Colour Doppler and duplex ultrasound assessment of Peyronie's disease in impotent men

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1993, The British Journal of Radiology, 66, 398-402 Colour Doppler and duplex ultrasound assessment of Peyronie's disease in impotent men 1 Z AMIN, MRCP, 1 U PATEL, MRCP, FRCR, 1 E P FRIEDMAN, MRCP,

1 1993, The British Journal of Radiology, 66, Colour Doppler and duplex ultrasound assessment of Peyronie's disease in impotent men 1 Z AMIN, MRCP, 1 U PATEL, MRCP, FRCR, 1 E P FRIEDMAN, MRCP, 2 J A VALE, FRCS, 2 R KIRBY, MD, FRCS and 1 W R LEES, FRCR department of Radiology, The Middlesex Hospital, Mortimer Street, London W1 N 8AA, UK and department of Urology, St Bartholomew's Hospital, West Smithfield, London EC1A 7BE, UK Abstract 280 patients (aged 28 to 74 years, mean 57) with erectile failure (EF) underwent colour Doppler and duplex ultrasound imaging (CDI) following intracorporeal papaverine. After achieving a full, or nearly full, erection visual inspection and palpation revealed plaques and/or constriction or deformity of the penis in 55 (20%) cases. 10 (4%) were known to have Peyronie's plaques prior to referral. Of these 55 patients ultrasound showed focal echogenic plaques in 14 (25%) and diffuse thickening of the tunica albuginea in 41 (75%). CDI diagnosed arteriogenic EF in 20 (36%) of these patients, venous leak in 10 (18%), arterial and venous in two (4%) and a normal response in 23 (42%). In 11 (20%) patients (seven with arteriogenic EF and four with venous leak) the plaque was seen to be affecting vessels. These results indicate that abnormalities of the tunica albuginea are far more common in patients presenting with erectile failure than previously thought. We believe that the diffuse thickening is a form of Peyronie's which is only recognized after pharmacological induction of penile erection. Peyronie's disease is a localized connective tissue disorder affecting the tunica albuginea of the corpora cavernosa (Somers et al, 1989; Gelbard et al, 1990) with irregular, dense plaques of fibrous tissue and associated abnormal curvature of the erect penis (Gingell & Desai, 1989). Patients presenting with Peyronie's disease complain of painful erection, abnormal penile curvature or erectile failure (Gingell & Desai, 1989; Gelbard et al, 1990). Severely deforming or disabling contracture of the tunica albuginea is rare, but minor inflammation and post-inflammatory fibrosis affecting the tunica are said to be early features and are relatively common (Smith, 1966; Vande Berg et al, 1981; Gelbard et al, 1990) Ultrasound assessment of Peyronie's disease often detects only focal, dense, echogenic plaques (Chou et al, 1987; Bock et al, 1988), but in a small number of cases a more diffuse thickening of the pericavernous fascia has been seen (Gelbard et al, 1981; Balconi et al, 1988; Lopez & Jarow, 1991) and is said to represent early change (Balconi et al, 1988). Some authors have concluded that ultrasound frequently shows no abnormality (Pohar et al, 1990; Lopez & Jarow, 1991). It is feasible that in the early stages of Peyronie's disease relatively widespread inflammation and fibrosis occur, which later may progress to focal or extensive plaques. Corresponding early findings on ultrasound are likely to be more diffuse and be seen as thickening of the tissue Received 21 September 1992 and in revised form 9 December 1992, accepted 11 January planes which may go unnoticed unless specifically sought. Erectile failure in patients with Peyronie's disease is often psychogenic, but may result from penile deformity or an associated vascular cause (Metz et al, 1983; Gingell & Desai, 1989). The plaque may be directly responsible for a venous leak (Metz et al, 1983) but there is little data on associated vascular insufficiency in patients with Peyronie's disease and impotence. Colour Doppler and duplex ultrasound imaging (CDI) is very useful in assessing patients with impotence and Peyronie's disease since it provides information about fibrous plaques/thickening (Hamm et al, 1986; Balconi et al, 1988) as well as about penile vasculature, non-invasively (Lue et al, 1985; Quam et al, 1989; Schwartz et al, 1989). We present our experience of CDI findings in impotent men who were found to have Peyronie's disease. Our objectives were: (1) to determine the incidence of Peyronie's disease in impotent men; (2) to assess the presence of diffuse thickening as well as plaques; (3) to evaluate the penile vasculature and its relationship to the plaque or thickening using colour flow Doppler imaging; (4) to ascertain the cause of the erectile failure in patients with Peyronie's disease. Patients and methods 280 patients (aged 28 to 74 years, mean 57) were referred for CDI assessment of their erectile failure. 398 The British Journal of Radiology, May 1993

Colour Doppler and duplex US assessment of Peyronie 's disease Patients had been evaluated initially with a thorough history and physical examination, including careful palpation of the penis for

5 MHz linear array transducer (Acuson 128, Mountain View, CA, USA).

2 Colour Doppler and duplex US assessment of Peyronie 's disease Patients had been evaluated initially with a thorough history and physical examination, including careful palpation of the penis for evidence of induration, as well as a hormonal assay. 40 to 80 mg of papaverine was injected intracorporeally and ultrasound scanning performed using a 7.5 MHz linear array transducer (Acuson 128, Mountain View, CA, USA). The corpora cavernosa and tunica albuginea were carefully scanned using grey-scale ultrasound and the presence of any focal echogenic plaques or diffuse thickening noted. On achieving a full, or nearly full, erection the penis was inspected for any bend or torsion along its axis and palpated for localized or widespread thickening. The presence of penile curvature or palpable thickening were taken to represent diagnostic evidence of Peyronie's disease. Ultrasound abnormalities were most frequently detected on the dorsum of the penis and to avoid problems with near field resolution the penis was laid on the anterior abdominal wall with the ultrasound transducer placed on its ventral surface. Colour flow imaging was used to define the penile vessels and, in those patients with evidence of fibrous plaques or thickening, to look for any distortion of the vessels. Duplex scanning of both cavernosal arteries was performed at the base of the penis, care being taken to ensure angle correction and sample the same point of each cavernosal artery every 2 min until the maximum blood flow velocity was obtained. The following parameters were derived from the duplex waveform: maximum systolic velocity (Vmax), minimum diastolic velocity (Vmin), pulsatility index (PI) and systolic rise time (delta T). Any significant differences between right and left cavernosal arteries was noted, and the presence or absence of a velocity gradient across fibrous plaques sought. Our criteria for diagnosing arteriogenic EF was a Vmax < 30 cm s" 1 in either cavernosal artery with a Vmin < 7 cm s" 1, or a (delta T) > 0.1 s, as well as failure to achieve a full erection. A venous leak was diagnosed if Vmin > 7 cm s" 1 for at least 5 min with an adequate inflow (Vmax > 30 cm s"') and failure to achieve a full erection. Patients who had a Vmax < 30 cm s" 1 and a Vmin > 7 cm s" 1 were diagnosed as having both an arterial and venous cause for their EF, although those with a Vmax below 25 cm s" 1 were classified as arteriogenic EF regardless of Vmin. Most of the patients with a suspected venous leak on CDI had cavernosography and cavernosometry to confirm the presence of a venous leak. Quam et al (1989) found CDI to be reliable in diagnosing venous leak, using Vmin > 5 cm s" 1, with cavernosography and cavernosometry as gold standards. In a similar study, but using Vmin > 7 cm s~', we found an improved sensitivity and specificity of 94% and 69%, respectively (Patel et al, 1992). Results Of the 280 patients only 10 (4%) were known to have Peyronie's plaques prior to CDI. 55 (20%) patients had visually obvious distortion or palpable thickening of the penile shaft, on achieving a full or nearly full erection. The 45 patients not previously known to have Peyronie's disease had been frequently unaware of any penile deformity. This may have been due to the erectile failure masking the abnormality. Ultrasound clearly demonstrated the two corpora cavernosa, with surrounding tunica albuginea as a thin (1-2 mm) echogenic band with well-defined margins. (a) (b) Figure 1. (a) Longitudinal scan showing a small echogenic plaque (arrow) and (b) transverse scan with a calcified plaque (arrow), cc, corpora cavernosa; t, tunica albuginea. Vol. 66, No

(18%) 2 (4%) 23 (42%) 55 96 (43%) 59 (26%) 15 (7%) 55 (24%) 225 The normal thickness of the tunica albuginea was measured carefully in 25 patients, and found to have a mean of 1.

3 Z Amin, U Patel, E Friedman et al Table I. CDI findings of 55 patients with Peyronie's and 225 patients without Peyronie's CDI diagnosis Peyronie's No Peyronie's Artenogemc EF Venous leak Arterial and venous Normal response Total 20 (36%) 10 (18%) 2 (4%) 23 (42%) (43%) 59 (26%) 15 (7%) 55 (24%) 225 The normal thickness of the tunica albuginea was measured carefully in 25 patients, and found to have a mean of 1.2 mm with a range of mm. The corpus spongiosum was seen lying ventrally in the midline. Focal, brightly echogenic plaques, sometimes with acoustic shadowing (indicating calcification) were seen in 14 (25%) of the 55 patients (Figure 1) with clinically obvious penile abnormality. In the remaining 41 (75%) there was widening and increased echogenicity of the tunica albuginea in the region of the clinical abnormality (Figure 2). This was clearly different from adjacent normal looking tunica albuginea, in a clinically normal part of the penis, and interpreted as a diffuse thickening of the tunica albuginea. The margins of the diffuse thickening were usually irregular and indistinct, making accurate measurement difficult. The maximum thickness varied from 3 to 10 mm, the milder forms associated with blurring of the margins of the tunica albuginea. Thickening of the tunica albuginea was seen most frequently on the dorsal aspect of the penis; it was often seen ventrally, and involving the septum. Using our CDI criteria patients were diagnosed as having either arteriogenic erectile failure (EF), venous leak, both arterial insufficiency and a venous leak or a normal response. These results are summarized in Table I for the 55 patients with Peyronie's and the 225 patients in whom no evidence of Peyronie's disease was found. Table II shows that impotent patients with Peyronie's disease are significantly more likely to have a non- Table II. Number of patients with and without Peyronie's who have a vasculogenic EF Peyronie's No Peyronie's Vasculogenic EF Normal response (chi-squared = , p < 0.01). Figure 2. Longitudinal (a) and transverse (b) scans showing diffuse thickening of the tunica albuginea (+). (c) Longitudinal scan showing the tunica albuginea in a normal penis for comparison (distance between is 1.1 mm). The bright echogenic line at the level of the lower cursor in (a), (b), and (c) represents the skin of the dorsal surface of the penis lying against the anterior abdominal wall, the transducer having been placed on the ventral surface of the penis. 400 The British Journal of Radiology, May 1993

Colour Doppler and duplex US assessment of Peyronie's disease Figure 3. Perivascular thickening ( +... + ) around a draining vein (arrow), passing though the tunica albuginea. cc, corpora cavernosa.

In 11 (20%) Peyronie's patients (seven with arteriogenic EF and four with venous leaks) CDI showed the fibrous plaque or thickening to be affecting vessels.

4 Colour Doppler and duplex US assessment of Peyronie's disease Figure 3. Perivascular thickening ( ) around a draining vein (arrow), passing though the tunica albuginea. cc, corpora cavernosa. vascular (psychogenic or neurogenic) cause for their EF compared with other patients with EF. In 11 (20%) Peyronie's patients (seven with arteriogenic EF and four with venous leaks) CDI showed the fibrous plaque or thickening to be affecting vessels. There was either clear distortion of the vessels or a velocity gradient was found across a cavernosal artery close to a plaque. In some cases there was obvious thickening around a draining vein in the tunica albuginea (Figure 3). Discussion The prevalence of Peyronie's disease in the normal population is unknown (Gelbard et al, 1990), but asymptomatic disease is said to be common (Smith, 1969) and has been reported as 1% in a medical school faculty (Vorstman & Lockhart, 1987). Peyronie's disease in impotent men is more common, being quoted as % (Metz et al, 1983; Gingell & Desai, 1989; Mulligan & Katz, 1989). We have found a much higher incidence of Peyronie's disease in impotent men (20%) than previously described, and the patient had frequently been unaware of the penile deformity detected following induction of an erection. This may be owing to several factors: erectile failure in Peyronie's may conceal other symptoms of the disease such as penile deviation, hence patients present earlier with impotence rather than penile deviation (Metz et al, 1983); careful palpation of the penile shaft with a full, or nearly full, erection enabled plaque/thickening to be detected, which would otherwise have been missed in the flaccid state; systematic ultrasound scanning using a high frequency transducer looking specifically for diffuse thickening as well as plaques; the public is becoming more aware of the treatment options for impotence, leading to earlier presentation of patients with erectile failure and, in those with Peyronie's, at an earlier stage of the disease. The majority (75%) of our patients with Peyronie's disease had diffuse thickening of the tunica albuginea. This finding has been recognized by some other groups (Gelbard et al, 1981; Balconi et al, 1988), with a reported incidence of up to 22% (Balconi et al, 1988). Lopez & Jarow (1991) also noted diffuse iso-echoic thickening of the tunica albuginea but felt this finding alone might be too subtle to be reliably detected with ultrasound; in their study ultrasound confirmed Peyronie's disease in only 13 out of 39 patients who were known to be affected. It may be that diffuse thickening was dismissed as an insignificant finding by some authors who have stated that ultrasound is not reliable in detecting Peyronie's disease (Pohar et al, 1990), although others have found ultrasound abnormalities in all of their affected patients (Chou et al, 1987; Balconi et al, 1988). There is limited histopathological data on Peyronie's disease, and the studies by Smith (1966; 1969) are the most comprehensive. He found chronic inflammatory changes and fibrosis (which were mostly perivascular) in the areolar connective tissue layer between the tunica albuginea and cavernosal sinusoids; in three out of 22 cases these changes extended into the corpus spongiosum. Early changes were predominantly inflammatory and these progressed to increasing fibrosis. More advanced cases revealed the presence of a thickened fibrous connective tissue plaque separating the tunica albuginea and corpus cavernosa, and with extension into these structures. Vande Berg et al (1981) performed an electron microscopic study of Peyronie's plaques, and their findings supported those of Smith (1966; 1969) that the disease process begins as a vasculitis in the tunica albuginea and subtunica, leading to fibrosis and possible calcification. These microscopic findings of inflammation and fibrosis in the tunica and subtunica could correspond to the diffuse thickening and illdefined margins of the tunica albuginea seen on ultrasound. The diffuse thickening may represent a relatively early form of Peyronie's disease which progresses to focal plaques of increased echogenicity (corresponding to increased fibrosis), sometimes with calcification. In this study CDI shows that 42% of patients with Peyronie's and impotence have a non-vasculogenic cause (i.e. psychogenic or neurogenic) of their erectile failure, and this is significantly greater than the proportion of impotent men without Peyronie's who have a non-vasculogenic impotence (24%). One would expect many of these patients to have psychogenic impotence (Gingell & Desai, 1988; Gelbard et al, 1990), although demyelination of nerve axons in Peyronie's plaques has been reported (Vande Berg et al, 1981) indicating that some of these patients may have a neurogenic cause for their erectile failure. 58% of our patients with Peyronie's disease and impotence were found to have a vasculogenic cause for their erectile failure. Lopez & Jarow (1991) reported Vol. 66, No

$However, they used a Vmax < 25 cm s" 1 to diagnose arteriogenic impotence as opposed to our criterion of Vmax < 30 cm s~\ which would have led to underdiagnosis of arteriogenic impotence.$

5 Z Amin, U Patel, E Friedman et al 27% of their patients with Peyronie's disease and impotence to have an arteriogenic cause for erectile failure and proposed that the remaining 73% had a venous leak. However, they used a Vmax < 25 cm s" 1 to diagnose arteriogenic impotence as opposed to our criterion of Vmax < 30 cm s~\ which would have led to underdiagnosis of arteriogenic impotence. Even so, it is a surprising finding to have no normal responders; this may partly be explained by their lower dose of papaverine. In 20% of our patients with Peyronie's and impotence there was vessel distortion and/or velocity gradient in arterial segments adjacent to fibrous plaques/thickening which suggests that the Peyronie's disease is directly responsible for the erectile failure in these patients. It is recognized that extensive plaque can cause band-like constriction or waisting of the penile shaft (Gingell & Desai, 1988). One can postulate that this results in a localized decrease in vessel compliance and hence a functional stenosis. In some of our patients the draining veins were surrounded by thick, echogenic walls (Figure 3). This may correspond to the histological findings of a perivascular inflammatory infiltrate and fibrosis (Smith, 1966). It has been proposed that a venoocclusive dysfunction is present in Peyronie's disease (Metz et al, 1983; Gasior et al, 1990) and that this might be secondary to fibrous tissue interfering mechanically with the venous drainage (Metz et al, 1983) or be a result of nerve demyelination destroying the regulation of the venous closure mechanism (Vande Berg et al, 1981; Metz et al, 1983). Our ultrasound findings would support the argument that at least in some patients with Peyronie's disease venous leak does occur and that this is likely to be secondary to a disturbance of the venous closure mechanism. However, this has not been found to be the predominant cause of impotence in these patients; psychogenic or neurogenic (possibly secondary to demyelination of the penile nerves) causes are more likely in comparison with impotent patients without Peyronie's. Conclusion Increasing public awareness of impotence and its treatment options is leading to earlier presentation. Our study shows that Peyronie's disease is far more common in patients presenting with erectile failure than previously thought. Ultrasound showed focal echogenic plaques in 25% of patients with Peyronie's disease and a diffuse thickening of the tunica albuginea in 75%. We believe that diffuse thickening is a common form of Peyronie's disease which is better recognized in the erect penis. Patients with Peyronie's disease and impotence are more likely to have a non-vasculogenic cause for their erectile failure than impotent patients without Peyronie's. However, a vasculogenic cause for the erectile failure in Peyronie's disease is common, occurring in 58% of patients and in a third of these CDI shows a direct association between the fibrous plaque/thickening and the vascular dysfunction. References BALCONI, G, ANGELI, E, NESSI, R & FLAVIIS, L, Ultrasonographic evaluation of Peyronie's disease. Urol. Radiol., 10, BOCK, E, SOLIVETTI, F M, CALUGI, V & ROSSI, P, Peyronie's disease. Ultrasonic evaluation. Radiologia Medica, 76, CHOU, Y H, TIU, C M, PAN, H B ET AL, High resolution real time ultrasound in Peyronie's disease. J. Ultrasound Med., 6, GASIOR, B L, LEVINE, F J, HOWANNESIAN, A ET AL, Plaque-associated corporal veno-occlusive dysfunction in idiopathic Peyronie's disease: a pharmacocavernosometric and pharmaco-cavernosographic study. World J. Urol., 8, GELBARD, M K, DOREY, F & JAMES, K, The natural history of Peyronie's disease. /. Urol., 144, GELBARD, M, SARTI, D & KAUFMAN, J J, Ultrasound imaging of Peyronie's plaques. J. Urol., 125, GINGELL, J C & DESAI, K M, Peyronie's disease. Br. Med. J., 297, GINGELL, J C & DESAI, K M, Review. Peyronie's disease. Br. J. Urol, 63, HAMM, B, FRIEDRICH, M & KELAMI, A, Ultrasound imaging in Peyronie's disease. Urology, 28, LOPEZ, J A & JAROW, J P, Duplex ultrasound findings in men with Peyronie's disease. Urol. Radiol., 12, LUE, T F, HRICAK, H, MARICH, K W & TANAGHO, E A, Vasculogenic impotence evaluated by high resolution ultrasonography and pulsed Doppler spectrum analysis. Radiology, 155, METZ, P, EBBEHOJ, J, UHRENHOLDT, A & WAGNER, G, Peyronie's disease and erectile failure. /. Urol., 130, MULLIGAN, T & KATZ, P G, Why aged men become impotent. Arch. Internal Med., 149, PATEL, U, AMIN, Z, FRIEDMAN, E ET AL, Colour flow Doppler imaging after papaverine induced penile erection in 220 impotent men. Study of temporal patterns and the role of repeated sampling, velocity asymmetry and vascular anomalies. Clin. Radiol. (in press). POHAR, S S, JACKSON, F I & GLAZEBROOK, G A, Ultrasonography and radiography in the diagnosis of Peyronie's disease. Can. Assoc. Radiol. J., 41, QUAM, J P, KING, B F, JAMES, E M ET AL, Duplex and colour Doppler sonographic evaluation of vasculogenic impotence. AJR, 153, SCHWARTZ, A N, WANG, K Y, MACK, L A ET AL, Evaluation of normal erectile function with colour flow Doppler sonography. AJR, 153, SMITH, B H, Peyronie's disease. Am. J. Clin. Pathoi, 45, SMITH, B H, Subclinical Peyronie's disease. Am. J. Clin. Pathoi., 52, SOMERS, K D, SISMOUR, E N, WRIGHT, G L Jr ET AL, Isolation and characterization of collagen in Peyronie's disease. J. Urol., 141, VANDE BERG, J S, DEVINE, C J, HORTON, C E ET AL, Peyronie's disease: An electron microscopic study. J. Urol., 126, VORSTMAN, B & LOCKHART, J, Peyronie's disease. Probl. Urol., 1, The British Journal of Radiology, May 1993

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