Priapism

Michael Silberman; Stephen Leslie; Eugene Hu

Priapism

Author: Michael Silberman Author: Stephen W. Leslie Editor: Eugene W. Hu Updated: 9/14/2025 9:55:37 PM

Introduction

Priapism is a disorder in which the penis maintains a prolonged, rigid erection in the absence of appropriate stimulation. Although definitions vary regarding duration, any unwanted erection lasting 4 hours or longer and not relieved by ejaculation is generally considered priapism.[1][2][3]

Priapism is classified into 3 broad categories—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 complete and permanent erectile dysfunction. Emergent management of this disease is directed toward achieving detumescence as well as relieving pain and preserving normal erectile function.[4][5]

Early intervention is essential for the functional recovery of erectile ability in patients with ischemic priapism.[1][6] If left untreated, penile corporal cellular and tissue damage occurs with necrosis and eventually fibrosis, resulting in penile shortening and permanent erectile dysfunction.[1]

Etiology

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Etiology

The etiology of priapism can broadly be categorized as ischemic (low-flow) and nonischemic (high-flow). The flow refers to arterial vascular blood streaming into the corpora cavernosa. The causes of ischemic priapism are numerous and include various hemoglobinopathies, such as sickle cell disease and thalassemia, as well as any hypercoagulable state.[7] Vasoactive medications, including erectile dysfunction medications such as phosphodiesterase (PDE) type 5 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.[8][9]

Antidepressants, such as trazodone; antipsychotics, especially those with alpha-1 adrenergic receptor blocking capability; and illicit drugs, including amphetamines and cocaine, may also cause priapism.[10][11][12][13] Trazodone is the single drug associated with the highest incidence of medication-induced priapism at about 16% of cases.[14][15] Alpha-1 adrenergic receptor blockage inhibits the ability of the sympathetic nervous system to cause detumescence.[10] Surprisingly, priapism following the use of PDE type 5 inhibitors, such as sildenafil, tadalafil, and vardenafil, is relatively rare. Antipsychotics and trazodone are more than twice as likely to cause priapism as PDE type 5 inhibitors.[16][17]

Less common causes include neoplastic processes, including leukemias, melanoma, prostate cancer, renal cancer, and especially bladder cancer; amyloidosis; dialysis; Fabry disease; fat embolisms; carbon monoxide poisoning; cauda equina syndrome; glucose-6-phosphate dehydrogenase deficiency; neurologic disorders; and infections that produce a hypercoagulable state.[18][19][20][21][22]

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 the disorder.[23]

Malignancies of the male pelvis can cause priapism due to either direct tumor infiltration or blockage of venous outflow, which can be identified with magnetic resonance imaging (MRI). The reported incidence of such malignant priapism is as high as 3.5% of patients presenting with priapism.[24]

Rare medication-related causes of priapism include hydroxyzine, drotaverine (a papaverine analog), low-molecular-weight heparin, and coagulopathy generally associated with coronavirus.[25][26][27][28] Other rare causes of priapism include chronic myeloid leukemia, COVID-19, thalassemias, amyloidosis, scorpion stings, spider bites, spinal cord injuries, and electronic cigarette use.[2][29][30][31]

Nonischemic high-flow priapism is far less common than the ischemic variety and typically results from direct perineal trauma or injury.[32] Nonischemic priapism can also result from iatrogenic injury during surgical interventions, congenital arterial malformations, or cancer.[32] In some cases, no underlying cause or explanation can be found for the disorder.[33][34]

Epidemiology

There are multiple causes of priapism. Approximately two-thirds of cases are caused by intracavernosal drugs to treat erectile dysfunction, followed by trazodone, chlorpromazine, and thioridazine, which exert alpha-1 antagonistic effects.[13][14][15][35][36]

Sickle cell disease also accounts for a large number of cases of adult priapism, with rates reported between 35% and 80%.[37][38][39] The majority of priapism cases from sickle cell disease occur in the African American population.[39] The disorder has a bimodal presentation with peaks at ages 7 to 10 years and 20 to 50 years.[40] Younger people tend to have priapism due to sickle cell disease, whereas medication effects are a more common etiology in older populations.[41] Please see StatPearls' companion resource, "Stuttering Priapism (Recurrent or Intermittent Priapism)," for further information

The overall incidence of priapism is estimated at 0.73 to 5.4 cases per 100,000 men per year.[42] The incidence of priapism following intracavernous injection therapy for erectile dysfunction is reportedly between 1.3% and 5.3%.[43] Rates of priapism following intracavernous injection therapy are higher in younger men and in patients with neurogenic or psychogenic erectile dysfunction.[43]

Priapism occurs 30% more frequently in the summer.[44]
Approximately 13% of patients who present to emergency departments with priapism are admitted.[44]
Priapism, by definition, is exclusively a disease of males, but rare cases of clitoral priapism have also been reported.[44]

Pathophysiology

Ischemic priapism

Ischemic priapism is the most common form of priapism. This condition results from 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.[45] Ischemic priapism is associated with little or no venous outflow, which reduces the arterial inflow into the corpora cavernosa, resulting in a rigid and prolonged erection.[2][15][46][47][48] This trapped blood causes increased intracorporal pressure, resulting in a compartment syndrome situation along with tissue ischemia, hypoxia, cavernosal acidosis, and penile pain.[2][15][46][47][48]

Alternatively, nonischemic priapism is caused by unregulated arterial blood flow into the corpora cavernosa without associated venous trapping. Patients typically do not develop tissue ischemia, and thus, this presentation is typically painless.[49]

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

Nitric oxide is a critical component of normal erectile function. PDE type 5 inhibitors, such as sildenafil, block the breakdown of cyclic guanosine monophosphate (cGMP), resulting in enhanced and prolonged intracavernosal smooth muscle relaxation.[50] This prolonged relaxation normally results in increased blood flow and a rigid erection.[50] 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.[51]

Underlying causes of priapism include excess neurotransmitter activity, impaired venous drainage from the corpora, often due to mechanical obstruction from sickle cell disease, parenteral lipids, and leukemia; dysfunction or paralysis of normal detumescence; or prolonged relaxation of cavernosal smooth muscle due to overdose or heightened sensitivity to vasoactive medications.

Although priapism is typically 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.[47] Permanent structural changes in the corporal smooth muscle tissue start to develop after 14 hours, beginning with trabecular interstitial edema, followed by the transformation of smooth muscle cells into fibroblasts.[47] Cellular damage 24 hours after the initiation of the priapism includes basement membrane skeletonization, increased platelet adherence, sinusoidal endothelial destruction, and necrosis from vascular stasis, acidosis, prolonged deoxygenation, and ischemia.[47] Thrombus collections in the sinusoidal spaces and direct damage to cavernosal smooth muscle tissue, leading to fibrosis and permanent erectile dysfunction, begin within 36 hours.[47]

Early treatment and detumescence generally do not result in long-term erection problems. If the priapism lasts longer than 24 hours, permanent damage begins, and up to 90% of such men cannot have normal sexual intercourse afterward.[2][52] After 72 hours, normal erectile function is destroyed and unrecoverable, so consideration should be given to implantation of a penile prosthesis.[53][54]

Recurrent priapism, also called stuttering priapism, is typically ischemic and often associated with sickle cell disease and, rarely, cannabis use.[55][56] 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 it is thought to be an intracavernosal regulatory problem involving PDE type 5 and nitric oxide.[57][58] Please see StatPearls' companion resource, "Stuttering Priapism (Recurrent or Intermittent Priapism)," for further information

Nonischemic Priapism

Nonischemic priapism is much less common and typically presents after a perineal trauma or injury, where a fistula forms between the cavernosal artery and the corpora.[32] The trauma may be blunt or penetrating and is often delivered directly to the penis or perineum. The priapism develops within 72 hours after the injury, but in some cases, this may take up to several weeks to develop.[2][32] Nonischemic high-flow priapism may rarely be idiopathic.[59] Unlike ischemic priapism, nonischemic priapism is not painful, does not typically require emergency medical care, and usually resolves spontaneously in the majority (62%) of cases, even if untreated.[60]

Priapism in Sickle Cell Disease

Priapism is a relatively common complication of sickle cell disease in affected males. Studies indicate that the overall prevalence of priapism among men with sickle cell disease ranges from 35% to 45%.[39][61] Priapism is uncommon in patients younger than 18 (3.6%) compared to adults (42%).[62]

In general, patients with sickle cell disease who develop priapism tend to have more severe disease, with more episodes of chest pain, cerebrovascular accident events, and increased hemolysis rates. The hemolysis releases arginine and free hemoglobin, which both reduce available nitric oxide. cGMP and nitric oxide are typically low in patients with sickle cell disease, which is expected to interfere with erections and minimize the risk of priapism. However, it is theorized that the corporal smooth muscle may become hypersensitive to nitric oxide and cGMP at levels that do not activate phosphodiesterases, resulting in prolonged erections.[58] This effect is exacerbated by oxidative stress.[63]

More than 95% of the priapism cases in sickle cell disease are ischemic.[64] High pressure in the venous channels of the corpora due to mechanical venous obstruction and dysfunction decreases the venous return, eventually leading to corporal engorgement along with minimal arterial inflow. This pathophysiology closely resembles compartment syndromes that occur elsewhere in the body.

Stuttering priapism, also known as recurrent ischemic priapism, is relatively common in patients with sickle cell disease. The typical duration is anywhere from a few minutes to 3 hours and generally tends to be painful but self-limiting.[65] Repeated episodes of ischemic priapism can lead to permanent penile damage and erectile dysfunction, which occurs in up to 40% of affected patients.[66]

Normal erections end when phosphodiesterases, such as PDE type 5, inactivate cGMP through hydrolysis, leading to smooth muscle contraction.[50] This erection reversal process appears to be defective in many patients with sickle cell disease.[51]

Priapism in sickle cell disease often occurs at night during rapid eye movement (REM) sleep and upon waking. Nocturnal erections are largely androgen-dependent, partly explaining the benefit of anti-androgen therapy in some patients with recurrent priapism.[67]

Please see StatPearls' companion resource, "Stuttering Priapism (Recurrent or Intermittent Priapism)," for further information.

Nocturnal painful erection is a rare disorder where patients are awakened from REM sleep due to painful, abnormal erections.[68] The structure and function of the penis are otherwise normal, and the condition is not associated with either priapism or erectile dysfunction.[68][69] Instead, nocturnal painful erection disorder is caused by obstructive sleep apnea, increased nocturnal testosterone levels, a neuroendocrine or neurotransmitter disorder, psychogenic issues brought on by anxiety and sleep deprivation, increased pain sensitivity during REM sleep, or ischemic penile compartment syndrome.[70][71][72][73][74]

Initial treatment is typically baclofen or possibly pregabalin.[68] Patients should be screened for obstructive sleep apnea, and continuous positive airway pressure therapy should be initiated as necessary. Combination therapy can then be used if additional treatment is needed. REM inhibitors include benzodiazepines, such as clonazepam and diazepam, and selective serotonin reuptake inhibitor antidepressants, such as clomipramine, paroxetine, fluoxetine, and sertraline.[68] Anti-androgen therapy typically involves finasteride or dutasteride, as other agents tend to have more undesirable sexual adverse effects.[68][70]

History and Physical

Upon initial assessment of a patient presenting with priapism, the exact duration of the abnormal erection should be elicited. The history and duration of the condition are beneficial 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 of priapism and treatments, current medications, and any history of underlying disorders known to precipitate priapism, such as sickle cell disease or trauma to the penis, pelvis, or perineum. Illicit drug use and alcoholic intoxication are contributing factors in up to 21% of cases of ischemic priapism.[2]

The duration of the condition before therapy is the single most important prognostic indicator for the resolution of ischemic priapism.[75]

The presence or absence of pain also helps differentiate ischemic from nonischemic causes of this disease, as a painless presentation suggests a high-flow, nonischemic pathology. Only in very rare and extreme cases does ischemic priapism present with gangrene, which ultimately results in partial or complete necrosis of the penis.[76]

On physical examination, the penis should be palpated to determine the presence of any pulsations that may represent arterial high-flow priapism, which is typically absent in ischemic conditions. In ischemic priapism, the corpora cavernosa are rigid, fully erect, and typically somewhat tender to palpation. The glans is typically soft or only partially engorged, but not rigid. The absence of tenderness or partially tumescent cavernosa tends to favor a diagnosis of nonischemic disease.

Nonischemic or high-flow priapism typically demonstrates reduced rigidity and much less pain than ischemic priapism. A corporal needle stick, traumatic injury to the perineum, or a recent urologic procedure can be the key precipitating event. Besides the genitalia, the perineum and abdomen should be carefully examined for signs of trauma, bruising, or possible malignancy. Obtaining a detailed history and performing a thorough physical examination helps determine the underlying etiology.

Evaluation

Evaluation of priapism begins with a detailed history and a thorough 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 G) may be used. A cavernous blood gas in ischemic priapism is acidic, generally with a pH less than 7.0, representing metabolic acidosis.[1] Additionally, pO₂ should be less than 30 mm Hg, and pCO₂ greater than 60 mmHg.[1]

Alternatively, high-flow nonischemic priapism reveals a 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.[1][77][78] Typically, aspirated blood from ischemic priapism is very dark and almost black, whereas corporal blood from nonischemic corpora is bright red with normal or near-normal oxygen, CO₂, and pH levels.

Aspirated Corporal Blood Gases in Acute Priapism

Ischemic (low-flow) priapism: pH <7.2, pO₂ <30 mm Hg, and pCO₂ >60 mmHg.
Nonischemic (high-flow) priapism: pH >7.2, pO₂ >90 mm Hg, and pCO₂ <40 mmHg.[1][79]

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 diagnosing priapism. A sickle cell test should be performed in all patients at risk for the condition. Drug toxicology testing and blood alcohol levels should be obtained as appropriate due to the association of priapism with drug abuse and high alcohol intake.

Penile imaging can be used to aid in the diagnosis of ischemic versus nonischemic causes of priapism. Intracorporal arterial blood flow can be analyzed using color duplex ultrasound. Absent blood flow in the cavernosal arteries suggests an ischemic etiology, whereas normal or increased arterial flow is characteristic of nonischemic priapism. Abnormal anatomy, including arterial fistulas or pseudoaneurysms, may also be identified on an ultrasound examination.

Current American Urological Association Guidelines recommend color duplex Doppler ultrasonography if available, as it can help differentiate ischemic from nonischemic priapism, can identify fistulas in about 70% of cases, and can be used in lieu of penile blood gas determinations.[2] Ischemic priapism shows minimal cavernosal arterial flow, whereas nonischemic priapism typically demonstrates normal or high vascular flow in these vessels.[2] Additionally, MRI or magnetic resonance angiography can be used to evaluate for malignancy or thrombosis. These modalities can also predict the viability of corporal tissue after prolonged or repeated episodes of priapism.[80]

Comprehensive blood work should be performed, including a CBC and a reticulocyte count. If sickle cell disease is even remotely suspected, hemoglobin S testing should be performed. In patients with sickle cell anemia, a type and screen is recommended, as some may require plasma exchange. Blood alcohol and toxicology drug screening should also be considered.

Sleep-related painful erections, also known as nocturnal penile tumescence accompanied by pain, is a rare condition that is somewhat similar to priapism.[68] This condition is defined as frequent awakenings due to penile pain during REM sleep from nocturnal erections, resulting in severe sleep disruptions.[68] The duration of the erections is insufficient to qualify these episodes as priapism, as they typically remain rigid for only 15 to 60 minutes.[68] 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.[68]

The exact cause is unknown, although untreated obstructive sleep apnea, hypertonicity of the pelvic floor muscles, psychological factors, neuroendocrine regulatory issues, neurogenic dysfunction of the ischiocavernosus and bulbocavernosus muscles, autonomic dysfunction, and pain threshold alterations have been implicated, and physical therapy appears to be helpful in some cases.[68][81] Baclofen combined with REM inhibitors and the use of continuous positive airway pressure for the sleep apnea are the most effective treatments.[56][68] Isolated case reports suggest that sodium oxybate or cinitapride may be useful in otherwise intractable cases.[81][82][83] Clozapine has been reported to be highly effective but can be dangerous.[82][84] Surgical interventions and penile prostheses are ineffective for relieving pain in this condition.[68][85]

Summary of Evaluation of Acute Priapism

Comprehensive history and physical.
Screening test for sickle cell disease, blood alcohol, and drug toxicology testing as appropriate.
Penile blood gases are optional (Low pO₂, low pH (<7.2), and high pCO₂ are consistent with ischemic priapism).
Imaging (optional) may include duplex ultrasound, MRI, or magnetic resonance angiography.

Treatment / Management

Ischemic (Low-Flow) Priapism

The initial approach to ischemic priapism is to treat it as a true emergency. Any priapism episode lasting 4 hours or longer requires early intervention to decrease the likelihood of irreversible corporal damage and future erectile dysfunction. Although treating a patient's underlying disease may reduce erectile rigidity, emergency management should focus on achieving actual detumescence. Several medications can be utilized for ischemic priapism, and oral therapies such as pseudoephedrine may be tried while awaiting equipment and supplies for more advanced interventions.

Oral terbutaline: Oral terbutaline has long been suggested as a priapism remedy in the past; however, it has not shown sufficient efficacy to be recommended currently, according to both the American Urological Association (AUA) and the European Association of Urology guidelines.[2] 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 normal saline or heparinized irrigation, followed by the administration of an intracavernosal injection of an appropriate sympathomimetic agent, typically phenylephrine.

Aspiration and irrigation: Aspiration and heparinized or normal saline irrigation are recommended as the initial medical therapy.[1][86] Performing a dorsal penile or ring block before aspiration, irrigation, and drug injection therapy is advisable to minimize patient discomfort. Aspiration is generally performed using a large diameter needle, butterfly, or angiocath (≥19 G) at either the 2 or 10 o'clock position on the penis near the base 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.[86][87] To achieve successful, prolonged detumescence, it must be combined with other treatments, such as irrigation with normal saline, heparinized saline, or diluted sympathomimetic agents. Aspiration with normal saline irrigation has been reported to successfully achieve detumescence in up to 66% of cases.[87](A1)

The same needle can be used for blood gas determinations, aspiration, irrigation, and sympathomimetic drug instillation. Although only one needle is required, some recommend two needles to facilitate the irrigation process. If one needle is placed near the base, the other should be placed distally for maximal irrigation. The inflow needle can be smaller than 19 G and can be placed into the distal corpora through the glans, which has the advantage of allowing any bleeding from the corpora to drain into the spongiosum.

Typically, after several rounds of aspiration and normal saline irrigation, oxygenated blood with a bright red color is observed. This reoxygenation of the corpora greatly enhances the smooth muscle contractile response to sympathomimetic injections.[2]

Intracavernosal drug therapy: This drug therapy is generally the next step in priapism treatment. Although several sympathomimetic agents are available for intracorporeal injection, phenylephrine is the most frequently utilized and recommended as the preferred first-line agent due to its efficacy and superior safety profile.[88] Phenylephrine needs to be diluted with normal saline before intracorporal injection. Approximately 100 to 500 mcg/mL is the recommended injectable diluted concentration.[60] A 1 mL injection of the diluted phenylephrine solution should be injected every 5 minutes for up to about 1 hour until full detumescence is achieved or a total dose of 1000 mcg has been administered.[60] The reported success rate of diluted phenylephrine injections alone is 58%, but this increases to 81% to 86% when combined with aspiration and irrigation if used within the first 24 to 36 hours after the priapism began.[89][90] Higher concentrations of phenylephrine solution have been associated with higher success rates, but this also increases the risk of cardiac and hypertensive complications.[89] (A1)

The American Urological Association Guidelines on priapism recommend 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 5 injections.[91] Providing the hospital pharmacy with a record or printout of the recommended dilution is advisable to facilitate rapid preparation in emergency situations. For convenience, the pharmacy can prepare a 10-mL syringe of normal saline with 200 mcg/mL of phenylephrine. (Dilution formula is 1 mL of 10 mg phenylephrine diluted in 49 mL of normal saline.) A 1 mL injection every 5 minutes, with up to 5 injections or 1000 mcg, is safe in most healthy individuals. Possible adverse effects include cardiac palpitations, dizziness, and headache.

A lower concentration and smaller injected volumes 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 adverse effects and is generally the preferred agent. When administered within 12 hours of priapism onset, this therapy has been reported in some studies to achieve near 100% success in producing detumescence.

All patients receiving intracorporal sympathomimetic agents should be continuously monitored for arrhythmias and elevated blood pressure.

Surgical intervention: Surgical intervention is required if medical therapy fails. A prolonged duration of the priapism (>15.5 hours) and the failure of 1000 mcg of injected, diluted phenylephrine solution after aspiration and normal saline irrigation suggest the likely need for surgical intervention, such as a shunt.[92] A history of prior episodes of priapism is another independent risk factor.[93] Surgical intervention primarily consists of shunt procedures to reduce corporal pressures, improve drainage, and, ultimately, reduce penile pain.[33][94][95] A shunt essentially creates a fistula between the corpora cavernosa and the corpora spongiosum, which generally retains normal venous drainage. Sometimes several shunts are needed. Several shunting techniques have been described, including the Winter, Ebbohoj, and Al-Ghorab procedures, as well as several modifications, including the T-shaped shunt, where a 10-blade is inserted into the distal corpora through the glans, pulled out, rotated 90°, and reinserted to make a T or crossed incision.[96]

All have roughly similar rates of priapism resolution. A preferred shunt is made directly through the glans with a cruciate incision into the distal end of the corpora on both sides. Blood is milked out of the corpora, and irrigation is continued until the color changes to a bright red, indicating adequate oxygenation. A shunt can also be created more proximally or directly to one of the superficial penile veins, the saphenous vein, or the deep dorsal vein.[97] These procedures are more technically complex, carry additional risks, and have not provided any significant, proven benefit. Therefore, they are generally not currently recommended.[2] (B2)

Corporal snake or tunneling maneuver: This maneuver can be tried if aspiration, irrigation, phenylephrine injections, and even distal shunting procedures are unsuccessful.[96][98][99][100][101] A small probe, such as a 7/8 Hegar dilator, is passed through the shunt opening in the glans into the corpora cavernosa all the way to the crura to create a clear vascular channel for drainage.[96] Reports of this corporal dilation/channeling procedure indicated a success rate of 80% in patients who presented with a mean priapism duration of 75 hours.[96][98][99][100][101] Success is clearly tied to the duration of the priapism before medical intervention. Patients with erections of more than 48 hours are likely to develop some degree of corporal smooth muscle necrosis and permanent erectile dysfunction.[98][99][100][101](B2)

Penoscrotal decompression: Penoscrotal decompression has been suggested as a better alternative procedure that avoids trauma to the glans and distal corpora.[101][102] This approach avoids increased susceptibility to potential future penile prosthesis erosion, remains effective even when distal shunting procedures fail, and provides a better cosmetic result.[101][103][104][105][106] A recent meta-analysis indicated that penoscrotal decompression achieved detumescence in otherwise intractable cases of ischemic priapism in 89.3% of cases, with preservation of normal erectile function in 54.8%.[104](A1)

Known as penoscrotal decompression, the initial surgical approach is the same as for a trans-scrotal penile prosthesis placement. The corpora are isolated and opened just enough to allow a pediatric Yankauer suction to enter, typically just 1 to 2 cm. Traction sutures are used to facilitate the corporal dilation. The Yankauer can then be advanced proximally and distally to evacuate debris and corporal thrombi.[101][102][103][104][105][106] Care must be taken to point the tip of the Yankauer laterally to avoid any potential injury to the urethra. Manual compression is used to express any remaining ischemic blood, followed by extensive irrigation of the corpora with saline. A malleable penile prosthesis may optionally be placed. The corporotomies are then closed with the traction sutures.(A1)

Although initially proposed for failed distal cavernosal-spongiosum shunts, it has since shown good efficacy as primary surgical therapy in patients with prolonged priapism (a mean of 71 hours).[101][103] About 55% to 60% of patients treated with this procedure were able to resume sexual activity either with or without oral medication support.[104] If erectile dysfunction persists, a penile prosthesis can be implanted, but placement should not be unduly delayed to minimize the risk of corporal fibrosis. Some experts now recommend going directly to penoscrotal decompression or some other method of corporal dilation, tunneling, or a snake maneuver, with or without penile prosthesis implantation, in cases of priapism presenting after more than 24 hours in duration. This approach avoids the surgical trauma and complications related to having a shunt procedure followed by a possible prosthesis at a later date.(A1)

Penile prosthesis placement: 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 patients who initially present with prolonged priapism of 48 to 72 hours or more, as their chances of recovery of normal erectile function are minimal.[107][108] Early implantation of a penile prosthesis is recommended in these cases (optimally <3 weeks), as a prolonged delay results in more fibrosis and a less satisfactory result.[109]

MRI imaging with contrast enhancement can help determine the relative health of the cavernosal smooth muscle tissue in cases of prolonged priapism.[80] Where there is substantial cavernosal injury due to prolonged priapism, typically considered 48 hours or more, immediate placement of a penile prosthesis should be considered and discussed with the patient. Early intervention can help prevent increased pain, additional fibrosis, penile curvature, and shortening of the penis.[110][111] In practice, a prosthesis may not be immediately available on an emergency basis. In this case, with the expectation that a prosthesis is likely necessary anyway, a limited channeling or even a full dilation of the corpora cavernosa with metal dilators can be performed. This approach essentially destroys the normal erectile mechanism and is typically short-term. A prosthesis is generally placed relatively quickly in these situations, preferably within a few weeks, before any significant penile shortening or fibrosis can develop. (B3)

Surgical intervention in priapism aims to relieve pain, cause detumescence, restore normal erectile function, and shorten the duration of corporal ischemia, which otherwise leads to continuing pain, fibrosis, and permanent erectile dysfunction. When a patient with prolonged priapism of 48 hours or longer presents for treatment, it may be prudent to explain that even with optimal care at that point, much damage has likely occurred to the erectile tissue and corpora already, which may not be reversible. In such cases of resistant ischemic priapism and those of 48 hours duration or longer, serious consideration should be given to full corporal dilation with immediate or early (within 3 weeks) penile prosthesis implantation.[1][53][112][113][114][115][116][117][118](A1)

Early placement of a penile prosthesis in patients with long-duration or intractable priapism demonstrates extremely high patient satisfaction scores and quality of life ratings.[113] If a penile prosthesis cannot be placed emergently, it should be implanted at the earliest opportunity, typically within 3 weeks after full corporal dilation if possible, as the dilated corpora cavernosa become densely fibrotic over time, making delayed penile prosthesis implantation far more difficult surgically with higher complication rates and lower patient satisfaction scores.[1][107][109][112][113][114][115][116][117][118][119][120](A1)

Patients with ischemic priapism lasting longer than 48 hours tend to achieve the best overall outcomes with immediate penile prosthesis placement as their definitive initial therapy. This approach is also recommended by the American Urological Association (AUA) Guidelines and the European Association of Urology (EAU) Sexual and Reproductive Health Guidelines Panel for such situations.[79][112][118] Placement of a penile prosthesis due to prolonged or intractable priapism tends to have increased risks, including infection of the cavernosa or prosthesis, distal erosion, and higher reoperation rates.[108](A1)

Antithrombotic therapy: Antithrombotic therapy has been suggested as a possible adjunct to shunting procedures for ischemic priapism. Theoretically, it may reduce the incidence of shunt thrombosis and recurrent priapism. A small study with 22 patients from a single institution suggested a substantial benefit in reduced priapism recurrence rates in those who had antithrombotic therapy in addition to their shunting procedures (11%) compared to those who only had the shunts (69%).[121] Although intriguing, this is still a preliminary finding from a small study in a single institution. Antithrombotic therapy requires dosage standardization and confirmation of efficacy and safety in controlled, randomized studies before it can be generally recommended.(B2)

Summary of management of acute ischemic (low-flow) priapism:

Oral pseudoephedrine
Penile local anesthetic block
Irrigation and aspiration of the corpora with heparinized or normal saline
Intracorporal injections of diluted phenylephrine (200 mcg/mL) every 5 minutes for 5 doses
Distal surgical cavernosal-spongiosum shunt (proximal shunts are not recommended)
Corporal tunneling (snake maneuver) with or without immediate penile prosthesis placement
Penoscrotal decompression
Penile prosthesis implantation

Recurrent or stuttering priapism: This 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 focus on acute therapy for erections of 3 to 4 hours 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. Many of these patients report waking up with a prolonged erection with increasing frequency and duration until they develop an ischemic priapism emergency.[122]

Estrogens have been used with reasonable success in the past, but are not currently recommended due to the risk of thromboembolism.[123] Antiandrogens and luteinizing hormone–releasing hormone (LHRH) agonist therapies are effective but are associated with significant adverse effects such as hot flashes, decreased libido, greater body fat, gynecomastia, and insulin resistance. In theory, LHRH antagonists such as degarelix should be effective, but there are no studies or reports on their use to date, so they cannot be recommended at this time. Terbutaline is no longer recommended in the treatment of priapism due to a lack of proven efficacy.(A1)

Medications for which there is evidence of efficacy in the treatment of stuttering priapism include:

Baclofen: Start at 10 mg tid, gradually increase weekly; maximum 90 mg daily. Recommended for patients with spinal cord injury or sleep-related painful erections only.
Casodex: 50 mg daily.
Finasteride/dutasteride: Finasteride 5 mg daily or dutasteride 10 mg daily; dosage may be tapered gradually in most patients.
Gabapentin: 300 to 600 mg tid.
Hydroxyurea: For patients with sickle cell disease only (see dosage guidelines below).
Ketoconazole plus prednisone: Ketoconazole 200 mg tid daily plus prednisone 5 mg for 2 weeks, followed by ketoconazole 200 mg at bedtime for 5 months.
LHRH Agonists: Leuprolide and goserelin.
Phenylephrine: Both oral and diluted for intracavernosal injection as needed.
Pseudoephedrine: 30 to 60 mg at bedtime with another 30 mg if priapism occurs.
Sildenafil or tadalafil: Sildenafil 50 mg daily or tadalafil 5 mg daily.

Please see StatPearls' companion resource, "Stuttering Priapism (Recurrent or Intermittent Priapism)," for further information.

Sickle cell disease: If a patient with priapism has sickle cell disease, 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 hemoglobin S concentration to 10% or less without iron or fluid overload, but these require specialized equipment and staffing.[85][124][125][126] Emergency management of acute priapism is otherwise the same in patients without sickle cell disease. However, recurrent priapism in male patients with sickle cell disease is a significant cause of erectile dysfunction due to permanent damage to the corpora cavernosa.(B3)

Patients with sickle cell disease with recurrent priapism generally respond well to hydroxyurea prophylaxis and automated exchange transfusions, which should be used when possible. Related symptoms include mental acuity changes, tachycardia, higher respiratory rate, and low oxygen saturation. Some patients with sickle cell disease 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.[127][128] Another option is to use sildenafil daily. Sildenafil works best in patients with priapism 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.[129][130][131](A1)

Hydroxyurea was originally designed as an anti-cancer drug. This drug affects bone marrow, causing an increase in fetal hemoglobin while decreasing normal adult hemoglobin production.[132][133] The net result is to reduce the overall concentration of hemoglobin S. Hydroxyurea also increases nitric oxide levels by reducing hemolysis and increasing intracellular nitric oxide production, resulting in direct vasodilation.[134] This drug is used for priapism prophylaxis only in patients with sickle cell disease.[135][136][137] The 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.(B3)

When hydroxyurea therapy fails to prevent recurrent priapism in patients with sickle cell disease, another approach uses regularly scheduled transfusions. The goal is to keep the hemoglobin S concentration to less than 50%. This regimen should be re-evaluated after 6 to 12 months and should be discontinued if it has not successfully reduced recurrent priapism episodes. Other treatments for recurrent priapism, such as sildenafil, as listed above, can be used concurrently.[129][131](A1)

Nonischemic (High-Flow) Priapism

Nonischemic priapism is generally managed conservatively due to the low probability of penile damage and lack of discomfort. Therefore, the initial intervention should be observed with treatment utilizing topical ice packs and compression. Although aspiration can be completed for diagnostic purposes, this procedure generally does not result in detumescence. Sympathomimetic intracorporal injections and surgical shunts are ineffective and not recommended in high-flow priapism. Supportive care with perineal compression and ice can be reasonably offered.

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 nonischemic priapism. Spontaneous resolution is reported in up to 62% of cases in published series.[138] Should a surgical procedure be desired, the initial recommended approach is arteriography with selective arterial embolization or direct ligation of the dysfunctional cavernous artery fistula.[139][140][141][142][143](A1)

The resolution of nonischemic high-flow priapism with selective arterial embolization is reported to be as high as 89%.[144]

Micro-coils may be recommended for embolization as alternative methods are reported to have higher recanalization rates.[145][146] If this is unsuccessful, arterial embolization can be repeated, or an open procedure to tie off the ruptured artery using intraoperative ultrasound guidance can be done. This has shown success after failed embolization attempts in nonischemic priapism.[141] The overall success rate of selective arterial embolization in nonischemic priapism is 89% to 100%, with 75% to 86% of patients retaining normal erectile capability post-embolization.[18] Recurrences are reported in up to 30% of patients treated with embolization. Repeat embolization is a possible option in these cases.[147](B3)

Superselective transcatheter arterial embolization for high-flow priapism using non-absorbable material has shown durable, long-term effectiveness beyond 10 years of follow-up.[148]

Adverse effects of embolization treatment include erectile dysfunction. If selective arterial embolization cannot be performed for some reason, a surgical approach may be considered, typically involving a corporal exploration, often with intraoperative Doppler ultrasound. Patients typically have to wait at least 1 month after the onset of the priapism to allow the fistula to mature before any surgical intervention.[18] Care must be taken to avoid inadvertent ligation of the cavernosal artery.[141](B3)

Summary of Current American Urological Association Priapism Treatment Guidelines

Ischemic priapism

May start treatment with oral pseudoephedrine. Oral terbutaline is ineffective.
Oral therapy is not recommended as the only treatment for ischemic priapism due to its overall lack of efficacy.
Intracavernous treatment is necessary for patients with an underlying disorder such as malignancy or sickle cell disease. At the same time, the primary condition should be treated.
Aspiration is vital if medical treatment is delayed. Irrigate with normal saline and aspirate while waiting for sympathomimetics.
For ischemic priapism, diluted phenylephrine is the recommended agent for intracavernosal injections as it has fewer adverse cardiac effects than alternative drugs.
Phenylephrine must be diluted before use. The recommended dilution is 100 to 500 mcg/mL.
Injections can be performed every 5 minutes for up to 5 total injections, 60 minutes, or 1000 mcg total phenylephrine dosage.
During intracavernous injections, the patient's vital signs, including electrocardiogram and blood pressure, need to be monitored.
If intracavernous injections fail, a distal surgical shunt should be considered. A cavernosa-spongiosum shunt through the glans is preferred as it has the fewest complications.
If distal shunts fail, remaining options include a snake maneuver (tunneling) or a penoscrotal decompression procedure. (Proximal shunts are not recommended.)
If all the above measures fail, a penile prosthesis should be implanted.[1]

Nonischemic priapism

Aspiration is only performed for diagnosis.
Nonischemic or high-flow priapism is relatively rare and comprises <5% of all priapism cases.
The primary treatment is observation.
Selective or superselective embolization, or surgery, can be performed if the patient wants these treatments.
Patients should be warned about failure rates and complications.
Embolization is performed using gels, clots, coils, and chemicals.
Selective transcatheter embolization is recommended over surgery when an interventional procedure is needed or requested.
Surgery is effective, but it is the last choice of treatment.

Differential Diagnosis

The differential diagnosis of priapism includes the following conditions, which may present with similar symptoms and should be carefully distinguished:

Cellulitis
Cocaine use
Insertion of a foreign body into the penis/urethra
Nocturnal painful erections
Paraphimosis
Pelvic malignancy
Penile fracture
Penile implant
Peyronie disease
Subcutaneous penile modifications, such as subcutaneous injections of vaseline and paraffin to alter the penile anatomy
Trauma to the genitals
Urethral rupture (partial or complete)

Prognosis

The outcome depends on the duration of symptoms, underlying pathology, comorbidities, and patient age. The longer the duration of symptoms, the poorer the outcome.[75] The risk of long-term or permanent erectile dysfunction is high, especially in cases of prolonged priapism, despite optimal treatment. In addition, patients who experience 1 episode of priapism are at risk for recurrent attacks.

Infection is another common cause of poor outcomes. Younger men with sickle cell disease should be taught about priapism, as early, rapid treatment helps minimize penile tissue damage and permanent erectile dysfunction.

Complications

Long-term erectile dysfunction due to damage from prolonged priapism is likely, starting at about 20 hours of duration.[75] The longer the duration of the priapism, the greater the damage to the corpora cavernosa tissues.[75]

Glans necrosis is a very severe but uncommon complication of priapism.[149][150] Non-surgical options, including a Winter or similar type of cavernosum-spongiosum shunt with continuous irrigation of normal or heparinized saline, have reportedly been more successful in treatment than immediate surgical excision.[149]

Deterrence and Patient Education

Follow-up is vital to ensure that the therapy has been successful. Patients at risk for recurrence should be prescribed 1 or more of the oral agents that have been identified as helpful in controlling recurrences. Commonly used options include bicalutamide, finasteride, sildenafil, baclofen, gabapentin, hydroxyurea (for patients with sickle cell disease only), phenylephrine, pseudoephedrine, and intramuscular leuprolide either alone or in some combination.

Pearls and Other Issues

Priapism is a challenging condition in the emergency department that requires prompt diagnosis—primarily distinguishing between ischemic and nonischemic priapism—and timely treatment. Typically, this can be easily achieved by a history, but a blood gas determination from aspirated penile corporal blood can be helpful in equivocal cases.

Nonischemic 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 in ischemic disease.

The primary goals of ischemic priapism management are achieving detumescence, relieving pain, and preserving erectile function.

Therapy typically proceeds in a stepwise fashion as follows:

Oral phenylephrine can be tried while waiting for additional supplies.
The first significant intervention is penile irrigation, aspiration, and diluted phenylephrine injections.
If these measures fail, the next step is a distal cavernosum-spongiosum shunt.
Should the distal shunt fail, a snake or tunneling maneuver can be tried, or a penoscrotal decompression procedure may be performed.
If all the above fail, consideration should be given to a penile prosthesis.

Enhancing Healthcare Team Outcomes

Priapism is not a fatal disorder, but it can lead to permanent erectile dysfunction in the future. Prevention relies heavily on patient education, with contributions from all members of the interprofessional healthcare team. At the time of discharge, nurses should educate patients on seeking medical help as soon as the condition develops. Older adults should be cautioned against the use of oral or injectable agents to treat erectile failure except as prescribed by their clinicians. These individuals should be cautioned against combining these agents, as the result is quite unpredictable. All patients with the first episode of priapism should be observed 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's condition and treatment must be well documented by all clinicians and healthcare professionals, as this disorder often leads to litigation. Follow-up with a urologist is mandatory, or one risks a malpractice suit. The interprofessional team members must exercise open communication to ensure that the patient receives the current standard of care. Pharmacists should discuss the risk of priapism with patients receiving drugs that have this possible adverse effect.[46][151]

Outcomes

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, 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 and longer durations are associated with a worse prognosis. The risk for recurrence is also high if 1 episode has already occurred. If the cause is associated with trauma, there is an increased risk of infection and fibrosis.[152][153]

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