disorder in which the penis maintains a prolonged, rigid erection in the absence of appropriate stimulation. Definitions vary regarding duration, but any erection lasting four hours or longer is generally considered priapism.

Three broad categories exist for this disease: ischemic, non-ischemic, and recurrent ischemic. Ischemic causes of priapism are a true emergency and require prompt intervention to prevent damage to the penis, which can progress to complete erectile dysfunction and permanent erectile dysfunction. Emergent management of this disease is directed toward achieving detumescence.[1][2]

Early intervention is essential for the functional recovery of erectile ability. If left untreated, penile corporal tissue necrosis and eventually fibrosis result along with permanent erectile dysfunction.


The etiology of priapism can broadly be categorized as low flow (ischemic) and high flow (non-ischemic). The flow refers to arterial flow. The causes of ischemic priapism are numerous and include various hemoglobinopathies, such as sickle cell disease and thalassemia, as well as any hypercoagulable state. Vasoactive medications, including erectile dysfunction medications (phosphodiesterase type five inhibitors and intracavernous injections), have been blamed for an increased incidence of this disorder and are thought to cause at least 25% of all cases.[3][4] Additionally, antidepressants (trazodone) and illicit drugs, including cocaine, may also cause priapism. Less common causes include neoplastic processes (leukemias, melanoma, prostate cancer, renal cancer, and especially bladder cancer), neurologic disorders, Fabry disease, dialysis, fat embolisms, cauda equina syndrome, amyloidosis, and infections that produce a hypercoagulable state. Recurrent ischemic causes of priapism share many of the same underlying etiologic factors as acute ischemic priapism, except for some defective regulatory mechanisms, which can result in abnormal signaling and intermittent, repeated episodes of priapism.

Rare causes of priapism include hydroxyzine, drotaverine (a papaverine analog), low molecular weight heparin, and coagulopathy generally associated with coronavirus.[5][6][7][8]

Non-ischemic priapism is less common and usually a result of direct trauma or injury. Priapism can also result from iatrogenic injury during surgical interventions, congenital arterial malformations, or cancer. In some, no underlying cause or explanation can be found for the disorder.[9][10]


There are multiple causes of priapism. It is estimated that in up to about two-thirds of patients, the cause is the use of intracavernosal drugs to treat erectile dysfunction. Sickle cell disease also accounts for a large number of cases of adult priapism, with rates reported between 40% and 80%. The majority of sickle cell cases of priapism are seen in African Americans, and the disease almost always affects the male. The disorder has a bimodal presentation with peaks at ages 7 to 10 and 20 to 50 years.[11] Younger people tend to have priapism due to sickle cell disease and the older population due to medications.[12] 

The overall incidence of priapism is estimated at 0.73 cases per 100,000 men per year.[13]

Priapism is exclusively a disease of males, but rare cases of clitoral priapism have also been reported.[14]


Ischemic priapism is the most common form of priapism. It is a disease process initiated by smooth muscle relaxation of the tissues and arteries in the corpora cavernosa. When detumescence is delayed due to an inability to reverse the arterial relaxation and smooth muscle paralysis that initiated the erection, ischemic priapism can occur.[15]  It is associated with a low arterial inflow into the corpora cavernosa and results in a rigid and prolonged erection. This trapped blood causes increased intracorporal pressure resulting in a compartment syndrome situation with tissue ischemia, hypoxia, cavernosal acidosis, and penile pain. Alternatively, non-ischemic priapism is caused by unregulated arterial blood flow into the corpora cavernosa without associated venous trapping. Patients usually do not develop tissue ischemia, and thus, this presentation is usually painless.[16]

Priapism does not generally cause engorgement of the glans penis and corpus spongiosum because these structures have a separate venous drainage system. The basis for surgical cavernosum to spongiosum shunt treatment for ischemic priapism is this alternate drainage route. 

Nitric oxide is a critical component of normal erectile function. Phosphodiesterase type 5 inhibitors, such as sildenafil, block the breakdown of cyclic guanosine monophosphate (cyclic GMP), resulting in enhanced and prolonged intracavernosal smooth muscle relaxation. This prolonged relaxation normally would result in increased blood flow and a rigid erection. A defect in the regulation of nitric oxide inside the corpora cavernosa has been proposed as the mechanism of priapism in some patients, especially in those with sickle cell disease.[17] 

Underlying causes of priapism include neurotransmitter excess, blockage of venous drainage from corpora (mechanical obstruction from sickle cell disease, parenteral lipids, leukemia, etc.), dysfunction or paralysis of normal detumescence or prolonged relaxation of cavernosal smooth muscle due to overdose or heightened sensitivity to vasoactive medications.

While priapism is usually defined as an erection that lasts 4 hours or longer, physiological changes and microscopic tissue damage inside the penis typically do not start until about 6 hours after onset.[18] Permanent structural changes of the corporal smooth muscle tissue begin to develop after 12 hours with trabecular interstitial edema.[18] Cellular damage starts 24 hours after priapism initiation with basement membrane skeletonization, increased platelet adherence, and sinusoidal endothelial destruction. Thrombus collections in the sinusoidal spaces and direct damage to cavernosal smooth muscle tissue leading to fibrosis and permanent ED begin by 36 hours. 

Early treatment and detumescence generally do not result in long-term erection problems. If the priapism lasts longer than 24 hours, permanent damage is done, and 90% of such men are unable to have normal sexual intercourse afterward.[19]

Recurrent priapism, also called "stuttering priapism," is usually ischemic and quite uncommon. It tends to be associated with sickle cell disease and, rarely, cannabis use.[20][21] Recurrent priapism typically occurs at night with relatively short periods of erectile rigidity, which gradually tend to develop longer durations. The exact pathophysiological mechanism of this type of priapism is not well understood but is thought to be an intracavernosal regulatory problem involving phosphodiesterase type 5 and nitric oxide.[22][23] 

Non-ischemic priapism is much less common and typically presents after a trauma or injury where there is a fistula forming between the cavernosal artery and the corpora. The trauma may be blunt or penetrating and is often delivered directly to the penis or perineum.  The priapism can develop up to 72 hours after the injury.  Unlike ischemic priapism, non-ischemic priapism is not painful, does not usually require emergency medical care, and will usually resolve spontaneously in the majority (62%) of cases, even if untreated.[24]

Priapism in Sickle Cell Disease

Priapism is a relatively common complication of sickle cell disease in affected males. Most studies put the prevalence among men with sickle cell disease at between 35% and 45%.[25] In general, patients with sickle cell disease who develop priapism tend to have more severe disease, with more episodes of chest pain, CVA events, and increased rates of hemolysis. The hemolysis releases arginine and free hemoglobin, which both reduce available nitric oxide. Cyclic GMP and nitric oxide are typically low in sickle cell patients who would be expected to interfere with erections and reduce priapism risk. It is theorized that the corporal smooth muscle may become hypersensitive to nitric oxide and cyclic GMP at levels that do not activate phosphodiesterase resulting in prolonged erections.[23]

More than 95% of the priapism cases in sickle cell disease are of the ischemic type.[26] High pressure in the venous channels of the corpora due to mechanical venous obstruction and dysfunction decreases the venous return and eventually leads to corporal engorgement along with minimal arterial inflow. This is very similar to compartment syndromes that occur elsewhere in the body.  

Stuttering priapism, also called recurrent ischemic priapism, is relatively common in sickle cell patients. Typical duration is anywhere from a few minutes to three hours and generally tends to be painful but self-limiting.[27] Repeated episodes of ischemic priapism can lead to permanent penile damage and erectile dysfunction, which occurs in up to 40% of patients so affected.[28]

Normal erections end when phosphodiesterases, such as PDE type 5, inactivate cyclic GMP through hydrolysis, leading to smooth muscle contraction. This erection reversal process appears to be defective in many sickle cell patients.[17] 

Sickle cell priapisms often happen at night during REM sleep and upon waking. Nocturnal erections are typically very androgen-dependent, which may partly explain the benefit of anti-androgen therapy in some priapism patients.[29] 

History and Physical

Upon initial assessment of patients presenting with priapism, the exact duration of the abnormal erection should be elicited. The history and duration of the condition are extremely helpful in determining its underlying etiology and help identify the specific type of priapism the patient is experiencing. Important clinical questions include the duration of symptoms, any treatments or injection therapy utilized, erectile function before the priapism episode, prior episodes and treatments, current medications, and any history of underlying disorders known to precipitate priapism, such as sickle cell disease or penile or perineal trauma. Additionally, the presence or absence of pain is important in determining ischemic versus non-ischemic causes of this disease as a painless presentation suggests a non-ischemic pathology. Only in very rare and extreme cases will ischemic priapism present with gangrene which ultimately results in necrosis of the entire penis.[30]  

On physical examination, the penis should be palpated to determine the presence of any pulsations that might represent arterial high-flow priapism and is usually absent in ischemic conditions. In ischemic priapism, the corpora cavernosa are usually somewhat tender to palpation, and the absence of tenderness or a partially tumescent cavernosa tends to favor a diagnosis of non-ischemic disease. Non-ischemic or high flow priapism will typically demonstrate reduced rigidity and much less pain than ischemic priapism. A corporal needle stick or a recent urologic procedure can be the precipitating event. Besides the genitalia, the perineum and abdomen should be carefully examined for signs of trauma or possible malignancy. A comprehensive history and physical exam help determine the underlying etiology.


Evaluation of priapism begins with a thorough and complete history and physical examination. If the etiology of priapism cannot be determined based on this information, then penile hemodynamics and intracorporal blood gases should be evaluated. Aspiration of the corpora cavernosa can be completed with laboratory evaluation of acquired blood. For blood cases, a small caliber needle (19 or 21 gauge) may be used. A cavernous blood gas in ischemic priapism will be low, generally with a pH less than 7.0, representing metabolic acidosis. Additionally, pO2 should be less than 30 mmHg, and pCO2 should be greater than 60 mmHg. Alternatively, high-flow non-ischemic priapism reveals more normal arterial blood on aspiration with a pH near 7.4 and pO2/pCO2 levels closer to 90 mm Hg and 40 mm Hg, respectively.[31][32] Typically, aspirated blood from ischemic priapism is very dark, almost black, while corporal blood from non-ischemic corpora is red with normal or near-normal levels of oxygen, CO2, and pH.

Summary of Aspirated Corporal Blood Gases in Priapism

  • Aspirated corporal blood gas in ischemic priapism: pH = 7 (or <7.2), pO2 < 30 mmHg and pCO2 > 60 mmHg.
  • Aspirated corporal blood gas in non-ischemic priapism: pH = 7.4 (or >7.2), pO2 > 90 mmHg and pCO2 < 40 mmHg. 

Further laboratory testing should be directed toward determining underlying or undiagnosed diseases that may be causing the patient’s condition. Lab tests, including complete blood count, reticulocyte counts, hemoglobin electrophoresis, serum lactic dehydrogenase, and urine toxicology, can all be employed to aid in the diagnostic evaluation of priapism. A sickle cell test should be done in all priapism patients at risk for the condition.

Penile imaging can be utilized to aid in the diagnosis of ischemic versus non-ischemic causes of priapism. Intracorporal arterial blood flow can be analyzed using color duplex ultrasound, with absent blood flow in the cavernosal arteries suggestive of an ischemic etiology while the normal arterial flow is characteristic of non-ischemic priapism. Abnormal anatomy, including arterial fistulas or pseudoaneurysms, may also be identified on US examination. Additionally, magnetic resonance imaging (MRI) or magnetic resonance angiography (MRA) can be utilized to evaluate for malignancy or thrombosis. It can also predict the viability of corpora tissue after prolonged or repeated episodes of priapism.

Complete blood work should be performed, including a complete blood count. If sickle cell disease is considered, then hemoglobin S measurements should be done. A type and screen test is recommended in sickle cell anemia as some patients may need a plasma exchange. 

"Sleep-related painful erections" is a rare condition that is somewhat similar to priapism. It is defined as frequent awakenings due to penile pain during REM sleep nocturnal erections resulting in severe sleep disruptions. The duration of the erections is insufficient to qualify these episodes as priapism as they typically remain rigid for only 15 to 60 minutes. Daytime, normal sexual activities are completely unaffected. Testosterone levels and libido are also normal, and there is no evidence of hematological disorders, which are common in stuttering priapism. The cause is unknown, although hypertonicity of the pelvic floor muscles has been implicated, and physical therapy appears to be helpful in some cases. The most effective treatment is baclofen.[21] Surgical interventions (penile prostheses) are ineffective for relieving pain in this condition.[33]

Summary of Evaluation of Acute Priapism

  • History and Physical
  • Screening test for sickle cell disease
  • Penile blood gases are optional (Low pO2 and high pCO2 are consistent with ischemic priapism)
  • Imaging (Optional) to include duplex ultrasound or MRI/MRA

Treatment / Management

Ischemic priapism is a true emergency, and any episode lasting four hours or longer requires early intervention to decrease the likelihood of irreversible corporal damage and future erectile dysfunction. Although the treatment of a patient’s underlying disease may decrease erectile rigidity, emergency management should focus on achieving actual detumescence.  Several medications can be utilized for ischemic priapism, and oral therapies such as pseudoephedrine or terbutaline may be tried while awaiting equipment and supplies for more advanced interventions. The dosage of oral terbutaline is 5 mg immediately, with another 5 mg taken 15 minutes later. Failure of oral therapies is common, with some studies reporting failure rates of 75%, resulting in the need to perform corporal aspiration of blood with the concurrent intracavernous injection of a sympathomimetic agent.

Aspiration is generally done at either the 2 o'clock or 10 o'clock position on the penis while milking the shaft. About 20 to 30 ml should be aspirated, and the color of the blood should be noted. Aspiration alone is only effective in about one-third of patients and must be combined with other treatments, such as diluted sympathomimetic agents, to achieve successful, prolonged detumescence.

It is recommended to perform a dorsal penile block before aspiration and injection to minimize patient discomfort. Although several sympathomimetic agents are available, phenylephrine is the most frequently utilized and recommended as the preferred first-line agent due to its efficacy and safety profile. Phenylephrine needs to be diluted with normal saline before intracorporal injection. The recommended injectable diluted concentration is from 100 to 500 mcg/ml.[24]  A 1 ml injection of the diluted phenylephrine solution should be injected every 3 to 5 minutes for up to about 1 hour or until full detumescence.[24] The American Urological Association Guidelines on priapism recommends an intracavernosal injection of 0.5 to 1 ml of a diluted phenylephrine concentration of 100 to 500 mcg/ml every 5 minutes for a total of up to 3 injections.[34]

A lower concentration and smaller injected volume should be utilized in children and those with severe cardiovascular disease.  Other potential sympathomimetic drugs include ephedrine, norepinephrine, and epinephrine. Of these, phenylephrine has relatively few cardiovascular side effects.  All patients receiving intracorporal sympathomimetic agents should be monitored for arrhythmias and elevated blood pressure. If completed within 12 hours of priapism onset, some studies have reported a near 100% success rate in achieving detumescence with this therapy.  

If medical therapy fails, surgical intervention may be required. Prolonged duration of priapism (>15.5 hours) and the failure of 950 mcg of injected, diluted phenylephrine solution suggests the likely need for surgical intervention such as a shunt.[35] A history of prior episodes of priapism is another independent risk factor.[36] Surgical intervention primarily consists of shunt procedures to reduce corporal pressures, drainage, and, ultimately, penile pain.[9][37][38] A shunt would essentially create a fistula between the corpora cavernosa to the corpora spongiosum, which generally retains normal venous drainage. Sometimes several shunts are needed. The initial shunt can be made directly through the glans with a cruciate incision into the distal end of the corpora, usually on both sides. If not successful, a small dilator can create a channel for drainage through the corpora cavernosa.[39] A shunt can also be created directly to one of the superficial penile veins.[40] The greater the degree of intervention, the lower the chances of eventual recovery of normal erectile function. Placement of a penile prosthesis at the time of the fistula surgery has been suggested for priapism patients who initially present with prolonged priapism of 72 hours or more as their chances of recovery of erectile function is minimal.[41][42] Early implantation of a penile prosthesis is recommended in these cases as a prolonged delay will result in more fibrosis and a less satisfactory result.[43] 

MRI imaging with contrast enhancement can help determine the relative health of the cavernosal smooth muscle tissue in cases of prolonged priapism.[44] In cases of substantial cavernosal injury due to prolonged priapism, a recommendation to proceed to an immediate placement of a penile prosthesis can be made and discussed with the patient. This will also help prevent pain, additional fibrosis, penile curvature, and shortening of the penis.[45][46] In practice, a prosthesis may not be immediately available on an emergency basis. In this case, with the expectation that a prosthesis will likely be needed anyway, a limited channeling or even a full dilation of the corpora cavernosa can be done with metal dilators. This will essentially destroy the normal erectile mechanism and is usually short-term as a prosthesis would generally be placed relatively quickly; before any significant penile shortening or fibrosis can develop. 

Summary of Management of Acute Ischemic Priapism

  • Oral terbutaline and/or oral pseudoephedrine.
  • Penile local anesthetic block.
  • Aspiration of corpora.
  • Intracorporal injections of diluted phenylephrine (100mcg - 500 mcg/ml) every 5 minutes x 3.
  • Surgical cavernosal - spongiosum shunt.
  • Corporal dilation with or without immediate penile prosthesis placement. 

Recurrent or "Stuttering" priapism shares many treatment goals with ischemic priapism, with acute therapy focused on achieving detumescence and chronic therapy focused on preventing recurrences. Emergency management should be focused on acute therapy for erections of 3 to 4 hours duration or longer with the same treatments utilized as in acute ischemic priapism. Avoidance of alpha-adrenergic receptor blockers, such as phenothiazines, is recommended as well as trazodone and similar medications. Many of these patients may have sickle cell disease, which should be investigated.  Estrogens have been used with reasonable success in the past but are not currently recommended due to the risk of thromboembolism.[47]

A number of therapies have been used for prophylaxis in stuttering priapism. These include:

  • Baclofen (start at 10 mg TID and gradually increase weekly.  Maximum is 90 mg daily.)
  • Casodex (50 mg daily)
  • Finasteride/dutasteride (finasteride 5 mg daily, dutasteride 10 mg daily.  May slowly reduce dosage in most patients.)
  • Gabapentin (300 - 600 mg TID)
  • Hydroxyurea (sickle cell patients only. See dosage below.)
  • Ketoconazole plus prednisone (200 mg TID daily plus prednisone 5 mg for two weeks followed by ketoconazole 200 mg HS for 5 months)
  • LHRH Agonists (Leuprolide, Eligard, etc.)
  • Phenylephrine (oral and diluted for intracavernosal injection as needed)
  • Pseudoephedrine (30 mg - 60 mg at bedtime with another 30 mg if priapism occurs)
  • Sildenafil (50 mg daily)
  • Terbutaline (5 - 10 mg daily)

More details on these therapies and "Stuttering Priapism" can be found in a separate, companion review article on the topic.[48]

Sickle Cell Disease: If a priapism patient has sickle cell disease, then aggressive hydration, alkalinization, oxygenation, and pain control are required in addition to the standard treatment of acute episodes of ischemic priapism. Exchange transfusions should be considered to lower the hemoglobin S for cases of acute priapism not responding to alternative therapies.  Good results have been reported with automated red blood cell exchange transfusions which can rapidly reduce the Hb S concentration to 10% or less without iron or fluid overload, but these require specialized equipment and staffing. Emergency treatment would otherwise be the same as for non-sickle cell patients with acute priapism. Recurrent priapism is a significant cause of erectile dysfunction in male sickle cell patients due to permanent damage to the corpora cavernosa.

Sickle cell patients with recurrent priapism generally respond well to hydroxyurea prophylaxis and automated exchange transfusions, which should be used when possible. There are related symptoms such as mental acuity changes, tachycardia, higher respiratory rate, and low O2 saturation. Some sickle cell patients with frequent recurrences can be taught self-administration of diluted phenylephrine (or a similar alpha agonist medication) injected into the corpora for erections lasting more than 2 hours.[49][50] Another option is to use sildenafil daily. Sildenafil works best in priapism patients who have nocturnal or early morning prolonged erections, which is fairly typical of recurrent priapism in sickle cell disease. Sildenafil is not used as a PDE type 5 inhibitor but to help regulate cavernosal smooth muscle tone, tension, and activity level.[51][52][53]

Hydroxyurea was originally designed as an anti-cancer drug. It affects bone marrow causing an increase in fetal hemoglobin while decreasing normal adult hemoglobin production.[54][55] The net result is to reduce the overall concentration of hemoglobin S. Hydroxyurea also increases nitric oxide levels by reducing hemolysis, increasing intracellular nitric oxide production, and direct vasodilation.[56] In priapism, it is used for prophylaxis only in sickle cell patients.[57][58][59] Dosage of hydroxyurea starts at 20 mg/kg daily and is then slowly increased to the maximum dose tolerated based on changes in the CBC.

When hydroxyurea therapy fails to prevent recurrent priapism in sickle cell disease patients, another approach uses regularly scheduled transfusions. The goal is to keep the hemoglobin S concentration to less than 50%. This program of regular transfusions should be re-evaluated after 6 to 12 months. It should be abandoned if it has not been successful in reducing recurrent priapism episodes. Other treatments for recurrent priapism, such as sildenafil, as listed above, can be used concurrently.[51][53]

Non-Ischemic Priapism is generally managed conservatively due to the low probability of penile damage, and thus the initial intervention should be observed with treatment utilizing topical ice packs. Although aspiration can be completed for diagnostic purposes, this procedure generally does not result in complete detumescence. Many patients elect to avoid surgery due to the inherent risks of erectile dysfunction, and some patients have been reported to maintain their capacity to obtain and maintain an erection despite years of non-ischemic priapism.  Should a surgical procedure be desired, the initial recommended approach is selective arterial embolization or direct ligation of the dysfunctional cavernous artery fistula.[60][61][62] The resolution of non-ischemic priapism with selective arterial embolization is reported to be as high as 89%.[63] Micro-coils may be recommended for embolization as alternative methods are reported to have higher recanalization rates.[64][65] If this is unsuccessful, arterial embolization can be repeated, or an open procedure to tie off the ruptured artery using ultrasound guidance has shown success after failed embolization attempts.[62]

Differential Diagnosis

  • Peyronie disease
  • Trauma to the genitals
  • Penile implant
  • Use of cocaine
  • Insertion of a foreign body into penis/urethra
  • Paraphimosis
  • Penile fracture


Current American Urological Association Guidelines

Ischemic Priapism

  1. May start treatment with oral pseudoephedrine or terbutaline (5 mg with an optional repeat dose after 15 minutes).
  2. Oral therapy is not recommended as the only treatment for ischemic priapism.
  3. Intracavernous treatment is necessary for patients with an underlying disorder like malignancy or sickle cell disease. At the same time, the primary condition should be treated.
  4. Aspiration is vital if there is a delay in starting medical treatment. Irrigate and aspirate while waiting for sympathomimetics.
  5. For ischemic priapism, diluted phenylephrine is the recommended agent for intracavernosal injections as it has fewer adverse cardiac effects than alternative drugs.
  6. The phenylephrine must be diluted before use. Recommended dilution is 100 to 500 mcg/ml.
  7. Injections can be performed every 5 minutes for up to 3 additional injections.  Others have recommended repeat injections up to 60 mins.
  8. During intracavernous injections, monitor the patient's vital signs, including EKG and blood pressure.
  9. If intracavernous injections fail, consider a surgical shunt. A cavernoglandular shunt is preferred as it has the fewest complications.

Non-Ischemic Priapism

  1. Aspiration is only done for diagnosis.
  2. Non-ischemic or high flow priapism is relatively rare and comprises <5% of all priapism cases.
  3. The primary treatment is observation.
  4. Embolization or surgery can be done if the patient wants these treatments. Patients should be warned about failure rates and complications.
  5. Selective embolization using gels, clots, coils, and chemicals can be performed.
  6. Surgery is the last choice of treatment.


The outcome depends on the duration of symptoms, underlying pathology, and patient age. The longer the duration of symptoms, the poorer the outcome. Long-term risk of erectile dysfunction is also very common, despite optimal treatment. In addition, patients who experience one episode of priapism are at risk for recurrent attacks. A common cause of poor outcomes is infection. Younger men with sickle cell should be taught about priapism as early; rapid treatment helps minimize permanent damage and erectile dysfunction. 


Long-term erectile dysfunction due to damage from prolonged priapism is possible. The longer the duration of the priapism, the greater the damage to corpora cavernosal tissues.

Glans necrosis is a very uncommon complication of priapism.  Non-surgical options, including a Winter type cavernosum - spongiosum shunt with continuous irrigation of heparinized saline, have reportedly been more successful in treatment than immediate surgical excision.[66]

Deterrence and Patient Education

Follow-up is vital to ensure that the therapy has been successful. Patients at risk for recurrence should be prescribed one or more of the oral agents that have been identified as helpful in controlling recurrences. The most commonly used include bicalutamide (casodex), finasteride, sildenafil, baclofen, gabapentin, hydroxyurea (sickle cell only patients), phenylephrine, sudafed, terbutaline, and IM leuprolide either alone or in some combination. 

Pearls and Other Issues

Priapism is a challenging disease in the emergency department and requires prompt diagnosis and treatment. The primary goal of ischemic priapism management is achieving detumescence, with several acceptable treatments available. Non-ischemic priapism can be safely managed conservatively in the majority of cases. Failure of rapid evaluation and treatment can result in significant morbidity, and intervention should not be delayed.

Enhancing Healthcare Team Outcomes

Priapism is not a fatal disorder, but it can lead to permanent erectile dysfunction in the future. The key to prevention is education, with all members of the interprofessional healthcare team contributing. At the time of discharge, the nurse should educate the patient on seeking medical help as soon the condition develops. Older adults should be cautioned against the use of oral or injectable agents used to treat erectile failure. All patients with the first episode of priapism should be seen by a mental health counselor as the condition is associated with severe anguish and anxiety. Patients need to be told that the condition can be associated with a poor outcome, despite adequate treatment. The patient condition and treatment must be documented by all clinicians as this disorder often leads to litigation. Follow-up by a urologist is mandatory, or one risks a malpractice suit. The interprofessional team members must exercise open communication to ensure that the patient is receiving the current standard of care. Pharmacists should discuss the risk of priapism with patients receiving drugs that have this possible side effect.[67][68] [Level 5]


The prognosis of patients with priapism depends on age, duration of symptoms, and the underlying cause. If the priapism is present for less than 24 hours, then the chances of remaining potent are high, but if the duration is more than 72 hours, the risk of remaining potent is greatly diminished. Erectile dysfunction is a long-term complication in many patients, and recurrent episodes of priapism, as well as longer durations, are associated with a worse prognosis. The risk for recurrence is also high if one episode has already occurred. If the cause is associated with trauma, there is an increased risk of infection and fibrosis.[69][70] [Level 5]

Article Details

Article Author

Michael Silberman

Article Author

Gavin Stormont

Article Editor:

Eugene Hu


1/13/2022 7:09:45 PM

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