Vasculogenic Erectile Dysfunction

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Chapter 28 Vasculogenic Erectile Dysfunction

Kirk A. Keegan, David F. Penson

Introduction

The first historical descriptions of erectile dysfunction (ED) date back to Egyptian papyrus nearly 4000 years ago. Egyptian scholars described two types of ED: a “natural” form in which the man was incapable of performing the sex act, and a “supernatural” form rooted in evil charms and spells.¹ Ancient thinkers such as Hippocrates and Aristotle also theorized on the etiology of ED. However, the first accurate depiction of penile anatomy and rudimentary analysis of erection was not published until 1585, when Ambroise Paré described it in his Ten Books on Surgery and the Book of Reproduction.² In these texts, Paré portrayed the penis as a tube with concentric coats of nerves, veins, arteries, two “ligaments” composed of the corpora cavernosa, and the urinary tract.

Over the succeeding centuries, there has been considerable investigation into the hemodynamic and anatomical mechanisms of male erection. Modern understanding of erectile physiology has been delineated only in the last 30 years. Central to our current theories of erectile physiology is the role of smooth muscle in control of arterial and venous flow, the architecture of the tunica albuginea, the role of nitric oxide (NO) as the principal neurotransmitter regulating tumescence, and the function of phosphodiesterases (PDEs) for detumescence. Recent research on the role of endothelial regulation of smooth muscle, the influence of ion channels, and the integral function of endothelial gap junctions has furthered our understanding. This chapter will review these findings, as well as the prevalence, clinical evaluation, diagnostic testing, medical and surgical management, clinical outcomes, and current guidelines regarding vasculogenic ED in detail.

Definition and Classifications

In 1992, the National Institutes of Health convened a Consensus Development Conference on Impotence. The group renamed impotence as male erectile dysfunction and defined it as “the inability to achieve or maintain an erection sufficient for satisfactory sexual performance.”³ Furthermore, they noted that erectile dysfunction represents the most appropriate term, given that sexual desire, orgasm, and ejaculation may be intact despite inability to achieve or maintain erection.

Multiple schema have been proposed to classify the different types of ED. Broadly, ED can be described in terms of organic and psychogenic dysfunction (Box 28-1). The main thrust of this chapter will center on vasculogenic ED, which comprises impaired endothelial function, arterial occlusive disease, veno-occlusive dysfunction, and structural changes to the corpora cavernosa.

Prevalence and Incidence

Erectile dysfunction is quite common, affecting approximately 30 million men in the United States.⁴ Several population-based studies have been performed to address male sexual function and specifically the prevalence and incidence of ED in the American male population. The 1992 National Health Social and Life Survey (NHSLS) was a national survey of 1410 American men between the ages of 18 and 59. In the study group, the prevalence of ED in men aged 18 to 29 years was 7%, aged 30 to 39 was 9%, aged 40 to 49 was 11%, and aged 50 to 59 was 18%.⁵ The Massachusetts Male Aging Study (MMAS), a longitudinal population-based study, evaluated 1709 men between the ages of 40 and 70 who returned questionnaires about a broad range of physiological measures, demographic information, and self-reported sexual function. Participants were surveyed between the years 1987 and 1989 and then reevaluated between 1995 and 1997. In this series, the age-adjusted prevalence of significant ED was 39% in men with coronary artery disease (CAD), 25% in men with diabetes mellitus, and 15% in men with hypertension. Incidence of ED on reevaluation was 25.9 cases per 1000 men per year (95% confidence interval [CI], 22.5-29.9).⁶ Using these data, it was estimated that for Caucasian men, 617,715 new cases of ED would present in the 40 to 69 age group each year.⁷ Data from European and Brazilian researchers suggest a similar incidence of ED in their respective countries.^8,⁹

Functional Anatomy

The functional anatomy of the human penis is composed of several key components. Principally, these are three cylindrical structures—two corpora cavernosa surrounded by a tough tunica albuginea, and the solitary corpus spongiosum which contains the urethra. Vascular components include arteries and arterioles, highly compliant sinusoids within the corpora cavernosa, and compressible venules and veins.

Corporal Bodies, Sinusoids, and Glans

The corpora cavernosa are paired spongy cylinders that lie on the superior aspect of the penis. They are enveloped by the tunica albuginea. The proximal ends of the corpora are separate structures anchored at the ischial ramus. The corpora then fuse underneath the pubic ramus and share a common septum distally towards the glans.

Within the corpora, interconnected sinusoids are enveloped by trabeculae of smooth muscle, collagen, and elastin (Fig. 28-1). The sinusoidal smooth muscle is in intimate association with the cavernous nerves and helicine arteries within the penis. The sinusoids are tonically constricted during the flaccid state. Arterial blood flow diffuses through larger central sinusoids to smaller peripheral sinusoids. In the flaccid state, this slow diffusion of arterial blood results in blood gas values similar to venous blood. During sexual stimulation, release of neurotransmitters causes the smooth muscle around the sinusoids to relax. This results in rapid influx of arterial blood, subsequent entrapment of blood within these expanding sinusoids, and occlusion of veins traversing the tunica albuginea. Subsequent tumescence results in pressure increases of several hundred mmHg and blood gas values approaching arterial levels.¹⁰

Figure 28-1 Drawing of three-dimensional anatomy of human penis, demonstrating inner circular layers and outer longitudinal layers of the tunica albuginea, intervening supports, sinusoidal tissue in corpora cavernosa, corpus spongiosum, and urethra.

The interior of the glans and corpus spongiosum share a similar sinusoidal architecture as the corpora cavernosa. However, the tunica surrounding the spongiosum is thinner and is completely absent around the glans. The corpus spongiosum is a highly compliant body that houses the urethra and facilitates expulsion of semen. The glans is exquisitely sensitive, conical in shape, eases intromission, and forms a cushion for the rigid corporal bodies. These areas engorge in a similar fashion as the corpora cavernosa but to a lesser degree, largely owing to an absence of the tunica albuginea and diminished venous trapping.

Tunica Albuginea

The tunica albuginea is composed primarily of tough type I collagen with a minority component of more flexible type III collagen and elastin. It is arranged in a bilayer, with inner circular layers and outer longitudinal layers (see Fig. 28-1). Intervening struts traverse the body of the corpora cavernosa and provide further support.¹¹ The longitudinal layers of the tunica are present from the glans to the proximal crura, where each corporal body inserts into its ischial ramus to form a foundation for support of the erect penis. Emissary veins (Fig. 28-2) pierce the tunica albuginea. During engorgement, these veins become compressed and allow entrapment of blood within the penis.

Figure 28-2 Penile erection.

A, When flaccid, the corpora cavernosa, including arterioles, sinusoids, and arteries, are contracted. This allows free flow of blood through intervening sinusoidal spaces. Blood exits the corpora cavernosa via emissary veins. B, During erection, arterioles, sinusoids, and arteries relax. This constricts venules and veins and effectively compresses emissary veins under the tunica albuginea. Vascular inflow exceeds outflow, effectively creating an erection.

Arterial System

The internal pudendal artery, a branch of the internal iliac artery (IIA), is the principal source of blood flow to the penis. Up to 70% of men may have accessory pudendal branches that originate from the external iliac, obturator, or vesical arteries.¹² The internal pudendal artery gives rise to the penile artery, which in turn branches in to the dorsal, bulbourethral, and cavernous arteries (Fig. 28-3). The cavernous artery supplies the corpus cavernosum via helicine arteries, which lie in close approximation to the sinusoidal tissue. During erection, these vessels dilate, resulting in engorgement.

Figure 28-3 Penile arterial supply.

Venous System

Venous drainage originates from the three corporal bodies. Venules interdigitate through the cavernosal sinusoids and coalesce below the tunica albuginea into a subtunical plexus. The plexi then form emissary veins that penetrate the tunica albuginea. From there, numerous subcutaneous veins course along the shaft of the penis to form the superficial dorsal vein and a deep dorsal venous system, which in turn drain into the saphenous vein and retropubic venous plexus, respectively ¹³ (Fig. 28-4; also see Fig. 28-2).

Figure 28-4 Penile venous drainage.

Nervous System

Penile innervation occurs via both autonomic (parasympathetic and sympathetic) and somatic (motor and sensory) pathways. Erection and detumescence are largely regulated via the autonomic system. Sympathetic and parasympathetic nerves coalesce to form the cavernous nerve, which penetrates the corpora cavernosa to exert its effect on erection (Fig. 28-5). Sensation and contraction of penile musculature occurs via the somatic nerves.

Figure 28-5 Penile nerves.

Autonomic pathways

Between the T11 and L2 spinal segments, the sympathetic trunk begins. These fibers then form the sympathetic chain ganglia, which continue caudally to the inferior mesenteric and superior hypogastric plexi. Further sympathetic fibers exit to form the hypogastric nerves, and ultimately the sympathetic portions of the pelvic plexus.¹⁴

Between the S2-S4 spinal cord segments, the parasympathetic pathway originates. These fibers also continue caudally to the pelvic plexus (see Fig. 28-5), where they join the aforementioned sympathetic nerves. Together, these nerves then join to form a network of nervous tissue that passes along the lateral and posterior aspect of the prostate to create the cavernous nerves.¹⁵ Stimulation of the sympathetic trunk via the cavernous nerves results in detumescence. Excitation of the parasympathetic aspects of the pelvic plexus and cavernous nerves is responsible for erection. To avoid iatrogenic ED, clear understanding of the location of these nerves is critical during pelvic surgery such as radical prostatectomy or abdominal perineal resection.

Somatic pathways

Sensory receptors in the penile skin and glans are unique in the human body.¹⁶ They are composed of free nerve endings comprising unmyelinated C fibers and thin myelinated A-delta fibers. These coalesce into the dorsal nerve of the penis, which ultimately forms the pudendal nerve. The pudendal nerve then enters the S2-S4 nerve roots at the spinal cord. Via spinothalamic and spinoreticular pathways, sensations such as touch, pain, and temperature are perceived.¹⁷ Interestingly, research by Burnett et al.¹⁸ suggests that the dorsal nerve of the penis carries both autonomic and somatic signals, and therefore contributes to penile sensation, erection, and ejaculation.

Pathophysiology of Erectile Dysfunction

Vasculogenic Erectile Dysfunction

As noted in Box 28-1, ED often represents a multifactorial disease state. Although the focus of this chapter is on the vasculogenic determinants of ED, it is worth noting that within an individual patient, neurological, hormonal, or psychological etiologies of ED may be of contributory or even primary importance. With that said, it is clear the vascular system is responsible for providing blood flow to the erectile tissues of the penis, so any dysfunction within the vascular system may affect erectile function.

Arteriogenic erectile dysfunction

Arteriogenic ED can be due to atherosclerotic or traumatic arterial occlusive disease. Michal and Ruzbarsky ¹⁹ noted impaired penile perfusion is an indicator of generalized atherosclerotic disease, and that the age of onset of ED and CAD is often similar. In fact, ED has been shown to be a bellwether for development of CAD in asymptomatic men,²⁰ and both diseases share the same risk factors—specifically smoking, diabetes, hypercholesterolemia, and hypertension.²¹

In arteriogenic ED, the corpora cavernosa demonstrate lower oxygen tension,²² which may result in a decreased volume of sinusoidal smooth muscle and subsequent venous leak.²³ In an experimental animal model, rabbits with iatrogenic iliac atherosclerotic disease demonstrated alterations in their downstream penile arteries and a reduction in cavernosal smooth muscle content.²⁴ These alterations were associated with decreased nitric oxide synthase (NOS)- and NO-mediated relaxation of corpora cavernosal tissue.²⁵ Erectile dysfunction due to traumatic stenosis of cavernous or pudendal arteries has been noted in young men with pelvic trauma²⁶ and in long-distance cyclists.²⁷

Venogenic erectile dysfunction

Not only can diabetes, hypertension, hypercholesterolemia, and penile injury result in penile arterial disease, these disorders can also result in loss of elastic fibers within the cavernosal venules and sinusoids. This loss of compliance results in diminished venous trapping and subsequent veno-occlusive dysfunction.²⁸ In fact, diminished venous occlusion may represent the most common form of vasculogenic ED.²⁹ Loss of smooth muscle relaxation due to heightened adrenergic tone or decreased NO release may exacerbate already poor compliance in these fibrotic sinusoids.³⁰ Finally, fibrosis leading to increased collagen deposition between cell membranes may abolish critical signaling and intercellular transmission via disrupted gap junctions.³¹

Drug-Induced (Iatrogenic) Erectile Dysfunction

The data are clear that diabetes, hypercholesterolemia, and hypertension have strong influences on ED. Not surprisingly, some of the medications used to treat these disorders have been implicated as contributing factors in its development. However, it is often difficult to ascertain the direction of causation in medication-induced ED. Of the cardiovascular medications, thiazide diuretics have the strongest association with development of ED. Chang et al.³² demonstrated that men treated with thiazide diuretics showed a significant increase in ED relative to those men prescribed placebo medication. Further evidence of the role of thiazides in ED was noted in the Treatment of Mild Hypertension Study (TOMHS), which demonstrated the prevalence of ED was twofold higher in men taking a thiazide versus placebo or other agent.³³ Curiously, after 4 years of treatment in this study, prevalence of ED within the placebo group approached that of those receiving thiazide. The significance of this finding is unclear but may be related to early unmasking of clinically undetected ED in those men receiving thiazides.

Nonselective β-blockers such as propranolol have been shown to inhibit erection compared to placebo, but this has not been demonstrated in selective β₁-antagonists.³⁴ In clinical series, there does not appear to be a deleterious influence of either angiotensin-converting enzyme (ACE) inhibitors or calcium channel blockers on erection.^33,³⁵ Interestingly, angiotensin receptor antagonists and some statins, such as atorvastatin, appear to improve erectile function.^36,³⁷ Of note, some α-blockers, such as terazosin, have occasionally been implicated in the development of priapism, or pathological erection, likely related to the α-adrenergic blockade of the sympathetic outflow necessary for detumescence.³⁸ Other medications implicated in the development of ED include spironolactone, some antipsychotics, selective serotonin reuptake inhibitors, opiates, and antiandrogens.³⁹

Evaluation of Erectile Dysfunction

Evaluation and treatment of a man presenting with ED has changed considerably over the last 30 years. This shift is largely due to the influence of oral therapies for treatment and a transition to a more patient-centered and evidence-based treatment plan. Evaluation should begin with an in-person and detailed medical, sexual, and psychosocial history (Fig. 28-6). Additionally, the use of a quantifiable questionnaire such as the International Index of Erectile Function (IIEF)⁴⁰ may be useful to establish baseline sexual function and to assess future treatment efficacy.

Figure 28-6 Algorithm for evaluation of erectile dysfunction (ED).

PDE, phosphodiesterase 5.

(Adapted from Lue TF, Giuliano F, Montorsi F, et al: Summary of the Recommendations on sexual dysfunctions in men, J Sex Med 1:6–23, 2004, and Lue, TF, Broderick, GA: Evaluation and nonsurgical management of erectile dysfunction and premature ejaculation. In Wein AJ, Kavoussi LR, Nocik AC, et al, editors: Campbell-Walsh Urology, ed 9, Philadelphia, 2007, Saunders, pp 751–752.)

History

The history should begin with a thorough discussion of the patient’s medical history, with particular attention to medical comorbidities. As previously mentioned, ED is an early marker for systemic atherosclerotic disease, and all patients should be questioned about their cardiovascular health.⁴¹ In particular, a detailed discussion regarding any chest pain, palpitations, dyspnea, and limb pain may reveal occult CAD, congestive heart failure, or peripheral artery disease. Querying the patient about his medication use may elucidate agents that contribute to ED or may be contraindications to oral PDE therapy (e.g., nitrates). A sexual history should focus on timing, duration, and severity of the patient’s ED, as well as the occurrence of other associated problems, such as premature ejaculation, desire, or anorgasmia. To complete the sexual history, a psychosocial evaluation may be relevant; sexual dysfunction may affect self-esteem and coping. Both depression and treatment for depression may be associated with ED.

Physical Examination

Physical examination may be equally revealing. The patient’s general appearance may alert the physician to serious underlying cardiovascular disease if the patient is cyanotic, dyspneic, emaciated, or plethoric. Additional pertinent findings on physical examination include general body habitus, secondary sex characteristics, staining of fingers associated with smoking, nail clubbing, lower-extremity ulcers, or edema. A thorough cardiopulmonary examination is required. Finally, an examination of the genitalia may demonstrate chordee, Peyronie disease, or signs of hypogonadism such as Kallmann’s or Klinefelter’s syndromes.

Laboratory Assessments

Laboratory testing for men with sexual dysfunction may include fasting glucose, lipid levels, sex hormone values (including morning free and total testosterone levels), and other endocrine tests, such as thyroid function tests and prolactin levels. Again, this testing may reveal comorbid conditions such as diabetes, hyperlipidemia, or hypogonadism that may contribute to ED. Prostate-specific antigen (PSA) testing may be considered in men over 40, men with a strong family history of prostate cancer, or men in whom testosterone replacement is being considered, although this is a point of debate in some circles.⁴² The optimal laboratory test panel for the evaluation of ED has yet to be determined.

Education and Referral

At this point in the medical interview, it is important to review with the patient the likely etiologies, pertinent anatomy and physiology, and potential treatment options. This refocusing lies at the center of the patient-centered approach and shared decision making. Additionally, the opportunity for patient education provides a chance to address modifiable risk factors, such as diet, exercise, smoking, alcohol abuse, and medication use, that may contribute to ED.

With the advent of oral PDE inhibitors, the majority of initial ED consultations now occur in the primary care physician’s office. However, based upon the findings of the history, physical examination, laboratory testing, or on initial oral drug treatment failure, it may be beneficial to refer the patient to a specialist (endocrinologist, cardiologist, urologist). Particularly germane to the urologist will be further evaluation of the penile vascular system via injection of vasodilators such as papaverine, phentolamine, or alprostadil.

Although rarely performed in 2010 and usually only after an empirical trial of oral PDE5 inhibitors, first-line urological evaluation of penile blood flow consists of a combined intracavernous injection of a single or combination of vasodilators and some form of penile stimulation. This testing allows the urologist to evaluate the specific mechanics of the erectile response and avoid the confounding influence of neurological or hormonal factors. Second-line urological evaluation includes intracavernous injection of a vasodilator and blood flow measurement with duplex ultrasonography, possibly Doppler waveform analysis, and peak systolic velocity calculations. Third-line evaluations may include calculations of cavernous arterial systolic occlusion pressures (CASOP), pharmacological arteriography, pharmacological cavernosometry, or cavernosography.⁴³ These increasingly invasive procedures are often reserved for young men with traumatic pelvic or penile arterial injuries who may be candidates for arterial revascularization.

Treatment

As noted previously, the initial step in penile tumescence is arousal and subsequent release of NO into vascular and cavernous smooth muscle cells (SMCs). This causes stimulation of guanylyl cyclase, with a concomitant rise in cyclic guanosine monophosphate (cGMP) and resultant reduction of cytoplasmic calcium. This leads to smooth muscle relaxation, increased arterial inflow, venous trapping, and subsequent erection.⁴⁴ With the discovery that PDE inhibitors prevent breakdown of cGMP,⁴⁵ and ensuing FDA approval of sildenafil in 1998, a new era in ED treatment was born.

Oral Agents

Sildenafil was the first specific PDE inhibitor approved for treatment of ED. Vardenafil and tadalafil have since followed suit. Multiple PDE subtypes have been identified, but PDE5 is present in high concentrations in corpora cavernosal tissues. As such, sildenafil, vardenafil, and tadalafil represent specific PDE5 inhibitors. These three medications appear to have equivalent efficacy and are generally well tolerated. Primary side effects include visual disturbances, flushing, and dyspepsia. Vardenafil should be avoided in patients who take type 1A antiarrhythmics such as quinidine or procainamide, type 3 antiarrhythmics such as sotalol or amiodarone, or in patients with congenital prolonged QT syndrome. Sildenafil, vardenafil, and tadalafil should all be avoided in patients taking nitrates. Each medication requires about 15 minutes to 1 hour to be effective. The half-lives of sildenafil and vardenafil are shorter, at approximately 5 hours, while the half-life of tadalafil is about 18 hours. For those patients who do not respond to oral treatment or are not candidates for oral PDE5 inhibitors, a number of other options are available, although all are more invasive.

Alprostadil (Prostaglandin E₁)

Prostaglandin E₁ (PGE1) mediates relaxation of corporal cavernosal tissue by activating prostaglandin (PG) receptors and subsequently increasing cyclic adenosine monophosphate (cAMP) levels in the corporal smooth muscle. Elevated cAMP results in reduction of cytosolic calcium and relaxation of smooth muscle. Alprostadil is formulated for both intraurethral placement and intracavernosal injection. Intraurethral administration involves insertion of a pellet approximately 3 mm in size, 2 to 3 cm within the distal urethra. Alprostadil is absorbed via the urethral mucosa, passes through the corpus spongiosum, and then via the emissary veins. The medication passes into the corpora cavernosa to exert its vasodilatory effects. Efficacy of intraurethral alprostadil is about 66% in office placement and about 50% in home placement.⁴⁶ Penile pain is often a significant side effect of alprostadil treatment.

Intracavernous injection of alprostadil works by the same mechanism as intraurethral placement. Researchers have noted higher efficacy with intracavernosal placement. However, alprostadil is still limited by pain during erections in 16.8% of patients, penile fibrosis in 2%, hematoma at the injection site in 1.5%, and priapism in 1.3% of patients.⁴⁷ Alprostadil is formulated in a powder and must be reconstituted and refrigerated.

Papaverine and Phentolamine

Other injectable agents include papaverine and phentolamine. Papaverine exerts its effect on penile erectile tissue by an inhibitory action on PDE, resulting in increased cAMP and cGMP as well as inhibition of voltage-gated calcium channels. These mechanisms each result in cavernosal smooth muscle relaxation and subsequent erection. Papaverine’s efficacy is approximately 50%, though it has not been expressly approved by the FDA for use in ED therapy. The incidence of priapism may be as high as 33% in patients receiving solitary papaverine treatment, and the incidence of penile fibrosis with this form of treatment is high.⁴³

Phentolamine is also used for injection therapy but works by a different mechanism; it functions as a competitive α-adrenergic antagonist. It is postulated to induce erection by releasing sympathetic tone and thereby increasing corporal blood flow. Systemic hypotension, reflex tachycardia, and nasal congestion are its principal side effects.⁴⁸

Typically these drugs are used in two- or three-drug combinations that allow dose reductions of each medication, increased efficacy approaching 90%, and decreased rates of pain, fibrosis, and priapism. For men unwilling or unable to inject themselves to induce erections, several other options exist.

Vacuum Erection Devices

In 1917, Otto Lederer was awarded the first patent for a surgical device to induce and maintain erection.⁴⁹ Since then, the vacuum erection device (VED) has been modified and perfected, yet the principle remains the same. The VED consists of a cylinder and suction pump that induces erection by negative pressure and subsequent increased corporal flow. A compression band is then placed at the base of the penis to trap engorged blood (Fig. 28-7). The erection is different than a physiological erection in that girth is increased, the penis is cooler, and it is less rigid than a natural erection. However, success rates are good, and patient and partner satisfaction are high. Cookson et al. noted a 90% chance of achieving a good-quality erection with satisfaction rates over 80%.⁵⁰ For patients failing the treatments discussed, surgery is typically reserved as a final treatment option.

Figure 28-7 Vacuum erection device.

Surgery

In 1936, a Russian surgeon named Bogoraz was the first person to create a functional autologous penile implant. He used rib cartilage in an attempt to correct ED. Although innovative, his success with this treatment was largely limited by resorption of the cartilage.⁵¹ In 1973, Scott ushered in the modern era of penile implantation with development of the three-piece inflatable penile prosthesis.⁵² Penile prostheses are typically reserved for men with organic ED who have failed or rejected treatments such as oral medications, vacuum erection devices, intraurethral alprostadil, or injection therapy. Three classes of penile implants exist: malleable, semirigid, and inflatable. Malleable and semirigid prostheses are typically placed via a distal penile approach. The inflatable prosthesis comes either as a two-piece or three-piece model that is composed of inflatable cylinders, tubing, a pump mechanism, and a reservoir (Fig. 28-8). Typically these are placed under general anesthetic, via a penoscrotal or infraumbilical incision. Infection rates vary from 3% to 8%.⁵³ Patient and partner satisfaction is over 90%, and freedom from mechanical failure ranges between 80% and 95% at 5 years.⁵⁴

Figure 28-8 Surgically implanted inflatable penile prosthesis.

Vascular Surgery

During the 1970s and 1980s, surgery for arteriogenic ED was routinely performed. However, a more contemporary understanding of the pathophysiology of ED has limited the use of vascular surgery for ED. We now understand that ED often represents a systemic disruption of vascular smooth muscle. Currently, the only patient group in whom penile revascularization surgery is likely to be successful is in nonsmoking, non-diabetic young men who have no demonstrable venous leak, and have stenosis of the internal pudendal artery due to trauma or congenital causes. As noted previously, these patients should undergo dynamic infusion cavernosography and cavernosometry (DICC) to rule out veno-occlusive dysfunction before embarking on surgical treatment.

Longitudinal Psychological Outcomes

There is significant interplay between psychological health and ED, but the direction of that relationship is not always clear. Few studies have evaluated the psychological benefit from ED treatment or baseline psychological characteristics of men with ED. In 2006, we evaluated 153 men in an observational ED registry and collected clinical and psychosocial data at baseline and during follow-up. Of those patients who responded to treatment, these men reported significant improvements in sexual self-efficacy, while nonresponders reported small decrements. Surprisingly, nearly 42% of the patients describing ED were not offered treatment by their physicians.⁵⁵ Given the benefits in psychological health suggested by this study, and the high incidence of occult cardiovascular disease noted in previous studies, this should be a call to all healthcare providers to actively diagnose and treat ED in their patients.

Guidelines

In 2005, the American Urologic Association convened a consensus group of experts within the discipline of erectile dysfunction.⁵⁶ The committee created a set of guidelines to help clarify the standard of care, recommended treatments, and offered expert opinions on treatment of ED. The primary findings of these guidelines are presented in Box 28-2 and form the basis of current standard practice.

Box 28-2 American Urological Association Management Guidelines for Erectile Dysfunction