Doppler Evaluation of Erectile Dysfunction - Part 1

D Golijanin; E Singer; R Davis; S Bhatt; A Seftel; V Dogra

Int J Impot Res. 2007;19(1):37-42. 

Abstract and Introduction


Erectile dysfunction (ED) is the consistent inability to achieve and maintain an erection sufficient for satisfactory sexual activity. Erectile dysfunction affects as many as 30 million men in America, with an increasing prevalence with age. Erectile dysfunction is secondary to organic, psychogenic and combined causes. The first part of this review article describes the guidelines for evaluation and treatment plans for men with ED. It also describes the normal sonographic anatomy of the penis, sonographic technique for evaluation of ED and the normal phases of erection.


National Institutes of Health defines erectile dysfunction (ED) as the consistent inability to achieve and maintain an erection sufficient for satisfactory sexual activity. Erectile dysfunction affects as many as 30 million American men.[1] The disorder is associated with age, with a 39% prevalence at the age of 40 years and a 67% prevalence at the age of 70 years. Massachusetts Male Aging Study reported on 52% of men aged 40–70 years having some degree of erectile difficulty.[2,3]

Erectile dysfunction includes organic, psychogenic and combined causes. Organic causes are found in 80–90% of patients and include vasculogenic (arterial, cavernosal and mixed), neurogenic, anatomic and endocrine causes. Psychogenic disorders with ED are performance anxiety, depression and inhibited sexual desire.

Guidelines for evaluation and treatment plans for men with ED have usually suggested a stepwise model.

Basic evaluation

Patients with ED undergo a preliminary assessment designed to address significant diseases such as diabetes, coronary artery disease (CAD) and hypertension before starting therapy, so non- or/and least invasive treatments are to be used first.[4,5,6] A basic diagnostic evaluation is the first step in ED assessment and is applied for the majority of men, whereas specific diagnostic procedures are implemented in a smaller subset of patients.[7,8] The basic evaluation is often commenced by the primary care physicians. Occasionally, a number of patients are diagnosed and treated by cardiologists, neurologists, endocrinologists and psychiatrists, who treat ED as a comorbidity of an underlying disease.[9,10]

Basic evaluation includes thorough medical, sexual and psycho-sexual history, physical examination and limited laboratory assessment. Radiological imaging in the field of ED has diminished in importance over the past 10 years with the introduction of new effective oral therapies and the recognition that surgical treatment of both penile venous leak and arterial insufficiency have poor long-term clinical outcomes. The introduction of phosphodiesterase-5 (PDE5) inhibitors has revolutionized the therapeutics of ED and radically changed the way in which men with ED are assessed and investigated.[11] Documentation of a good quality erection in response to a PDE5-inhibiting drug confirms grossly adequate arterial flow and patent veno-occlusive mechanisms. However, color Doppler ultrasound continues to have a role in the evaluation of specific patients with ED and has an increasing role in the detection of silent CAD in men presenting with ED.[12]

Specific evaluation

Vascular evaluation and imaging may be indicated in patients with (a) arterial/arteriolar arteriogenic dysfunction, (b) veno-occlusive disorder, (c) Peyronie's disease, (d) high-flow priapism, (e) penile trauma (fracture) and (f) in patients without symptomatic peripheral vascular disease presenting with ED where penile Doppler is used to assess the risk of cardiovascular disease and need for further cardiac or peripheral vascular assessment. In the last group, significant risk factors such as hypertension, smoking, trauma, hyperlipidemia, diabetes mellitus, obesity and inactivity are closely related to ED and decrease in sexual ability is regarded as one of the first clinical parameters of increased risk of significant CAD or peripheral vascular disease.[13,14,15] Erectile dysfunction is now being recognized as one of the earliest manifestations of endothelial dysfunction and peripheral vascular disease. Montorsi et al.[16] have demonstrated that ED presents about 39 months before CAD possibly because the smaller penile arteries reach critical narrowing and decreasing blood flow earlier than larger vessels. He has demonstrated that a normal penile Doppler test virtually excludes CAD with a 98% negative predictive value, whereas an abnormal penile Doppler test had a 30% positive predictive value for CAD – a value many times higher than 4% found in the general population.[17] El-Sakka and Morsy[18] in evaluation of men with ED found that 77% of those with high-grade ischemic heart disease had an abnormal penile Doppler test with peak systolic velocity (PSV) of less than 25 cm/s. Gazzaruso et al.[19] demonstrated in asymptomatic type II diabetics that those with angiographically confirmed silent CAD had over seven times the rate of ED (33.8% vs 4.7%) than control type II diabetics without CAD. As more information accrues confirming ED as an early manifestation of peripheral vascular disease, penile Doppler testing may play a key role in selecting those who do or do not need further coronary artery vascular assessment.

Vasculogenic imaging is usually reserved for men with ED who have a potentially surgically treatable cause. These patients are frequently young, have often suffered traumatic straddle injuries to the penis and may be unresponsive to oral and intracavernosal therapy. In this group of men, the mainstay of investigation is color Doppler ultrasound of the penile vasculature.[20] In addition to penile color Doppler ultrasound evaluation, several other tests of penile function and anatomy are available, including, dynamic infusion cavernosometry, cavernosography, selective penile angiography, penile nuclear magnetic resonance and near-infrared spectrophotometry.[21]

The use of Doppler ultrasound in the assessment of the penile vasculature was first described in 1985.[22] Advantages of penile Doppler and pharmacologic duplex ultrasonography include objective, minimally invasive evaluation of penile hemodynamics at a relatively low cost. Intracavernosal injection of vasoactive substances including prostaglandin E1, papaverine and phentolamine permits testing penile circulation not only at rest when the flow is minimal but also under maximal direct pharmacologic stimulation, when arterial insufficiency may be observed.[23,24,25] These substances may be administrated as a single drug or in combination,[23,24] with reported efficacy rates of up to 94%. Intracavernosal injections are routinely given with color Doppler ultrasound, but despite this the tests have been less than completely reliable possibly owing to the negative effects of anxiety and adrenergic output on the testing results. A variety of techniques has been used to minimize anxiety and maximize the reproducibility of the investigations, including a quiet and private environment, manual stimulation and visual sexual stimulation.[26] Others have used avoidance of injection giving high doses of PDE5 inhibitors and visual stimulation to promote blood flow and erection during testing, gaining from a less invasive procedure but losing on the certainty of maximal vascular relaxation stimulation.[27,28,29,30,31,32,33,34,35,36,37,38,39] In addition to various techniques employed to stimulate penile blood flow and an erection during testing, in order to increase observer ability to precisely assess vasculogenic causes of ED, interpretation of penile Doppler ultrasound findings remain very difficult in some cases. First, there is a gray area in the criteria for identifying arteriogenic ED. The parameter that is most commonly used to define arteriogenic ED is peak systolic blood flow in the penile arteries. Peak flow rates less than 25 cm/s are abnormally low and peak flow rates greater than 35 cm/s are normal, but the range of 25–35 cm/s is equivocal. Recently, Speel et al.[40] reported that acceleration time was the most valid parameter to detect cavernous atherosclerotic pathology. Blood flow velocity in the cavernous artery following pharmacostimulation was determined with duplex ultrasonography in 106 patients with ED. The cutoff point for acceleration time to discriminate between atherosclerotic and non-atherosclerotic ED was determined at acceleration time 100 ms or greater. Sensitivity was 66% and specificity was 71%.

Secondly, the criteria for diagnosing veno-occlusive dysfunction are also not very convincing. During a complete erection, the end-diastolic velocity (EDV) of the cavernosal arteries should be zero, or reverse flow may also be observed as a result of the increased intracavernosal pressure in the rigid stage of erection. In men with veno-occlusive disorder, the usual criterion for diagnosing veno-occlusive dysfunction has been an EDV greater than 5 cm/s.[41,42] This observation was not confirmed in all studies and there is a poor correlation of color Doppler ultrasound findings and veno-occlusive dysfunction when diagnosis was made using gold standard method, which is cavernosogram with infusion cavernosometry.[39]. Although the accurate diagnostic procedure for venous leak diagnosis is infusion cavernosometry after maximal vasodilatation, this is rarely employed owing to poor surgical results of venous leak repair.

Sonographic penile anatomy

The penis is composed of two dorsal corpora cavernosa and one ventral corpus spongiosum. The two corpora cavernosa are enclosed in a fibrous sheath, the tunica albuginea, which partially covers the corpus spongiosum. The tunica albuginea is composed of elastic fibers that form an irregular, criss-crossing strips network on which collagen fibers rest. The corpora cavernosa are composed of sinusoidal spaces lined by smooth muscles (erectile tissue) and endothelium. The glans penis is formed by expansion of the corpus spongiosum. The corpus spongiosum is traversed throughout its length by the anterior urethra, which begins at the perineal membrane. The corpus spongiosum provides support to the urethra and helps with the expulsion of semen from the urethra. Buck's fascia surrounds both cavernosal bodies dorsally and splits to surround the spongiosum ventrally (Figure 1a and b). The penile blood vessels arise from the internal pudendal artery. The penile artery divides into two main branches, the dorsal penile artery and the cavernosal artery. The cavernosal artery enters the corpus cavernosum on the superomedial surface of the penis. The branches of this artery are called the helicine arteries and subsequently divide into smaller vessels that communicate with the lacunae of the corpus cavernosum (Figure 1c and d). The venous blood is returned by the venous plexus beneath the tunica albuginea. The emissary veins perforate the tunica albuginea, and the blood is drained by the venae circumflexae into the deep dorsal veins.

Figure 1.


Normal sonogram of penis. (a) Transverse gray-scale ultrasound of the penis demonstrates the two corpora cavernosa (CC) surrounded by the tunica albuginea (arrowhead). The corpus spongiosum (CS) is seen inferior to the corpora cavernosa. All three corpora are surrounded by the Buck's fascia (arrow). (b) The corresponding line diagram. (c) Longitudinal color flow Doppler ultrasound of normal cavernosal bodies and flow through cavernosal artery (arrow) and the helicine branches (arrowheads). (d) The corresponding line drawing of the blood supply to the penis.

Applied color Doppler ultrasonography technique

Sonographic examination of the penis is performed with the patient in either the supine or lithotomy (frog leg) position with the penis lying on the anterior abdominal wall or supported with towels between the thighs. High-frequency (7.5–14 MHz) linear array transducers are used to obtain high-resolution images of the penis. A sufficient amount of sonographic acoustic gel should be used on the surface of the penis to obtain good-quality images, and excessive compression by the transducer should be avoided, especially in patients with trauma. The examination is performed in transverse and longitudinal planes starting at the level of the glans and moving down to the base of the penis. A transperineal approach may be used if required to assess the base of the penis. The two corpora cavernosa are homogeneous in echo texture and identified as two hypoechoic circular structures. The tunica albuginea is visualized as a linear hyperechoic structure covering the corpora cavernosa. The cavernosal artery is visualized on the medial portion of the corpora cavernosa. The corpus spongiosum is often compressed and difficult to visualize optimally from the ventral aspect. Color Doppler examination of the penis should be performed in both transverse and longitudinal planes. Peak systolic velocities of the cavernosal arteries should also be recorded. Owing to the variation in the PSV of the cavernosal artery at different locations across the shaft of the penis (PSV is higher proximally), PSV should be consistently measured at the junction of the proximal one-third and distal two-third of the penile shaft where the cavernosal artery bends (Figure 2). Cavernosal artery velocities in healthy volunteers measure 10–15 cm/s in the non-erect condition. Cavernous arteries should be identified and their action potential dimension measured. When pharmacological testing is required, prostaglandin E1 injection 10–20 μg, is injected to one of the corpora cavernosa laterally in the distal part of the penis with a 30-gauge needle. Injection should always be made in the distal two-third part of the penis on one side only because of the presence of a septum in between the two corpora cavernosa in the proximal part of the penis, which is deficient distally, thus allowing bilateral perfusion of the injected vasoactive substance. Besides prostaglandin E1, other vasoactive agents used are papaverine 30–60 mg and Trimix (combination of papaverine, phentolamine and prostaglandin E1). Trimix is reserved for those patients who do not respond to prostaglandin. An oral vasoactive agent, sildenafil citrate, plus visual sexual stimulation can be used as an alternative to intracavernosal injection of vasoactive agents for penile Doppler evaluation with similar results.

Figure 2.


Cavernosal artery peak systolic velocity (PSV). Peak systolic velocity of the cavernosal artery decreases from base of the penis to the glans penis. (a) A higher PSV of the cavernosal artery (measured more proximally) as compared to distal measurement in the same patient (b).

The injection of the vasoactive substance results in physiological response of erection in normal people, and thus helps to differentiate patients with neurogenic or psychogenic dysfunction from those with vascular disturbances.

Similarly, PDE5 inhibitors could be used for pharmacological testing with increased time frame in between examinations. Tumescence and rigidity are observed and recorded, as well as the angle-corrected velocities, in both cavernosal arteries at 5, 10, 15, 20, 25 and 30 min after injection. Velocities in deep dorsal vein should also be recorded.

Phases of erection

The erection process may be divided into four phases. First, the flaccid phase during which corporeal volume is small, approximately one-fifth of maximal volume, and corporeal pressure is around 20 mm Hg. In the filling and tumescence phase, the corporeal smooth muscle is relaxed owing to reduction in the sympathetic tonus of the arteries allowing brief arterial inflow. The corpora cavernosa are engorged with blood. This results in increase of pressure inside corpora cavernosa, causing pressure at the level of the relaxed veins against the tunica albuginea and preventing outflow. The hemodynamic resistance of the veins increases significantly. This leads to fourth phase of rigidity, where intracavernosal volume grows almost five times baseline and intracorporeal pressure is close to systolic systemic arterial pressure. Final rigidity is obtained by contraction of the perineal muscles that generate high-pressure peaks giving the rigidity required for full erection. Doppler ultrasonography accurately divides phases of erection with characteristically different spectral waveforms as seen in Figure 3.

Figure 3.


Phases of erection. (a) Flaccid phase. Spectral Doppler waveform demonstrates high resistance waveform. Velocities are in the range of 5–15 cm/s. (b) Filling phase. Spectral Doppler waveform demonstrates increased systolic velocity and increased diastolic flow. (c) Tumescent phase. The systolic velocities stabilize, diastolic flow decreases or becomes reversed. (d) Rigid phase. Spectral Doppler waveform demonstrates very high resistance waveform with no diastolic flow and minimal systolic flow. The peak systolic velocities decrease.

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