Overview

Since the introduction of several effective oral treatments for erectile dysfunction (ED), primary care physicians and midlevel providers manage most patients wishing treatment of male sexual dysfunction. ED is defined as the consistent or recurrent inability to attain and/or maintain penile erection sufficient for sexual performance. ED constitutes an evolving public health concern. Studies from the 1990s estimated that half of men older than 40 years had ED. Public awareness, pharmaceutical marketing, and new areas of research, such as cancer survivorship, are also increasing. In aggregate, this research and awareness is increasing the demand for treatment to the primary provider. Failure or poor efficacy of first-line treatments often leads to specialty referral. Other reasons for specialty referral may be trauma, uncertainty of diagnoses, or simply, the wish of the patient or provider.

Broadly categorized, there are 3 types of ED: neurogenic, psychogenic, and vasculogenic. Neurogenic and psychogenic causes are discussed by Altof and Needle elsewhere in this issue. Vasculogenic causes can be arterial, venoocclusive, or some combination of the two. Vasculogenic ED may account for up to 60% to 80% of all cases reported.

There has been considerable research into diagnostic techniques over the past few decades. Without invasive testing, the urologist was limited to inferences made from physical examination and patient-based questionnaires. More data were often required to make solid clinical and surgical decisions. This requirement of data prompted several different types of investigations. The first-line diagnostic test for vasculogenic ED has been combined intracavernous injection and stimulation (CIS) and direct assessment by an observer. This test is used to bypass both neurologic and hormonal influences and allow the provider to directly evaluate the vascular status of the penis. A normal response from CIS is associated with appropriate venous occlusion. False-negative results are found in as many as 20% of patients with intermediate arterial inflow. False-positive result could also commonly occur.

If more testing is thought to be needed or an operative intervention is being considered, such as for Peyronie’s disease or for pelvic trauma, a second-line study is warranted. The pharmacopenile Doppler ultrasonography (PDDU) is a diagnostic modality useful in determining the subtype of vasculogenic ED as well as the magnitude of its severity. PDDU involves injecting a vasoactive penile stimulant followed by genital self-stimulation, audiovisual stimulation, or in some cases, repeat injection during which blood flow is assessed by color duplex Doppler ultrasonography. This procedure allows for both a direct and a quantifiable evaluation of ED. Ultrasonography is also able to provide information on the underlying soft tissue abnormalities such as a Peyronie’s plaque.

Penile anatomy

Three cylindrical structures, the corpus spongiosum, ventrally containing the urethra, and the paired corpora cavernosa, form the penis. The corpora cavernosa are covered by a 2-layer tunica with outer longitudinal fibers and inner circular fibers. There are also fibrous struts that help add support to the erect penis. The intracavernosal septum incompletely divides the 2 cylinders. Clinically, this anatomy is advantageous because only a single injection to the corporal body is required. The medication will circulate to the contralateral side. The tunica albuginea itself is also covered with a more superficial Buck fascia and a loose connective tissue and skin ( Fig. 1 ). On ultrasonography, the corpora cavernosa appears hypoechoic and encased in a hyperechoic tunica.

Cross section of the penis demonstrating the visual anatomy noted on a typical study.

Arterial supply to the penis is from the branches of the common penile artery, which is the direct continuation of the internal pudendal artery bilaterally. This artery branches into 3 named arteries. The cavernosal artery pierces the corporal body and travels in the center of the erectile tissue. These arteries are evaluated during the ultrasonographic study as discussed later. The bulbourethral artery enters the spongiosum superiorly and supplies the urethra, the spongiosum, and the glans penis. The third artery is the dorsal artery of the penis that courses between the dorsal vein and penile nerves. It gives off branches to the cavernous bodies and circumferential branches to the spongiosum. As with much of the pelvic vasculature, considerable variations have been found in the arterial supply to the penis. On ultrasonography, the arteries can be found in several imaging planes and are easily seen as bright parallel lines because the arterial walls are hyperechoic ( Fig. 2 ). The venous drainage of the corpora begin with the intersinusoidal and subtunical venous plexuses. This venous drainage continues to the emissary veins and then to larger channels such as the dorsal vein of the penis. The venous function in ED is described later.

A cavernous artery is seen in this sagittal ultrasonography. The appearance of the arterial walls is consistent with arthrosclerosis and/or calcification. RCA, right cavernous artery.

Penile anatomy

Three cylindrical structures, the corpus spongiosum, ventrally containing the urethra, and the paired corpora cavernosa, form the penis. The corpora cavernosa are covered by a 2-layer tunica with outer longitudinal fibers and inner circular fibers. There are also fibrous struts that help add support to the erect penis. The intracavernosal septum incompletely divides the 2 cylinders. Clinically, this anatomy is advantageous because only a single injection to the corporal body is required. The medication will circulate to the contralateral side. The tunica albuginea itself is also covered with a more superficial Buck fascia and a loose connective tissue and skin ( Fig. 1 ). On ultrasonography, the corpora cavernosa appears hypoechoic and encased in a hyperechoic tunica.

Cross section of the penis demonstrating the visual anatomy noted on a typical study.

Arterial supply to the penis is from the branches of the common penile artery, which is the direct continuation of the internal pudendal artery bilaterally. This artery branches into 3 named arteries. The cavernosal artery pierces the corporal body and travels in the center of the erectile tissue. These arteries are evaluated during the ultrasonographic study as discussed later. The bulbourethral artery enters the spongiosum superiorly and supplies the urethra, the spongiosum, and the glans penis. The third artery is the dorsal artery of the penis that courses between the dorsal vein and penile nerves. It gives off branches to the cavernous bodies and circumferential branches to the spongiosum. As with much of the pelvic vasculature, considerable variations have been found in the arterial supply to the penis. On ultrasonography, the arteries can be found in several imaging planes and are easily seen as bright parallel lines because the arterial walls are hyperechoic ( Fig. 2 ). The venous drainage of the corpora begin with the intersinusoidal and subtunical venous plexuses. This venous drainage continues to the emissary veins and then to larger channels such as the dorsal vein of the penis. The venous function in ED is described later.

A cavernous artery is seen in this sagittal ultrasonography. The appearance of the arterial walls is consistent with arthrosclerosis and/or calcification. RCA, right cavernous artery.

Physiology of erection

In a flaccid state, the subtunical and intersinusoidal veins freely flow to the emissary veins. The arterioles and sinusoids maintain a high resting tone, which limits the inflow into the corpora. When combined, these yield a flaccid penis. After appropriate neural stimulation, a cascade of neurotransmitters, such as nitric oxide, affect the vascular supply to the penis. This starts with relaxation of the smooth muscle in the cavernosal arteries and then proceeds to the sinusoids. This relaxation promotes a high inflow to the corporal bodies. Tumescence continues as the sinusoids fill with blood and begin to engorge. As the tunica elongates and expands, it begins to occlude the emissary veins between the inner circular and outer longitudinal layers described earlier. ( Fig. 3 ) The occlusion propagates the erection because inflow is high and vascular outflow is at a minimum. Eventually, the intracorporal pressure increases to systemic levels and the inflow becomes reduced as well. Initially, the glans penis and corpora spongiosum react similarly in regard to flow. The major difference is the lack of tunical coverings and thus minimal venous occlusion. These structures continue to have high arterial inflow and function similar to an arteriovenous shunt. Just as tumescence proceeds step-wise, detumescence does so as well, with several separate stages proceeding according to penile pressure as the penis returns to its normal state.

Physiology of erection revealing the changes in the corporal smooth muscle and the accompanying vasculature. ( A ) The normal anatomy and physiology in the erect phallus, ( B ) the normal anatomy and physiology in the flaccid phallus.

Patient selection

As with most diagnostic interventions, the patient selection process begins only after a satisfactory evaluation has been performed. A full patient history should be obtained, including a medical, surgical, sexual, and psychosocial history. The use of a patient self-assessment such as the International Index of Erectile Function or the Sexual Health Inventory for Men is also helpful in the standard evaluation. Given the considerable patient, and potentially even physician awkwardness of this type of interaction, the authors recommend an attitude of comfort and adaptability throughout the evaluation process. Physical examination should include a broad screening for medical comorbid conditions relevant to ED, such as body habitus and blood pressure measurements. Urologic evaluation may reveal physical findings such as Peyronie’s plaques, and neurologic evaluation may yield clues to neurogenic causes including presence of the bulbocavernosus reflex or peripheral neuropathy suggesting diabetes. Laboratory studies to identify or confirm a specific cause, such as hypogonadism, may be used as appropriate.

Many patients have an obvious and often severe cause of ED, such as Peyronie’s disease, pelvic surgery, or metabolic syndrome. Another large subset of patients would have tried and failed oral treatments with phosphodiesterase 5 inhibitors. Further testing to confirm the cause is not mandatory for the urologist. First and foremost, the provider should review the medications tried and their doses to ensure that first-line trials have been appropriate. The provider may then pursue other empirical treatments such as intracavernosal injections, but the patient should have an option of undergoing more definitive studies. Some patients who have undergone CIS report that even though they had an appropriate response in the clinic, it does not correlate with their “home” experience. This report might be an indication of venous leak, and PDDU may be helpful to better understand the cause of the patient’s ED. Another indication for PDDU is operative planning. If, for example, the urologist is deciding between plaque excision and grafting and a penile implant for Peyronie’s disease, a quantifiable examination of penile blood flow may provide the data needed for the decision.