Priapism 

  • Author: Hosam S Al-Qudah, MD; Chief Editor: Edward David Kim, MD, FACS   more...
 
Updated: Jan 20, 2012
 

Background

Priapism is defined as an abnormal persistent erection of the penis. It is an involuntary prolonged erection unrelated to sexual stimulation and unrelieved by ejaculation. As with many medical emergencies, the saying "time is tissue" holds true for priapism. This condition is a true urologic emergency, and early intervention allows the best chance for functional recovery.[1]

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Pathophysiology

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

Priapism. Corporeal relaxation causes external prePriapism. Corporeal relaxation causes external pressure on the emissary veins exiting the tunica albuginea, trapping blood in the penis and causing erection.

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

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

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

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

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

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Epidemiology

Frequency

United States

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

Mortality/Morbidity

  • Priapism is painful at onset. Corporeal fibrosis due to persistent priapism can result in deep-tissue infections of the penis.
  • The major chronic morbidity associated with all types of priapism is persistent erectile dysfunction and impotence.
  • The duration of symptoms is the most important factor affecting outcome. A recent Scandinavian study reported that 92% of patients with priapism for less than 24 hours remained potent, while only 22% of patients with priapism that lasted longer than 7 days remained potent.[2]

Race

  • Priapism is common in African Americans with SCD.

Sex

  • Priapism occurs exclusively in males.

Age

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

Hosam S Al-Qudah, MD  Consultant Urologist, Department of General Surgery, Saad Specialist Hospital, Al-Khobar, Saudi Arabia

Disclosure: Nothing to disclose.

Coauthor(s)

Osama Al-Omar, MD  Chief of Urology, Warren General Hospital

Osama Al-Omar, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Urological Association, Michigan State Medical Society, National Arab American Medical Association, and Society for Fetal Urology

Disclosure: Nothing to disclose.

Monica Parraga-Marquez, MD  Consulting Staff, Department of Emergency Medicine, Metropolitan Hospital Center; Clinical Assistant Professor, Department of Emergency Medicine, New York Medical College

Monica Parraga-Marquez, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Richard A Santucci, MD, FACS  Specialist-in-Chief, Department of Urology, Detroit Medical Center; Chief of Urology, Detroit Receiving Hospital; Director, The Center for Urologic Reconstruction; Clinical Professor of Urology, Michigan State University College of Medicine

Richard A Santucci, MD, FACS is a member of the following medical societies: American College of Surgeons, American Urological Association, and Société Internationale d'Urologie (International Society of Urology)

Disclosure: Nothing to disclose.

Paul S Wahlheim, MD  Staff Physician, Department of Emergency Medicine, St Joseph's Hospital and Medical Center

Paul S Wahlheim, MD is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians

Disclosure: Nothing to disclose.

Specialty Editor Board

Edward David Kim, MD, FACS  Professor of Surgery, Division of Urology, University of Tennessee Graduate School of Medicine; Consulting Staff, University of Tennessee Medical Center

Edward David Kim, MD, FACS is a member of the following medical societies: American College of Surgeons, American Society for Reproductive Medicine, American Society of Andrology, American Urological Association, Sexual Medicine Society of North America, and Tennessee Medical Association

Disclosure: Lilly Consulting fee Advisor; Astellas Consulting fee Speaking and teaching; Watson Consulting fee Speaking and teaching; Allergan Consulting fee Speaking and teaching

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

J Stuart Wolf Jr, MD, FACS  The David A Bloom Professor of Urology, Director, Division of Endourology and Stone Disease, Department of Urology, University of Michigan Medical School

J Stuart Wolf Jr, MD, FACS is a member of the following medical societies: American College of Surgeons, American Urological Association, Catholic Medical Association, Endourological Society, Society for Urology and Engineering, Society of Laparoendoscopic Surgeons, Society of University Urologists, and Society of Urologic Oncology

Disclosure: Nothing to disclose.

Chief Editor

Edward David Kim, MD, FACS  Professor of Surgery, Division of Urology, University of Tennessee Graduate School of Medicine; Consulting Staff, University of Tennessee Medical Center

Edward David Kim, MD, FACS is a member of the following medical societies: American College of Surgeons, American Society for Reproductive Medicine, American Society of Andrology, American Urological Association, Sexual Medicine Society of North America, and Tennessee Medical Association

Disclosure: Lilly Consulting fee Advisor; Astellas Consulting fee Speaking and teaching; Watson Consulting fee Speaking and teaching; Allergan Consulting fee Speaking and teaching

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Priapism. Corporeal relaxation causes external pressure on the emissary veins exiting the tunica albuginea, trapping blood in the penis and causing erection.
Priapism. Sexual stimulation causes the release of nitric oxide (NO) via stimulation of nonadrenergic noncholinergic neurons. NO-activated intracellular guanylate cyclase, converting guanosine triphosphate (GTP) to cyclic guanosine monophosphate (cGMP), causes relaxation of cavernosal arteries and increased penile blood flow, resulting in erection.
Priapism. Winter shunt placed by biopsy needle, usually under local anesthetic.
Priapism. Proximal cavernosal-spongiosum shunt (Quackel shunt) surgically connects the proximal corpora cavernosa to the corpora spongiosum.
Priapism. Proximal cavernosal-saphenous shunt (Grayhack shunt) surgically connects the proximal corpora cavernosum to the saphenous vein.
 
 
 
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