Penile Doppler sonographyin the investigation of

erectile dysfunctionRAD Magazine, 36, 424, 19-20

By James Halls and Uday PatelDepartment of Radiology, St George’s Hospital,

London

Although there are many causes of erectile dys-function, the physical aetiologies can be dividedinto arterial inflow problems, abnormalities of thevenous occlusion mechanism and structuralpenile abnormalities. This review will brieflydescribe the anatomy and physiology of penileerection, the technique itself and illustrate themain abnormalities that may be encountered.

Analysis of the cavernosal artery flow dynamics usingpenile Doppler sonography (PDS) was first investigated byLue et al in 1985.1 Its role has subsequently evolved, par-ticularly since the introduction of oral PDE5 inhibitors, suchas Sildenafil.2 A successful trial of these oral agents in effectconfirms an adequate arterial inflow and a satisfactoryvenous occlusion mechanism, thereby precluding furtherinvestigation. As such, PDS is reserved for those patientswith limited or equivocal response or those with complexproblems that may require corrective surgery, such as ayoung patient with pelvic/perineal trauma.3

In order to understand a penile Doppler study, a briefreview of normal anatomy and erectile physiology is neces-sary. When viewed with standard transverse grey scaleultrasound the paired hypoechoic corpora cavernosa are vis-ible, surrounded by the thick echogenic tunica albuginea(figure 1). The ventrally-located single corpora spongiosum(which is surrounded by a thinner layer of tunica albuginea)is seen to surround the penile urethra. The corpora caver-nosa constitute multiple smooth muscle and endothelial-lined sinusoids which, with onset of erection, distend withblood and are capable of considerable volume expansion.Although penile arterial anatomy is variable, the penis issupplied by branches of the internal pudendal artery (itselfa branch of the internal iliac artery). The penile artery (hav-ing given off the bulbar artery) divides into the dorsal arteryand the cavernosal arteries. As their name suggests, thecavernosal arteries run centrally within the length of thecorpora cavernosa and are easily identified by their parallelechogenic walls. These arteries supply the cavernosa vianumerous helicine arteries and supply the sinusoids viaarterioles. Communication of blood across the midlinebetween cavernosa is permitted by perforations in the inter-cavernous septum. Emissary veins that pierce the tunicaalbuginea drain into the deep dorsal vein via the spongiosal,circumflex and cavernosal veins.

The resting smooth muscle tone of the cavernosal arteri-oles and sinusoids in the flaccid penis is high, with resultantlow volume inflow and outflow. Erection begins with neu-rochemically driven relaxation of smooth muscles of sinu-soids and cavernosal arterioles. This results in significantlyincreased cavernosal artery flow. This increased inflowengorges the cavernosal sinusoids, which distend and causepenile tumescence. The distending sinusoids will eventuallycompress the exiting venules and emissary veins, therebyrestricting venous outflow. The resultant situation of higharterial inflow with restricted venous outflow produces arapid increase in intracorporal pressure and penile erection.

A PDS study involves intrapenile injection of a pharma-

costimulant with assessment of the cavernosal arteries andtheir temporal velocity and spectral waveform evolution.Although individual techniques vary, the fundamental prin-ciple is to ensure regular assessment of the waveforms, untilpredetermined haemodynamic parameters are met.4-9 Inorder to reduce catecholamine-induced increase in vasculartone and minimise anxiety, the procedure should be per-formed in a quiet environment. Informed consent shouldinclude a 1-2% risk of inducing priapism.10 The patient liessupine and 10-20mcg of PGE-1 is injected into one of thecorpora cavernosa. Bilateral injection is unnecessary as dif-fusion occurs freely between the cavernosa. In order toreduce the chance of priapism, those who are treatmentnaïve or if psychogenic impotence is felt likely, should bestarted with 5mcg, with further doses as required.

Once tumescence starts, the penis is assessed with stan-dard grey scale ultrasound for non-vascular abnormalitiessuch as Peyronie’s plaques, areas of fibrosis and tunicaalbuginea defects. Care should be taken not to misinterpretthe tiny echogenic foci of injected air (a result of the caver-nosal injection) as pathology. The authors’ preference is toscan the penis dorsally, transversally in the early stagesand oblique-longitudinal upon tumescence. By angling theprobe 20-30° cephalad, the artery in the root of the caver-nosa can be studied. As flow in this region is towards theprobe, the artery can be insonated at a Doppler angle of 0°.Angle correction should be corrected to the direction of theartery and kept less than 60°. Velocity measurements aremost accurate and reproducible at the base of the penis.11

At the start of the study, the cavernosal arteries are typi-cally difficult to visualise but become demonstrable after 1-3 minutes. At this point, image capture and measurementshould be repeated every five minutes until maximal peaksystolic velocity (PSV) and minimal diastolic velocity havebeen reached (sometimes up to 25 minutes post-injection).Both cavernosal arteries should be assessed and the qualityof the erection recorded. The waveform progression issequentially assessed, the first few typically showing ele-vating velocities as a consequence of the smooth musclerelaxation. From this point the PSV is followed. The study iscomplete once minimal diastolic velocity is reached. In addi-tion to sequential waveform analysis, the entire length ofthe cavernosal arteries should be visualised to identifypotential anomalies in the vascular supply.12

A normal study (figure 2)As described earlier, prior to stimulation the cavernosalarteries are difficult to appreciate. Following injection andprior to sinusoidal engorgement, the cavernosal sinusoidsrepresent a low resistance bed allowing forward flowthroughout the cardiac cycle with a high diastolic velocity.The PSV should continue to increase. As the sinusoidsengorge and restrict venous outflow, the system becomeshigh resistance and forward flow is achieved only duringthe high-pressure systolic portion of the cardiac cycle/spec-tral waveform. Consequential changes in the spectral wave-form and measurements can be identified, such as a dicroticnotch. As the intracavernosal pressure continues to rise, theshortened duration of systolic flow causes a narrowing ofthe systolic waveform. Diastolic flow should be reduced toclose to zero. When intracavernosal pressure exceeds dias-tolic pressure, end-diastolic flow reversal is demonstrated.With maximal penile rigidity, the intracavernosal pressuremay approach that of systolic pressure with a reduction insystolic velocity.

Although threshold values for normal systolic and dias-tolic velocities are debated, the authors use a PSV greaterthan 35cm/sec and an EDV being either negative or nearzero.Arterial insufficiency (figure 3)An exact threshold PSV value for definitively diagnosingarterial insufficiency as the cause of erectile dysfunctionvaries, with values between 25 and 35cm/sec suggested byauthors.1,13-15

By correlating measurements of PSV with selective angio-graphic findings, Benson et al concluded that a PSV lessthan 25cm/sec was associated with a strong likelihood ofsevere arterial disease.16

Venous incompetence (figure 4)In the normal subject, as the engorging sinusoids impedevenous outflow, there is an elevation in intracavernosal pres-sure with consequential reduction in diastolic flow and enddiastolic flow reversal. Elevated end diastolic flow valuesare therefore suggestive of venous incompetence (also called‘venous leakage’). Again, exact threshold figures are debated,with some authors suggesting an EDV greater than 5cm/secto be highly suggestive.14,17 Others use 7cm/sec as a diag-nostic cut-off.18

It is worth mentioning that the specificity of EDV in diag-nosing venous incompetence is low when associated with co-existing arterial insufficiency.7 In this situation, the moreinvasive dynamic infusion cavernosometry and cavernosog-raphy (DICC) is recommended due to its ability to quantifyoutflow resistance independent of arterial inflow.19 This isparticularly true if surgery is contemplated.20

Peyronie’s Disease (figure 5)First described in 1743 by the physician of France’s KingLouis XVI, Peyronie’s disease is a relatively common benignconnective tissue disease characterised by fibrous thickeningof the tunica albuginea. On grey scale imaging, theseplaques of fibrosis appear as echogenic irregular thicken-ings of the tunica often with associated calcification.21 Theiridentification may allow patient selection for lithotripsy.7

There is a strong association between erectile dysfunc-tion and Peyronie’s.22,23 Although likely multifactorial, manyhave suggested vascular abnormalities to be the main aeti-ology.22,24-26 Identification of the underlying cause is impor-tant for planning future management.PriapismPriapism is a persistent penile erection that continuesbeyond, or is unrelated to, sexual stimulation.27 The morecommon ‘low-flow’ (ischaemic) priapism is a consequence ofsinusoidal thrombosis and veno-occlusion and results in apainful, rigid erection. PDS demonstrates an absence of cav-ernosal flow with a high resistance, low velocity trace fromthe artery. Prompt treatment is necessary to prevent irre-versible ischaemia and sinusoidal fibrosis.28 ‘High-flow’ (non-ischaemic) priapism is classically a consequence ofpenile/perineal trauma with the development of an arterio-cavernous fistula.29 The penis is classically only partly rigidand pain free. PDS can accurately visualise the fistulae,with sensitivity approaching 100%.29 The PSV is typicallyelevated with high diastolic flow and often prominence ofthe draining veins.7 Diagnostic distinction is essential as thetreatment of the two conditions differs, with the low-flowgroup requiring prompt aspiration and the high-flow typerequiring transcatheter embolisation.

References1, Lue T F et al. Vasculogenic impotence evaluated by high-resolution

ultrasonography and pulsed Doppler spectrum analysis. Radiology 1985;155(3):777-81.

2, Speel T G et al. The value of sildenafil as mode of stimulation in phar-maco-penile duplex ultrasonography. Int J Impot Res 2001;13(4):189-91.

3, Meuleman E J, Diemont W L. Investigation of erectile dysfunction.Diagnostic testing for vascular factors in erectile dysfunction. Urol Clin NorthAm 1995;22(4):803-19.

4, Fitzgerald S W et al. Colour Doppler sonography in the evaluation oferectile dysfunction. Radiographics, 1992;12(1):3-17; discussion 18-9.

5, Golijanin D et al. Doppler evaluation of erectile dysfunction – part 1. IntJ Impot Res 2007;19(1):37-42.

6, Connolly J A, Borirakchanyavat S, Lue T F. Ultrasound evaluation ofthe penis for assessment of impotence. J Clin Ultrasound 1996;24(8):481-6.

7, Wilkins C J, Sriprasad S, Sidhu P S. Colour Doppler ultrasound of thepenis. Clin Radiol 2003;58(7):514-23.

8, Aversa A, Sarteschi L M. The role of penile colour-duplex ultrasound forthe evaluation of erectile dysfunction. J Sex Med 2007;4(5):1437-47.

9, Halls J, Bydawell G, Patel U. Erectile dysfunction; the role of penileDoppler ultrasound in diagnosis. Abdom Imaging 2009;34(6):712-25.

10, Gontero P et al. Phentolamine re-dosing during penile dynamic colourDoppler ultrasound; a practical method to abolish a false diagnosis of venousleakage in patients with erectile dysfunction. Br J Radiol 2004;77(923):922-6.

11, Kim S H et al. Doppler sonography of deep cavernosal artery of thepenis; variation of peak systolic velocity according to sampling location. JUltrasound Med 1994;13(8):591-4.

12, Mancini M et al. The presence of arterial anatomical variations canaffect the results of duplex sonographic evaluation of penile vessels in impotentpatients. J Urol 1996;155(6):1919-23.

13, Quam J P et al. Duplex and colour Doppler sonographic evaluation ofvasculogenic impotence. AJR Am J Roentgenol 1989;153(6):1141-7.

14, Benson C B, Vickers M A. Sexual impotence caused by vascular dis-ease; diagnosis with duplex sonography. AJR Am J Roentgenol 1989;153(6):1149-53.

15, Collins J P, Lewandowski B J. Experience with intracorporeal injectionof papaverine and duplex ultrasound scanning for assessment of arteriogenicimpotence. Br J Urol 1987;59(1):84-8.

16, Benson C B, Aruny J E, Vickers, Jr M A. Correlation of duplex sonog-raphy with arteriography in patients with erectile dysfunction. AJR Am JRoentgenol 1993;160(1):71-3.

17, Fitzgerald S W et al. Colour Doppler sonography in the evaluation oferectile dysfunction: patterns of temporal response to papaverine. AJR Am JRoentgenol 1991;157(2):331-6.

18, Patel U et al. Colour flow and spectral Doppler imaging after papaver-ine-induced penile erection in 220 impotent men; study of temporal patternsand the importance of repeated sampling, velocity asymmetry and vascularanomalies. Clin Radiol 1993;48(1):18-24.

19, Bassiouny H S, Levine L A. Penile duplex sonography in the diagno-sis of venogenic impotence. J Vasc Surg 1991;13(1):75-82; discussion 82-3.

20, Fowlis G A et al. Preliminary report – combined surgical and radio-logical penile vein occlusion for the management of impotence caused byvenous-sinusoidal incompetence. Br J Urol 1994;74(4):492-6.

21, Golijanin D et al. Doppler evaluation of erectile dysfunction – part 2.Int J Impot Res 2007;19(1):43-8.

22, Lopez J A, Jarow J P. Penile vascular evaluation of men withPeyronie’s disease. J Urol 1993;149(1):53-5.

23, Devine C J Jr, Horton C E. Peyronie’s disease. Clin Plast Surg 1988;15(3):405-9.

24, Weidner W et al. Sexual dysfunction in Peyronie’s disease; an analysisof 222 patients without previous local plaque therapy. J Urol 1997;157(1):325-8.

25, Montorsi F et al. Vascular abnormalities in Peyronie’s disease; therole of colour Doppler sonography. J Urol 1994;151(2):373-5.

26, Brock G, Kadioglu A, Lue T F. Peyronie’s disease; a modified treat-ment. Urology 1993;42(3):300-4.

27, Pautler S E, Brock G B. Priapism. From Priapus to the present time.Urol Clin North Am 2001;28(2):391-403.

28, Spycher M A, Hauri D. The ultrastructure of the erectile tissue in pri-apism. J Urol 1986;135(1):142-7.

29, Bastuba M D et al. Arterial priapism; diagnosis, treatment and long-term follow-up. J Urol 1994;151(5):1231-7.

FIGURE 1Normal grey-scale images of the penis.A. Transverse. Note the echogenic tunica albuginea

(long arrow) surrounding the paired corpora cav-ernosa and single corpus spongiosum.

B. Longitudinal. Note the parallel echogenic walls ofthe cavernosal artery (long closed arrow). A gradi-ent of cavernosal distension can be observed, withthose sinusoids closest to the artery (short closedarrow) distending first and thereby having a morehypoechoic appearance.

FIGURE 3Arterial insufficiencyA–D. Images taken at approximately five minuteintervals after an injection of full dose of Caverject.Diastolic flow is positive, indicating pharmacologicalresponse, but the PSV is <10cm/sec throughout thestudy indicating severe arterial insufficiency. No sig-nificant penile erection was obtained.

FIGURE 4A. Thick echogenic calcified Peyronie’s plaque (open

arrow). Note the posterior acoustic shadowing.Distortion of the underlying cavernosal arteriesmay be observed.

B. Significant cavernosal fibrosis (closed arrows) as asequelae of low-flow priapism. Note the echogenic,distorted cavernosa.

FIGURE 2 A normal penile Dopplerstudy. A. A few minutes after

injection, as tumes-cence begins; note theelevating systolic anddiastolic velocities

B. After approximately10 minutes post-stim-ulation, with increas-ing intracavernosalpressure there is areduction in diastolicflow.

C. PSV has peakedabove 50cm/sec, indi-cating normal arterialinflow. There is end-diastolic flow rever-sal, indicating anintact venous occlu-sion mechanism.Later in the samestudy a reduction insystolic velocity mayoccur (not shown).