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Treatment of High-Flow Priapism and Erectile Dysfunction
Superselective embolization of terminal branches of the male internal pudendal artery is a highly successful procedure in the treatment of high-flow arterial priapism. Vascular imaging and treatment in patients with erectile dysfunction (ED) using cavernosography and internal pudendal artery angiography and angioplasty remains a controversial topic.
† Deceased
Priapism
Priapism is a pathologically persisting erection of the penis not associated with sexual stimulation. It is a result of imbalance of arterial inflow and venous outflow involving the corpora cavernosa. The incidence in the general population is low, between 0.5 and 2.9 per 100,000 person-years, and is higher in patients with sickle cell anemia and in men using intracorporal injections.
There are two types—low-flow/ischemic and high-flow/arterial—and these are grouped based on the pathophysiology, with implications for subsequent treatment options and outcomes.
Low-Flow/Ischemic/Venoocclusive Priapism
Incidence
-
This is the most common type.
Etiology
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Any prothrombotic state
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Intracavernous vasodilator injections for treatment of ED
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Postembolization or surgery for venous leak
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Neurogenic
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Drugs
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Idiopathic
Pathophysiology
Low-flow priapism is caused by decreased outflow of blood due to venous thrombosis; thus there results a compartment syndrome–like pathophysiology, with the risk of gangrene.
Clinical Presentation
Acute onset of severe pain, rigidity, and other compartment syndrome clinical findings are noted. Venous blood is evident on aspiration of the corpora cavernosa. Doppler studies show no or low velocities in cavernosal arteries.
Management
Priapism is a medical emergency, and if not treated within 24 hours, leads to irreversible ischemia and tissue necrosis. This type of priapism is usually treated by a consultant urologist. †
First-line treatment is aspiration that confirms the diagnosis and at the same time decompresses. This is followed by irrigation with a sympathomimetic pharmaceutical agent and, if necessary, a surgical shunt. The management is slightly different but follows the same principles for the sickle cell anemia variant of venoocclusive priapism.
High-Flow/Nonischemic/Arterial Priapism
Incidence
-
Less common than the low-flow type; in adults, 80%–90% have a single fistula causing the priapism, but in children, 50% have multiple fistulas.
Etiology
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Mostly traumatic
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Typically a straddle injury to the perineum
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Sometimes results from complications of low-flow priapism
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Can be idiopathic without a recognizable event
Pathophysiology
There is unregulated blood flow in an arteriolacunar (not arteriovenous) fistula between one of the terminal branches of the internal pudendal artery (most commonly the cavernosal artery) and lacunar spaces of the corpora cavernosa. The bulbar and dorsal penile arteries are less frequently involved. Venous outflow is not restricted, because there is no compression of subtunical veins, normally produced by neural stimulation; hence there is a constant state of inflow/outflow without pooling of blood. Shearing forces on the endothelium cause release of increased levels of nitric oxide and activation of the cyclic guanosine monophosphate pathway, resulting in relaxation of smooth muscle.
Clinical Presentation
Unlike the low-flow/occlusive type, there is no ischemia or pain, hence it is not an emergency. The onset is usually delayed after injury, but typically it is clinically evident within 72 hours. Aspiration of the cavernosa reveals arterial blood. Doppler studies show normal or high velocities in cavernosal arteries. The actual site of the arteriolacunar fistula can usually be accurately determined.
Management
American Urological Association guidelines suggest initial conservative management, with 62% of cases resolving spontaneously. However, we believe early interventional radiology management with embolization of the fistula provides a better outcome for high-flow fistulas.
Erectile Dysfunction
Erectile dysfunction is defined as inability to reach or maintain erection sufficient for satisfactory sexual performance. ED is commonly associated with diabetes mellitus (threefold increased risk of ED), hypertension, vascular disease, dyslipidemia, hypogonadism, and depression.
Incidence
-
ED affects up to one-third of men throughout their lives and more than 150 million men worldwide.
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Prevalence increases with age: 12% are younger than 59 years, 22% are 60–69, and 30% are older than 69.
Etiology
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ED may result from organic causes, psychological causes, or a combination of both.
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Possible organic causes could be vascular, neurogenic, hormonal, anatomic, or drug-induced.
Pathophysiology
A normal sexual erectile response results from the production of nitric oxide from endothelial cells after parasympathetic stimuli. Nitric oxide causes smooth muscle relaxation, which leads to arterial influx of blood into the corpus cavernosum, followed by compression of venous return, producing an erection. This neurovascular function must be integrated with sexual perception and desire. Other smooth muscle relaxants (e.g., prostaglandin E 1 analogs and α-adrenergic antagonists) can cause sufficient cavernosal relaxation to result in erection. Many of the drugs that have been developed to treat ED act at this level.
Vascular causes of ED may be arterial or venous or both, and these are the ones amenable to endovascular treatment. Generalized penile arterial insufficiency may result from stenotic arterial lesions of the internal pudendal arteries or from microangiopathy of the arteries of the corpora cavernosa. Failure of the veins to close completely during an erection ( venoocclusive dysfunction) may occur in men with large venous channels that drain the corpora cavernosa, and may be studied by cavernosography. Evidence is accumulating in favor of ED as a vascular disorder in most patients.
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