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Table of Contents
REVIEW ARTICLE
Year : 2018  |  Volume : 29  |  Issue : 1  |  Page : 2-6

Interventional management of low-flow priapism: A protocol proposal


1 Department of Surgery School of Medicine, Universidad del Valle; Department of Surgery, School of Medicine, UROGIV Research Group at Universidad del Valle, Cali, Colombia
2 Department of Surgery, School of Medicine, UROGIV Research Group at Universidad del Valle, Cali, Colombia
3 Department of Surgery, School of Medicine, UROGIV Research Group at Universidad del Valle; Department of Epidemiology, Universidad Libre, Cali, Colombia
4 Department of Surgery, Fundación Valle del Lili, Cali, Colombia

Date of Web Publication23-Feb-2018

Correspondence Address:
Herney Andrés Garcia-Perdomo
Universidad Del Valle, Cll 4b#36-00, Cali
Colombia
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/UROS.UROS_4_18

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  Abstract 

Priapism is an involuntary prolonged erection that lasts for more than 4 h. Although several interventions have been proposed to manage the condition, these strategies are based on expert panel opinions, and little evidence exists regarding prognosis and outcomes. To synthetize information about interventions to treat priapism and to make evidence-based recommendations, we performed a literature search of Medline via Ovid, Scopus (including Embase) and Lilacs from 1980 to the current day with the following keywords: ischemic priapism, erectile function, drainage, and shunt. The length of the ischemic priapism is an important variable for the prognosis because of the pathophysiology of this condition. Here, we propose a step-by-step approach based on the time and invasiveness of the intervention. However, it is important to note that we could not find any clinical trial that supports this approach, and more research is needed for the future statements.

Keywords: General urology, operative treatments, penis, priapism


How to cite this article:
Garcia-Perdomo HA, Gómez-Puerto DA, Zapata-Copete J, Manzano-Núñez R. Interventional management of low-flow priapism: A protocol proposal. Urol Sci 2018;29:2-6

How to cite this URL:
Garcia-Perdomo HA, Gómez-Puerto DA, Zapata-Copete J, Manzano-Núñez R. Interventional management of low-flow priapism: A protocol proposal. Urol Sci [serial online] 2018 [cited 2018 Sep 23];29:2-6. Available from: http://www.e-urol-sci.com/text.asp?2018/29/1/2/226030


  Introduction Top


Priapism is a prolonged erection that is involuntary, lasts more than 4 h, is unrelated to sexual stimulation and is unrelieved by ejaculation. It constitutes a true disorder of erection physiology where the penis is recognized as the typically affected organ although priapism of the clitoris has been reported.[1] Recent advances have been made regarding the scientific understanding of the pathophysiology, prognosis, and outcomes of patients presenting with this condition at the emergency department. Therefore, interventions aiming to establish effective, evidence-based therapeutics for priapism are needed. Priapism remains a poorly recognized condition by many medical professionals, and therefore, there is no clear consensus or evidence regarding its management. This article reviews recent clinical developments in the medical and surgical management of priapism surveying scientific research activity and experience in this rapidly evolving field of study, proposing a best practice suggestion for the management of low-flow priapism in the emergency setting.


  Methods Top


We performed a literature search in Medline via Ovid, Scopus (Includes Embase), and LILACS from 1980 to the current day. We used the following keywords: ischemic priapism, low-flow priapism, erectile function, drainage, and shunt.


  Epidemiology Top


Priapism epidemiology is variable and depends on the populations being considered. This regional variation may be multifactorial and could be explained by fluctuations in black and Hispanic populations, as well as by climatic variability.[2],[3],[4] In Western populations, agents to treat erectile dysfunction are common causes of adult priapism. In other populations, sickle cell disease predominates as the cause of adult priapism.

Studies have shown that priapism occurs at nearly all ages with a bimodal distribution with peaks at 5–10 years and 20–50 years. Kulmala et al.,[5] in a study of 193 cases of priapism over 26 years in the Finnish population, showed a baseline incidence of 0.3–0.52/100,000 person-years. In the United States, the incidence of priapism has been estimated to be 5.3/100,000 person-years, with ischemic priapism (associated with hyperviscosity syndromes such as sickle cell disease) being the most frequent type of priapism.[4] In the Netherlands, a retrospective cohort composed of 145,071 males found that priapism occurred mainly in men 40 years or older and that the overall incidence rate was 1.5/100,000 person-years.[6] Similar results were found in Australia, where the reported incidence was 0.84/100000 person-years.[3] In Japan, the incidence of priapism has been estimated to be 0.13/100,000 person-years, which is lower than that in other parts of the world; the lower incidence may be explained by racial differences since there were no patients with sickle cell disease among the Japanese population.[7]


  Pathophysiology Top


Priapism can be seen to be a dysfunctional hemodynamic process of the penis involving an imbalanced erectile tissue response.[8] Although the underlying cause of priapism is usually not known, the understanding of its pathophysiology has advanced significantly. Currently, there are three different types of priapism: (1) Low-flow, ischemic, or anoxic priapism; (2) high-flow well-oxygenated priapism; and (3) recurrent or stuttering priapism [Table 1]. The main issues discussed here will relate to the first type; the other two are out of the scope of this review.
Table 1: Characteristics of types of priapism

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  Ischemic Priapism Top


Ischemic priapism is the most common presentation of this condition. An erection begins with the relaxation of the smooth muscle of cavernosal arteries and tissue, leading to increased nonischemic inflow, and decreased venous outflow.[9] As the intracorporal pressure rises to the mean arterial pressure, the inflow of blood decreases. This process usually does not involve the glans penis or corpus spongiosum. The persistence of the erection and failure of detumescence as well as persistent relaxation and failure of contraction of the cavernous smooth muscle are associated with rising pCO2 levels and acidosis. Urgent medical attention is needed when this condition lasts more than 4 h; prolonged ischemia is associated with tissue edema that causes a compartment syndrome resulting in muscle necrosis and fibrosis. Irreversible damage is identified after 24–48 h of priapism.[10]

Nitric oxide (NO) is the primary erectile-mediating neurotransmitter. This gaseous mediator is synthesized in the cavernous nerves to initiate an erection, and endothelial NO synthase in the endothelium maintains the erection during sexual stimulation. Studies have revealed that an altered NO signaling pathway can result in excessive erections, and this mechanism has been proposed for some patients with priapism, particularly those with sickle cell disease.[11]


  Clinical Presentation and Diagnosis Top


An accurate clinical history yields the information necessary to set the diagnosis of priapism and its severity. The presence of a persistent erection for more than 4 h; degree of pain; duration of pain; prior priapism episodes; prior treatments and drugs used; history of pelvic, genital or perineal trauma; and erectile function before the episode are important information that defines the management and prognosis.[12] A thorough history and physical examination should address the patient as a whole. It is important to be aware of the penile color, rigidity, penile discharge, lesions, and evidence of local trauma or injection sites. In addition, it is important to be aware of the following: The presence of prosthetic devices since malfunction may cause pseudopriapism;[13] evaluate regional lymphadenopathy because it could be a result of malignancy and finally, but not less important, evaluate rectal tone since high spinal cord lesions, or stenosis can also cause priapism.

It is vital that the physician distinguishes between the two basic types of priapism, high flow (non-ischemic), and low flow (ischemic). Pain is one of the most important differentiating features of ischemic priapism.[14] The corpora cavernosa are usually rigid and tender to palpation. Other characteristics of ischemic priapism include a soft glans, painful penile shaft, thick dark (hypoxic) aspirates of corpus cavernosum and if necessary, a Doppler indicating low arterial flow. A painless erection of the cavernous bodies with a flaccid corpus spongiosum and firm glans, bright red (oxygenated) aspirates of corpus cavernosum, evidence of trauma, recurrent event, and Doppler indicating elevated arterial flow are signs of nonischemic priapism.[15]

Blood gas testing and color duplex ultrasonography are reliable diagnostic methods for distinguishing ischemic from nonischemic priapism. Cavernosal blood gases in men with ischemic priapism typically have a PO2 of <30 mmHg, a pCO2 of >60 mmHg, and a pH <7.25. Cavernous blood gases in men with nonischemic priapism are similar to the blood gases of arterial blood.[12]

A laboratory evaluation of priapism should include a complete blood count, white blood cell differential, and platelet count. Acute infections or hematologic abnormalities can cause priapism, such as sickle cell anemia, leukemia, and platelet abnormalities.[14] In the emergency department, when there is a suspicion of sickle cell anemia, screening should be performed by either the sickledex test or examination of a peripheral smear and subsequent confirmation using hemoglobin electrophoresis.[12]


  Surgical Treatment Top


Management of ischemic priapism should achieve resolution as promptly as possible. Maintaining tissue oxygenation following episodes of priapism is essential to reduce the damage caused by red blood cell stasis and fibrosis of the corpora cavernosa and thus preserve erectile function. Invasive options for the treatment of priapism include corpus cavernosum aspiration/irrigation and distal and proximal shunting. In general, the principle behind surgery for priapism involves shunting blood away from the corpus cavernosum to the corpus spongiosum, relieving vascular occlusion. While each of these options has been reported in limited clinical series, there are no randomized controlled trials of early surgical interventions.


  Direct Injection Top


Blood aspiration can be performed with percutaneous needle access on both lateral aspects of the proximal penile shaft. Vasoactive irrigation is conducted with a direct injection of a sympathomimetic agent, such as phenylephrine (dosed 100–200 mg every 5–10 min until detumescence, with a 1000 mg maximum dose), using a 27G–30G needle, without prior aspiration of blood from the corpora cavernosa.[16] A dorsal nerve block or local penile shaft block can be used as a preceding penile anesthetic maneuver.[17] The injection of a sympathomimetic drug alone without aspiration/irrigation yields a resolution in approximately 58% of cases.[12] Resolution is achieved by sympathomimetic injection in 77% of patients who had undergone prior aspiration or irrigation.[12] Intervention with blood aspiration after 72 h of priapism may relieve pathologic erection and pain; however, there is no benefit in terms of erectile function preservation.[18]


  Distal Glandular Drainage Top


Penile drainage and/or vasoactive irrigation are early treatment choices for patients with ischemic priapism.[19] Blood aspiration can be performed with intracorporeal access through the glans under general or local anesthesia and must be continued until fresh red oxygenated blood is aspired. Aspiration alone without the use of sympathomimetics, with or without corporal irrigation, resolves the erection in up to 36% of patients; however, the addition of a sympathomimetic injection increases efficacy by up to 81%.[12]


  Distal Shunt Top


In most cases, surgical management is reserved for males who do not achieve detumescence promptly. Failure to achieve detumescence by repeated aspiration over the course of at least 1 h is suggestive of a permanent injury of the smooth muscle, and at this point, surgery should be considered.[17] Failure of the shunt to achieve detumescence is derived from muscle necrosis. A cavernoglanular/corporoglanular shunt should be one of the first choices for the shunting procedures because it is relatively easy to perform, and the complications are very rare.[12] The shunting procedure can be performed with a large biopsy needle or a scalpel inserted percutaneously through the glans [Table 2]. It can also be performed by excising a piece of the tunica albuginea at the tip of the corpus cavernosum (Al-Ghorab). Distal shunts have lower erectile dysfunction (<25%) compared with 50% when a proximal shunt procedure is performed.[20] Proximal shunting using the Quackels or Grayhack procedures may be warranted if more distal shunting procedures have failed to relieve the priapism.[12]
Table 2: Characteristics of shunts

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It is recommended to perform the least invasive surgical procedure at the beginning (direct injection or distal penile procedures), and if this procedure fails, the next step is to continue with proximal shunts.[14]


  Proximal Shunt Top


A surgical fistula can be created between the corpus cavernosum and the corpus spongiosum or one of the penile veins. Proximal shunting can be considered if distal procedures have failed to relieve priapism. Data of postoperative recovery rates of erectile function in men submitted to shunt surgery for prolonged erections are unreliable.[19] The most common proximal shunt procedure is the Quackels (corporospongiosal shunt). At lithotomy position, the bulbocavernosus muscle is dissected and separated from the corpus spongiosum with both corporal bodies incised. The other proximal shunt operation is the corporo-saphenous vein or superficial/deep dorsal vein shunts (Grayhack or Barry shunt), where one of the saphenous veins is ligated and anastomosed with the corpora cavernosa.[20]

Given the morbidity associated with shunt procedures is important to find strategies to diminish postoperative thrombotic complications. Lue and Garcia observed the success of perioperative anticoagulation therapy in preventing premature shunt closure, resulting in better outcomes,[21] they propose it as an integral part of shunt procedures; however, this is not a regular and accepted practice.


  Penile Prosthesis Top


Corporal fibrosis is commonly seen after prolonged ischemic priapism (>72 h or fails to respond to more conservative interventions); therefore, implanting a prosthesis could be difficult later on. Furthermore, implants are far easier to place in the early postpriapism period when the tissue is more elastic and more conducive to dilation. Implants after 6 months are challenging and always require some degree of sharp dissection of the fibrotic tissue or some degree of excision of the tissue.[22],[23]

One study reported the use of malleable devices in early management with a nonabsorbable suture being used to attach the device to the tunica albuginea at the site of the corporotomies. No infections or distal cylinder migration was reported (mean follow-up 15 months).[24] Larger series studied men who presented with prolonged ischemic priapism that was unresponsive to conventional treatment and were therefore given malleable or inflatable prostheses, choosing the device based on the amount of bruising and edema with the thought that patients with minimal bruising and edema were at lower risk for infection and thus were better candidates for an inflatable device. After a median follow-up of 15.7 months (4–60 months), 84% reported successful sexual intercourse. Prosthesis infection occurred in 6% of patients, which was managed by explantation and delayed reinsertion. No patient complained of penile shortening, and the overall satisfaction rate was 96%.[25]

Other studies of early penile prosthesis implantation in refractory priapism found that in patients who underwent surgery 7 days after priapism occurred, 80% of patients required additional corporotomies and downsized cylinders. These complications were not seen in the early implant group.[26]

In conclusion, there is no consensus on performing this type of procedure (Penile Prothesis) early in priapism to prevent erectile dysfunction; however, it is an excellent choice.[10]


  Best Practice and Proposal Top


According to the literature review shown in this article, we propose the step-by-step flowchart presented in [Figure 1].
Figure 1: Step-by-step

Click here to view



  Conclusions Top


The length of the ischemic priapism is an important variable for the prognosis because of the pathophysiology of this condition. Here, we propose a step-by-step approach based on the time and invasiveness of the intervention. However, it is important to note that we could not find any clinical trial evidence that supports this process, and more research is needed for the future statements.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

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Monllor J, Taño F, Arteaga PR, Galbis F. Priapism of the clitoris. Eur Urol 1996;30:521-2.  Back to cited text no. 1
    
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Adediran A, Wright K, Akinbami A, Dosunmu A, Oshinaike O, Osikomaiya B, et al. Prevalence of priapism and its awareness amongst male homozygous sickle cell patients in Lagos, Nigeria. Adv Urol 2013;2013:890328.  Back to cited text no. 2
[PUBMED]    
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Earle CM, Stuckey BG, Ching HL, Wisniewski ZS. The incidence and management of priapism in Western Australia: A 16 year audit. Int J Impot Res 2003;15:272-6.  Back to cited text no. 3
    
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Roghmann F, Becker A, Sammon JD, Ouerghi M, Sun M, Sukumar S, et al. Incidence of priapism in emergency departments in the United States. J Urol 2013;190:1275-80.  Back to cited text no. 4
    
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Kulmala RV, Lehtonen TA, Tammela TL. Priapism, its incidence and seasonal distribution in Finland. Scand J Urol Nephrol 1995;29:93-6.  Back to cited text no. 5
    
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Sugihara T, Yasunaga H, Horiguchi H, Nishimatsu H, Matsuda S, Homma Y, et al. Incidence and clinical features of priapism in japan: 46 cases from the japanese diagnosis procedure combination database 2006-2008. Int J Impot Res 2011;23:76-80.  Back to cited text no. 7
    
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Burnett AL. Pathophysiology of priapism: Dysregulatory erection physiology thesis. J Urol 2003;170:26-34.  Back to cited text no. 8
    
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Berger R, Billups K, Brock G, Broderick GA, Dhabuwala CB, Goldstein I, et al. Report of the American Foundation for Urologic Disease (AFUD) Thought Leader Panel for evaluation and treatment of priapism. Int J Impot Res 2001;13 Suppl 5:S39-43.  Back to cited text no. 17
    
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Bassett J, Rajfer J. Diagnostic and therapeutic options for the management of ischemic and nonischemic priapism. Rev Urol 2010;12:56-63.  Back to cited text no. 18
    
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Salonia A, Eardley I, Giuliano F, Hatzichristou D, Moncada I, Vardi Y, et al. European association of urology guidelines on priapism. Eur Urol 2014;65:480-9.  Back to cited text no. 19
    
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Lue TF, Garcia M. Should perioperative anticoagulation be an integral part of the priapism shunting procedure? Transl Androl Urol 2013;2:316-20.  Back to cited text no. 21
    
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Levine LA, Becher E, Bella A, Brant W, Kohler T, Martinez-Salamanca JI, et al. Penile prosthesis surgery: Current recommendations from the international consultation on sexual medicine. J Sex Med 2016;13:489-518.  Back to cited text no. 22
    
23.
Stember DS, Mulhall JP. Ischemic priapism and implant surgery with sharp corporal fibrosis excision. J Sex Med 2010;7:1987-90.  Back to cited text no. 23
    
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25.
Ralph DJ, Garaffa G, Muneer A, Freeman A, Rees R, Christopher AN, et al. The immediate insertion of a penile prosthesis for acute ischaemic priapism. Eur Urol 2009;56:1033-8.  Back to cited text no. 25
    
26.
Zacharakis E, Garaffa G, Raheem AA, Christopher AN, Muneer A, Ralph DJ, et al. Penile prosthesis insertion in patients with refractory ischaemic priapism: Early vs. delayed implantation. BJU Int 2014;114:576-81.  Back to cited text no. 26
    


    Figures

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    Tables

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  In this article
Abstract
Introduction
Methods
Epidemiology
Pathophysiology
Ischemic Priapism
Clinical Present...
Surgical Treatment
Direct Injection
Distal Glandular...
Distal Shunt
Proximal Shunt
Penile Prosthesis
Best Practice an...
Conclusions
References
Article Figures
Article Tables

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