Penile Vascular Surgery

JACK M. ZUCKERMAN

KURT MCCAMMON

Erectile dysfunction (ED) negatively impacts quality of life for a diverse spectrum of the worldwide population. In the United States, its prevalence in men 40 to 70 years of age has been estimated around 50% (1), and the incidence of ED increases with each decade of life (2). Many patients with ED have a variety of risk factors, including atherosclerotic arterial disease, diabetes mellitus, hypertension, and tobacco abuse leading to arteriogenic or neurogenic ED. Not surprisingly, coronary artery disease (CAD) has been shown to have a direct correlation with pudendal artery stenosis leading to arterial insufficiency and ED (3).

In the aging male, ED most commonly is a manifestation of the patients overall health, specifically vascular health. Sustaining a rigid erection requires adequate perfusion of the corpora cavernosa through a robust arterial inflow as well as increased resistance to venous outflow. Systemic risk factors affecting either arterial inflow or venous outflow, therefore, can be expected to negatively impact erectile function. Endothelial dysfunction commonly affects both pudendal and coronary arteries (4). For patients without known vascular disease, a new ED diagnosis may represent a harbinger of future adverse events, such as myocardial infarction or cerebrovascular insult. Montorsi and colleagues identified a significant lag of 39 months between presentation of ED and CAD, suggesting that the smaller penile vessels are affected by arterial disease prior to the larger caliber coronary arteries (5).

Although common in the elderly population, young and middle-aged men (age teens to 40 or 50 years) present less often for evaluation of ED. Although practitioners now commonly consider vascular disease in the older patient with ED, younger men are more likely to be diagnosed with a psychogenic etiology for their impotence. Ironically, as these young men are often otherwise healthy, it is this very population who may be found to have isolated vascular lesions amenable to curative surgical intervention.

Traumatic injuries are a less frequent etiology of ED. Pelvic fractures, which are the primary traumatic injury associated with ED, are relatively rare and occur in less than 10% of blunt trauma (6,7). Pelvic fractures most often result from a high-energy impact, which has implications for nearby genitourinary organs, primarily bladder and urethra. Pelvic fracture urethral injuries (PFUIs) with disruption of the membranous urethra have been reported in up to 10%, and bladder injuries occur slightly more frequently (6,7,8,9). Despite the polytrauma setting in which most pelvic fractures occur, improvements in trauma resuscitation have resulted in dramatically reduced mortality for these patients. Demetriades and colleagues described a large series of traumatic pelvic fractures and found an overall mortality rate of only 13.6%, of which less than 1% died as a direct result of the pelvic fracture (6). These improvements in survivability subsequently result in a larger portion of these patients suffering from chronic problems related to their injuries, including sexual dysfunction. This is particularly problematic for the young adult patient at the beginning of his sexual life.

The distal internal pudendal, common penile, and cavernosal arteries are also susceptible to blunt trauma less obvious than an injury that causes a pelvic fracture. Given their location within Alcock canal and proximity to the ischiopubic rami, these arteries can be injured simply bicycle riding or by a straddle injury, such as perineal trauma attempting advanced “rail tricks” on a skateboard or snowboard (10).

Similar to focal arterial insufficiency, ED secondary to venoocclusive disease (venogenic ED [VED]) is an etiology found in a portion of younger patients and may be amenable to surgical intervention. Failure of full expansion of the sinus spaces secondary to diffuse smooth muscle dysfunction or replacement with fibrous tissue accounts for much of the identified venoocclusive dysfunction. Additionally, alterations within the tunica albuginea, specifically atrophy of the collagen composition leading to tissue laxity, have been suggested to account for a portion of patients with diffuse veno-occlusive dysfunction (11). These etiologies are thought to occur primarily in older men, especially those with other associated conditions, such as having undergone radical prostatectomy or pelvic radiation (12,13). However, in younger patients, focal defects in the integrity of the tunica albuginea or congenital abnormal venous channels may also result in VED. These patients often present with primary ED, present since initial sexual encounters. Penile trauma, surgery for priapism or Peyronie disease, and previous endoscopic incisions of urethral strictures can all lead to defects in the corporal veno-occlusive mechanism (14).

In this chapter, we will discuss the vascular surgical management for ED in patients with focal anatomic defects in either arterial inflow or venous outflow. We review the diagnosis, patient selection, evaluation and treatment outcomes, and complications.

PHYSIOLOGY OF ERECTILE FUNCTION

Penile erection begins with autonomic cavernosal nerve stimulation (15). Nitric oxide (NO) synthase, an enzyme in lacunar space vascular endothelial cells and autonomic cavernosal nerve endings, facilitates the synthesis of NO from molecular oxygen and L-arginine. During sexual stimulation, NO activates guanylyl cyclase, an enzyme that facilitates the synthesis of the second messenger, cyclic guanosine monophosphate (cGMP) from guanosine triphosphate. The elevated concentrations of cGMP result in lowered intracellular calcium, thus promoting penile smooth muscle relaxation. Biologic consequences of
NO-cGMP relaxation include increased arterial blood inflow, engorgement of the lacunar spaces, lengthening and enlargement of the corporal erectile tissue within the constrained tunica albuginea, and eventual subtunical venule occlusion with increased penile venous outflow resistance and corporal venoocclusive function (16).

DIAGNOSIS

Younger men with ED and the absence of other vascular risk factors represent the ideal patient population to evaluate for vasculogenic and/or VED. Evaluation should begin with a comprehensive history and physical examination, specifically a detailed past urologic history. Common risk factors for ED should be ruled out, such as medication side effects, cardiovascular disease, diabetes, tobacco use, and psychological disorders. History may reveal a history of pelvic fracture or penile/perineal trauma. Distance bicycle riding is a known risk factor for pudendal arterial injury, which may lead to arteriogenic ED and should be assessed (17). Patients with congenital venoocclusive dysfunction may complain of complete lifelong ED or rapid loss of erection. Any past genitourinary procedures, especially penile surgeries must be documented. A limited endocrine evaluation should be obtained, including a morning testosterone.

FIGURE 70.1 Diagnostic algorithm for arterial or venogenic erectile dysfunction (VED). DICC, direct infusion cavernosometry and cavernosography; EDV, end diastolic velocity; ICI, intra-cavernosal injection; RI, resistive index; PDE5, phosphodiesterase type 5.

Patients suspected of either arteriogenic or VED should be offered a progressive diagnostic evaluation (Fig. 70.1). Penile color duplex Doppler ultrasonography is the best initial study. This test allows a rapid assessment of both penile arterial inflow and veno-occlusion. Additionally, it allows direct observation of the erectile response to intracavernosal injection of a vasodilating agent. Patients are administered 20 µg of prostaglandin E1, and the duplex is performed 10 minutes following administration. We determine patients to have arterial insufficiency if their peak systolic velocities for the dorsal or cavernosal arteries are less than 30 cm per second (18,19). Prolonged systolic rise time, especially greater than 100 milliseconds, is also associated with atherosclerotic ED.

In patients with normal arterial inflow, venous leak is ruled out if the resistive index is >0.9 and/or the end-diastolic velocity approaches zero (less than 5 cm per second). Venous leak is suggested when the resistive index is <0.75 and the dorsal vein velocity is >10 cm per second (18). Finally, during the penile duplex ultrasound, the deep inferior epigastric arteries (DIEA) are also evaluated, giving us important information about vessel size, blood flow within the vessel, and where the vessel begins its intramuscular course in the event these vessels
are used for arterial bypass surgery. During the entire procedure, it is crucial to provide a private, quiet, and comfortable environment for testing because patient anxiety will effectively counteract the dilatory effect of the injected agent and reduce the reliability of the results. Those patients not achieving a sufficient erection following injection of the vasodilating agent, whether secondary to anxiety and sympathetic discharge or concomitant arterial pathology, cannot be adequately evaluated for veno-occlusive dysfunction. Penile duplex interpreted in that scenario have been shown more commonly to falsely diagnose venous leak (20). Conversely, patients achieving a normal rigid erection following administration of a vasoactive intracavernosal agent lessen the likelihood of significant arterial or venous pathology.

If arterial insufficiency is suggested, patients being considered for surgical intervention should undergo a selective internal pudendal angiogram to evaluate for pudendal or common penile artery occlusion. We also evaluate the inferior epigastric arteries during this angiogram because these will serve as the donor vessels during any future revascularization. More recently, we have obtained computerized tomography (CT) angiography to help clarify the course of the deep inferior epigastric artery (DIEA). We have found this especially helpful in those patients who show an early entry of the DIEA into the rectus muscle. Patients in whom venogenic impotence is suggested on penile duplex do not require a pudendal angiogram.

Direct infusion cavernosometry and cavernosography (DICC) are the definitive tests for diagnosing VED and identifying sites of leakage. We perform this study in all patients being considered for venous surgery. Small gauge needles are placed into each of the corpora cavernosa. One is connected to a pressure transducer, and the other is connected to an infusion pump with metered delivery rates of heparinized saline. After injection of a vasodilating agent, the need for a flow rate of >20 mL per minute of saline to maintain a rigid erection at an intracorporeal pressure of at least 90 mm Hg is indicative of corporal veno-occlusive dysfunction. A maintenance flow rate between 10 and 20 mL per minute is considered borderline for venous leakage. Excessively high maintenance flows (>50 mL per minute) usually indicate massive venous runoff, and these patients do not do well with veno-occlusive surgery (21). Pressure decay of more than 30 mm Hg within 30 seconds is also suggestive of venous leak. Isosmotic contrast material is then infused into the corpora at the previously defined maintenance flow rate from cavernosometry and then anteroposterior and oblique radiographs of the penis are taken. The most common sites of venous leakage seen in patients with veno-occlusive dysfunction are the deep dorsal vein, the cavernosal veins, and the circumflex veins at the base of the penis. A large amount of drainage into all of these systems is also a contraindication to surgery.

More recently, CT imaging has been suggested in lieu of DICC to evaluate the penile venous drainage. After injection of a vasodilating agent, Virag and Paul reported on 38 patients who had dilute contrast injected into the corporal bodies and three-dimensional CT reconstructions obtained to evaluate prominent venous drainage (22). They suggest that this may be an option in the future that is less invasive and easier to perform. At this time, however, protocols for its use in the diagnosis of venous leak are not well defined, and we continue to perform DICC prior to any venous procedure for VED.

ALTERNATIVE TREATMENT OPTIONS

All men thought to have either focal arteriogenic or VED should undergo a trial of medical management. Many patients, regardless of the etiology of their ED, will respond to medical management with oral phosphodiesterase type 5 (PDE5) inhibitors. It has been suggested that a PDE5 trial may be performed in most men even prior to an extensive workup because their efficacy lessens the likelihood of surgically significant arterial or venous pathology (23). Other conservative options include a vacuum erection device with or without a penile band. The band is an especially useful conservative option in patients with VED because it acts to counteract the leak. Patients not responding to these agents should be offered a trial of intracavernosal injections with either prostaglandin E1, papaverine, and/or phentolamine. Intraurethral prostaglandin (MUSE) is also an option for patients not willing to attempt penile injections. Patients not responsive to more conservative measures should be counseled on available surgical options, including arterial or venous surgery (when indicated) or penile prosthesis placement.

ARTERIOGENIC ERECTILE DYSFUNCTION

Patient Selection

Patient selection is paramount when considering penile arterial bypass for the treatment of ED. All patients should have a normal neurologic and endocrine evaluation. Younger patients without associated vascular comorbidities will achieve the most optimal outcome, although limited comorbid conditions are not an absolute contraindication. Current and past tobacco use will lead to worse outcomes, and patients should be counseled accordingly (24). All patients should have the diagnosis confirmed with penile duplex ultrasound without suggestion of veno-occlusive dysfunction. Focal lesions should be confirmed with selective pudendal angiography and appropriate recipient and donor vessels should be identified. At our institution, we primarily offer revascularization to patients with bilateral complete occlusion of the internal pudendal or common penile arteries without reconstitution through collaterals; however, arterial bypass has been performed in patients with unilateral lesions only.

Surgical Technique

All our penile revascularization surgeries are performed in a similar fashion, by anastomosing the deep inferior epigastric artery (IEA) to the dorsal penile artery in an end-to-side fashion (Fig. 70.2). The side chosen for anastomosis is based on the vessel with the largest diameter both on angiogram and intraoperative findings. Occasionally, we do anastomose the right IEA to the left dorsal penile artery, or vice versa, but this is rare. Each surgery is performed using a two-team approach with urology and plastic and reconstructive surgery working simultaneously. All anastomoses are performed using standard microvascular technique.