CHAPTER
32
INTRODUCTION
Ultrasound of the penis
Anthony J. Edey, C. Jason Wilkins and Paul S. Sidhu
621
NORMAL ANATOMY AND ULTRASOUND
APPEARANCES 621
ERECTILE DYSFUNCTION 621
Background 621
Physiology of the erectile process 623
STIMULATED COLOUR DOPPLER ULTRASOUND
Pharmacological agents 623
Technique 623
Baseline imaging 623
Normal response 624
Arteriogenic erectile dysfunction 624
Veno-occlusive erectile dysfunction 624
Further imaging 625
False venous leak 626
623
PRIAPISM 627
Non-ischaemic priapism 627
Ischaemic priapism 627
PEYRONIE’S DISEASE
PENILE FIBROSIS
627
628
PENILE MASSES
628
PENILE TRAUMA
629
URETHRAL ULTRASOUND
629
INTRODUCTION
Ultrasound plays an important role in the evaluation of penile
pathology. High-frequency ‘small parts’ linear transducers allow
interrogation of the greyscale anatomy and dynamic vascular
imaging of the normal and diseased penis. Diagnostic images can
be obtained with few artefacts in a non-invasive manner and
without exposure to ionising radiation. Ultrasound of the penis has
been useful in the assessment of erectile dysfunction, but is also
valuable in the assessment of Peyronie’s disease, penile masses,
priapism and following trauma.
NORMAL ANATOMY AND ULTRASOUND
APPEARANCES
The penis is composed of three cylindrical structures of erectile
tissue: two dorsal corpora cavernosa and a ventral corpus spongiosum containing the penile urethra. The spongiosum is smaller
proximally but expands distally to form the glans penis (Fig. 32.1).
The corpora cavernosa contain sinusoidal tissue which is markedly
distensible and is essential to the erectile process. A tough,
non-distensible fibrous capsule, the tunica albuginea, invests the
corpora cavernosa, with a much thinner layer covering the corpus
spongiosum.1 There are two layers of fascia enveloping the shaft of
the penis beneath the skin. The dartos fascia is superficial and is in
continuity with Scarpa’s fascia of the abdomen and the dartos fascia
of the scrotum. Deep to the dartos fascia lies Buck’s fascia, which
covers the corpora cavernosa and corpus spongiosum and attaches
posteriorly to the suspensory ligaments of the penis, allowing the
erect penis to achieve a horizontal or greater angle.2 The normal
arterial supply to the penis is via the internal pudendal artery (a
branch of the anterior division of the internal iliac artery), which
divides into terminal branches, the dorsal penile artery (supplying
the glans penis), the cavernosal artery (supplying the corpora cavernosa) and the bulbar artery (supplying the bulb and the corpus
spongiosum) (Fig. 32.2). The cavernosal arteries give the main contribution to erectile function and anatomical variations are common.
Emissary veins pierce the tunica albuginea, and drain into the deep
dorsal vein via the spongiosal, circumflex and cavernosal veins.3
Ultrasound identifies the paired corpora cavernosa, the cavernosal arteries, the tunica albuginea and the corpus spongiosum (Fig.
32.3). The corpora cavernosa are of intermediate reflectivity. Buck’s
fascia and the tunica albuginea are indistinguishable as they surround the corpora and appear as a thin low reflective envelope
(<2 mm thick). Overlying the corpus spongiosum, Buck’s fascia is
visible as a separate high reflectivity line. The corpus spongiosum
is of slightly higher reflectivity than the corpora cavernosa. The
highly reflective walls of the cavernosal arteries are usually clearly
identified at the base of the penis and can often be identified as two
parallel, highly reflective lines on longitudinal imaging (Fig. 32.4).
The normal urethra is not identified.
Anatomy
• Ventral highly reflective corpus spongiosum expands to form the
glans penis.
• Dorsal paired low reflective corpora cavernosa
• enveloped by the thin highly reflective tunica albuginea
• distensible sinusoidal tissue essential for erectile function.
• Internal pudendal artery divides into
• dorsal penile artery, bulbar artery and the cavernosal arteries.
• Venous drainage via the superficial and deep dorsal veins
• emissary veins pierce the tunica albuginea, draining into dorsal
veins via cavernosal, spongiosal and circumflex veins
• the emissary vein/tunica region is the site of the venoocclusive mechanism.
ERECTILE DYSFUNCTION
Background
Erectile dysfunction is defined as the inability to achieve or maintain an erection adequate for sexual satisfaction. The Massachusetts
Male Aging Study found that 35% of men aged 40–70 years reported
moderate or complete erectile dysfunction.4 Severity and
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CHAPTER 32 • Ultrasound of the penis
Superficial dorsal vein
Cavernosal artery
Dorsal penile artery
Dartos fascia
Deep dorsal vein
Dorsal nerve
of the penis
Helicine artery
Internal pudendal arteries
Dorsal artery
Bulbar artery
Buck’s fascia
Circumflex veins
Corpus
cavernosum
Tunica albuginea
Cavernosal artery
Corpus spongiosum
Urethra
Corpus cavernosa
Urethral artery
Corpus spongiosum
Figure 32.1 Anatomy of the penis. (Modified from Baxter GM
and Sidhu PS. Ultrasound of the Urogenital System. Thieme,
Stuttgart, 2006, Ch. 12, Diseases of the penis with functional
evaluation by Wilkins CJ, Sidhu PS.)
Glans
Figure 32.2 Arterial supply of the penis.
A
B
Figure 32.3 Ultrasound appearances of the penis. A: In the flaccid state, the paired corpora cavernosa (long arrows) are of low
reflectivity and contain the cavernosal arteries (short arrows). The higher reflective corpora spongiosum (arrowhead) contains the urethra.
B: During tumescence, the corpora cavernosa expand with blood resulting in pockets of low reflectivity forming (short arrows). The
cavernosal arteries are more prominent (long arrow).
prevalence increase with age and it is estimated that between 20
and 30 million men in the USA are affected by erectile
dysfunction.5
Following the discovery that intra-cavernosal injection of vasoactive agents can produce an erection in the absence of sexual arousal,
our understanding of the physiology of the erectile process has
improved.6 Recently, the introduction of effective oral therapies
such as sildenafil, a phosphodiesterase type 5 (PDE-5) inhibitor, has
revolutionised the management of erectile dysfunction. There has
been a decline in the role of stimulated colour Doppler ultrasound
(CDUS) and other radiological tests in the evaluation of erectile
dysfunction. Often a ‘trial’ of a PDE-5 inhibitor serves as an initial
diagnostic test: efficacy confirms the adequacy of penile arterial
inflow and veno-occlusive erectile mechanisms and eliminates the
need for further testing. Furthermore, surgical procedures for the
622
Figure 32.4 Longitudinal image of the prominent cavernosal
artery (arrow).
Stimulated colour Doppler ultrasound
treatment of venous leaks have poor long-term clinical outcomes.
Despite this, patient pressure means that surgical correction for
venous leak, whilst controversial, is still carried out in some centres.
The use of arterial reconstructive surgery is indicated only in a
small group of patients with new onset focal arterial occlusion with
few or no features of systemic vascular disease.7,8
However, a CDUS examination remains useful; experience shows
that many patients benefit psychologically from a normal test
result. Additionally, CDUS imaging of the penis is important in the
pre-assessment of patients due to undergo revascularisation surgery
following penile trauma, and to document vascularity prior to
surgery for Peyronie’s disease.9 There is also evidence that erectile
dysfunction may be an early marker of peripheral and coronary
atherosclerotic disease.10 Pooled data suggests that a normal arterial
response to prostaglandin E1 has a negative predictive value for the
presence of coronary artery disease of 84%, whilst a diminished
response has a positive predictive value of 32%.
Physiology of the erectile process
Penile erection is the consequence of neurovascular events triggered by a combination of psychological and hormonal factors.
Increased cavernosal artery blood flow results in filling of the sinusoids of the corpora cavernosa. This leads to an elevation of pressure in the corpora as the sinusoids distend within the non-compliant
tunica albuginea. The rise in intra-tunica pressure compresses the
sub-tunica venous plexuses between the trabecula and tunica
albuginea. In turn, this partially occludes venous drainage from the
penis and results in tumescence. Complete occlusion of venous
outflow is achieved during sexual activity by compression of the
engorged corpora cavernosa at their base by contraction of the
ischio-cavernosal muscles. This final stage results in rigidity. During
tumescence intra-cavernous pressures reach approximately
100 mmHg and when rigid the pressure may rise to several hundred
mmHg.
Erectile dysfunction is the result of a failure of this process and
may be due to neurogenic, psychogenic, vascular (arterial or
venous) causes, or as the result of disruption of the tunica albuginea, post-traumatic or more commonly due to Peyronie’s disease.
Alternatively it may be due to patient medication or systemic disorders such as diabetes mellitus with multifactorial causes not
uncommon.
absence of diastolic flow is a frequent occurrence in the ‘normal’
responder, and is not a sinister finding.13 More recent work has
found that the absence of systolic flow at 1 hour following intracavernosal injection of a stimulant is a more useful predictor and
warrants immediate treatment and admission.14 Imaging all patients
at 1 hour post procedure would be impractical and a 4-hour return
to receive prompt treatment based on patient self-assessment has
been shown to work well.3
Technique
The stimulated CDUS examination should be performed with a
chaperone, in a setting that offers patient privacy with little possibility of interruption. A high-frequency linear ‘small parts’ transducer with a small footprint is required. Intra-cavernosal injection
of PGE-1 is performed with a small-bore needle (typically 30G). The
ideal injection site is between the proximal and mid thirds of the
shaft at the dorsolateral aspect. Following injection of the vasoactive
substance the angle-corrected velocity of either the left or the right
cavernosal artery is recorded at 5-minute intervals from baseline up
to 30 minutes.15 Tumescence and rigidity are documented.
Colour flow Doppler ultrasound of the cavernosal arteries should
be performed with the probe positioned at the base of the penis on
the ventral surface. The angle for Doppler analysis needs to be
optimised (<60°) with box-steering, angle correction and orientation
of the probe to ensure reproducible, valid measurements. The peak
systolic velocity (PSV) of the cavernosal artery varies according to
the location of sampling, with higher velocities more proximally.16
Measurement of the spectral Doppler trace is most reproducible at
the base of penis where the angle of the cavernosal vessel is not
parallel with the probe.9 Self-stimulation has been advocated as an
adjunct to pharmacological stimulation in order to obtain a maximal
response, although the risk of ejaculation (which would necessitate
a repeat of the test on a separate occasion) needs to be considered
and patients should be advised to stop prior to this.17
Baseline imaging
Pharmacological agents
Baseline B-mode US imaging is performed in longitudinal and
transverse planes with the penis held by the patient in the anatomical position. Before injection of the stimulant detailed ultrasound
examination of the penis is required. This allows selection of an
appropriate site for injection. Significant abnormalities such as
fibrotic plaque disease, focal cavernosal fibrosis, arterial calcification or tunica disruption may be detected. Ultrasound imaging
prior to injection allows the observer to distinguish between true
calcification/fibrosis abnormalities and the spurious appearance of
calcification/fibrosis of the corpora which may occur following
inadvertent intra-cavernosal injection of air bubbles18 (Fig. 32.5).
The cavernosal arteries range in diameter from 0.3 mm in the flaccid
Prostaglandin E-1 (PGE-1) is the most widely used agent for pharmacological stimulation of the penis. The normal dosage of PGE-1
is between 10 and 20 µg. Practice varies, but most commonly 20 µg
is administered at the outset of the test. An alternative is to assess
the erectile response after an initial dose of 10 µg and if inadequate
a second 10 µg injection is administered. However, the examination
is significantly shortened with the single dose method and use of a
single dose minimises patient discomfort and anxiety. PGE-1 is
widely reported as a safe treatment but there is a small risk of priapism (less than 1%).11 Papaverine, the second most commonly used
stimulant, has a reported incidence of iatrogenic priapism of up to
18%.12 Regardless, patients should be fully informed of the risks and
given appropriate advice. One possible strategy is that patients with
an erection lasting longer than 4 hours be given direct access to an
on-site urology opinion to ensure prompt treatment. During stimulated CDUS, absence of cavernosal artery flow or a resistance index
greater than 1.00 (absent diastolic flow) was thought to be highly
specific in predicting priapism. However, experience suggests that
Figure 32.5 Air in the corpora cavernosa. Following the
intra-cavernosal injection of a vasoactive substance, air (arrows)
causing acoustic shadowing is present at the injection site in the
corpora cavernosa.
STIMULATED COLOUR DOPPLER
ULTRASOUND
623
CHAPTER 32 • Ultrasound of the penis
Figure 32.6 Cavernosal artery duplication. In this transverse
image of the penis, there are two (arrows) cavernosal arteries
present in the left corpora cavernosa.
state to 1.0 mm during erection.6,7,19 The PSV of the cavernosal
artery in the flaccid penis in normal patients is 10–15 cm/s. This
value should be documented and further sampling during the
study should be performed in the same location.
Normal response
During the pharmacologically induced erection, dynamic assessment of the spectral Doppler waveform is performed. Maximal
arterial engorgement occurs early in tumescence and allows colour
mapping of the vessels. Variations such as bifurcation, duplication
and a common origin of the cavernosal arteries are often seen20 (Fig.
32.6). Cross communications between left and right cavernosal
arteries are present in virtually all patients.19 Anomalies may lead
to a reduction in the PSV in the absence of significant arterial insufficiency and therefore measurements obtained may result in false
positive results.21 If there is definite asymmetry of the cavernosal
arteries, this should be documented and both arteries sampled
during the course of the assessment. A focal stenosis may result in
high-velocity ‘jets’ at the site of narrowing on colour Doppler US
and, more distally, in damped pulsatility. The helicine arteries are
not visible in the flaccid penis but become apparent during the
onset of erection and branch in a radial direction from the cavernosal arteries (Fig. 32.7). During the course of tumescence, erection
and full rigidity the helicine arteries become less visible as progressive venous occlusion leads to a reduction and finally cessation of
penile inflow.19
Pharmacologically induced erection follows a predictable
sequence of changes on CDUS in patients without erectile dysfunction. Schwartz et al.22 divided this sequence into stages.
n
n
n
624
Phase 0: Prior to injection the dorsal arteries of the penis are
more clearly identified than the cavernosal arteries. In about
one-third of patients colour and spectral Doppler analysis of
the cavernosal artery prior to stimulation is not possible. The
normal spectral waveform at this stage is monophasic with a
high resistance pattern showing minimal or no diastolic flow.
Phase 1: Follows pharmaco-stimulation and marks the onset
of erection. During phase 1 the systolic and diastolic flow
increase results in continuous flow throughout the cardiac
cycle. In normal volunteers PSV is usually greater than
35 cm/s and the peak end-diastolic velocity (EDV) is greater
then 8 cm/s.
Phase 2: As pressure increases within the corpora cavernosa
there is a progressive decrease in the diastolic flow. The
Figure 32.7 Helicine branches of the cavernosal artery
following pharmaco-stimulation.
n
n
n
development of tumescence and subsequent veno-occlusion
results in a reduction in diastolic flow.
Phase 3: Corresponds to no diastolic flow.
Phase 4: Characterised by reversal of diastolic flow and
represents full erection (Fig. 32.8).
Phase 5: The final stage of rigidity, usually not seen in clinical
practice, shows a decrease in systolic velocities, which may
approach zero.22
This sequence of events has a variable time course. Assessment
over 30 minutes is occasionally required to ensure that the maximal
effect has been attained, although 20 minutes is normally
sufficient.23
Arteriogenic erectile dysfunction
Maximal PSV of the cavernosal artery following injection of vasoactive agents is the most accurate indicator of arterial disease. The
average PSV in normal volunteers is between 30 and 40 cm/s.24 A
PSV of ≥35 cm/s is unequivocally normal, whilst a PSV of <25 cm/s
following adequate stimulation indicates definite arterial insufficiency.18 Intermediate values are not specific and in this group
sildenafil is often used as some will have mild to moderate arterial
insufficiency and may benefit25 (Fig. 32.9).
Some authors suggest that arteriogenic erectile dysfunction can
be diagnosed on the basis of the PSV in the flaccid penis. One study
showed that a cut-off value of 10 cm/s for the PSV in the non-erect
penis was 96% sensitive and 92% specific in the diagnosis of arteriogenic erectile dysfunction.26 The degree of change in the diameter
of the cavernosal artery during the erectile process provides some
insight into the degree of arterial insufficiency. In normal patients
the vessel increases in size by 75–100%, whereas in patients with
arteriogenic erectile dysfunction this figure is usually less than
75%.23 However, the increase in the baseline diameter following
pharmacological stimulation does not correlate with either the
measured PSV or clinical grading of erection and it is not routine
to measure arterial diameters.27
Veno-occlusive erectile dysfunction
Ultrasound may be used to diagnose veno-occlusive dysfunction in
patients with normal arterial inflow. Having established a normal
arterial response with a PSV >35 cm/s, an EDV of >5 cm/s is
usually accepted as the level above which a venous leak is
Stimulated colour Doppler ultrasound
A
C
B
Figure 32.8 Normal pharmaco-stimulated colour Doppler
ultrasound examination of the penis. A: At 5 minutes postinjection, there is increased flow into the penis with forward flow in
diastole, measured at 6.6 cm/s. B: At 10 minutes, the peak systolic
velocity measures 67.3 cm/s; this indicates that there is no arterial
abnormality to compromise blood flow into the penis. The enddiastolic velocity remains above the baseline. C: At 15 minutes, the
end-diastolic velocity is a negative value, −5.3 cm/s; there is
integrity of the venous drainage with no leaking of blood from the
penis.
present.28,29 The resistive index (RI) may be used as an alternative
measure for the diagnosis. An RI of less than 0.8 with a normal PSV
is also regarded as diagnostic of a venous leak.30 An RI of 1.0 is
normal. In young patients with good arterial input, reversal of EDV
should normally be seen and it may be appropriate to lower the
EDV threshold in this group. As well as forward diastolic flow in
the cavernosal artery, continuous flow in the dorsal vein or other
abnormal draining veins may also be seen, but is not a requisite for
diagnosis3 (Fig. 32.10).
Further imaging
Figure 32.9 Arterial erectile dysfunction. The peak systolic
velocity remains at 27.5 cm/s despite three doses of PGE-1. The
end-diastolic velocity remains elevated at 6.7 cm/s; venous integrity
cannot be assessed in the presence of arterial erectile dysfunction.
The diagnosis of venous incompetence on ultrasound requires
normal arterial inflow. In cases with mixed aetiology of erectile
dysfunction an indeterminate result may be obtained and reflects
both arterial inflow insufficiency and venous leak. In this group of
patients, cavernosography and arteriography may be required.
Cavernosography with cavernosometry remains the diagnostic reference standard for the diagnosis of venous leak, as this technique
measures outflow resistance without the need for adequate arterial
inflow as well as mapping the sites of incompetence.31 Therefore,
following a positive CDUS for venous leak, cavernosography is
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CHAPTER 32 • Ultrasound of the penis
usually required if surgical venous ligation is planned. As previously discussed, surgical intervention for venous leak has a limited
success rate and its effects may be short-lived. However, it is a relatively minor surgical procedure and may be the treatment option
of choice for young patients, providing a temporary improvement
in symptoms. An alternative treatment is coil embolisation via a
direct approach using a draining vein.32
False venous leak
Anxiety following injection of PGE-1 may lead to a false positive
result for venous leak due to elevated adrenergic tone.11 Increased
levels of adrenaline prevent complete relaxation of the sinusoidal
smooth muscle in the corpora cavernosa and result in a failure of
the normal veno-occlusive mechanism required for an erection. On
CDUS this is characterised by forward flow in the cavernosal artery
throughout the cardiac cycle and is indistinguishable from a positive finding of venous incompetence. In patients with a suboptimal
response to PGE-1 injection and features of venous incompetence
the study may be supplemented by an intra-cavernosal injection of
phentolamine. Phentolamine is an alpha-adrenoreceptor antagonist
and has been found to be safe at an intra-cavernosal dose of 2 mg
with no significant impact on systemic blood pressure. In a study
by Aversa et al.33 phentolamine normalised erectile response in
20/26 patients initially diagnosed with venous leak following injection with PGE-1 (Fig. 32.11). Phentolamine led to a statistically
significant increase in the grade of erection, PSV and a decrease in
EDV in this study.33 Similar results have been reported in other
studies.11 The concern that intra-cavernosal injection of multiple
vasoactive agents may lead to an increased risk of priapism is
unfounded.11,33
The marked reduction in false positive results has led many
authors to recommend that intra-cavernosal phentolamine is necessary before a venous leak can be diagnosed by CDUS assessment
in the younger patient. Furthermore, phentolamine, as an oral preparation, may offer a therapeutic approach in this very specific group
of patients.34,35 Venous leak not reversed by phentolamine is highly
predictive of a structurally based abnormality.
Haemodynamic parameters for stimulated colour Doppler ultrasound
Figure 32.10 Venous erectile dysfunction. At 20 minutes
following pharmaco-stimulation, the peak systolic velocity measures
52.1 cm/s; there is no arterial erectile dysfunction. However, the
end-diastolic velocity measures 13.7 cm/s; this is a clear example
of a venous cause for erectile dysfunction.
A
Adequate arterial inflow if PSV >35 cm/s.
Borderline arterial inflow if PSV between 35 cm/s and 25 cm/s.
Arterial insufficiency if PSV <25 cm/s.
If PSV >35 cm/s a venous leak is diagnosed if EDV >5 cm/s.
Reversal of end-diastolic flow is expected in younger patients
with an adequate arterial inflow.
• Phentolamine may be required in young patients to avoid a
spurious diagnosis secondary to anxiety-induced adrenergic
drive.
•
•
•
•
•
B
Figure 32.11 Colour Doppler ultrasound response to intra-cavernosal phentolamine. A: Following pharmaco-stimulation with
PGE-1 in this young patient, the peak systolic velocity and the end-diastolic velocity are difficult to interpret; arterial input may be
insufficient to prevent a venous leak. B: At 25 minutes, 5 minutes after a 2 mg dose of phentolamine, the peak systolic velocity increases
to 75.7 cm/s and the end-diastolic velocity is negative at −5.4 cm/s; the arterial and venous mechanisms are intact.
626
Peyronie’s disease
PRIAPISM
Priapism is defined as an erection that is maintained in the absence
of sexual stimulation.17 There are two principal categories: nonischaemic and ischaemic priapism. A further subgroup of ‘stuttering’ or recurrent priapism has been proposed.36 Rarely, priapism
may be a manifestation of an aorto-caval fistula.37 Diagnosis of priapism is clinical and relies on the history, examination and analysis
of blood aspirated from the cavernosa. However, ultrasound provides clinically useful information that may help management.38
Non-ischaemic priapism
Non-ischaemic, high-flow or post-traumatic priapism is a manifestation of damage to the cavernosal arteries resulting in fistula formation between the high-pressure arterial system and the
low-pressure cavernosal sinusoids.17 Clinically patients present
with prolonged tumescence from the time of injury. On aspiration
the cavernosal blood is oxygenated. Presentation may not be
immediate as it is usually painless. Patients with non-ischaemic
priapism may still be able to achieve an erection following
sexual stimulation.
B-mode imaging reveals a hypoechoic intra-cavernosal region
around the damaged cavernosal artery. This abnormality is localised to the site of cavernosal disruption and haematoma formation
resulting from arterial extravasation.38 There is elevation of the cavernosal artery PSV and high forward diastolic flow at spectral
Doppler US examination. The draining veins are often prominent
and may exhibit arterialised waveforms.18 Colour Doppler ultrasound allows direct imaging of the arterio-sinusoidal fistula. This
is identified as a focus of high-velocity, turbulent flow superimposed on the hypoechoic region demonstrated on greyscale
imaging.39 Elective arterial embolisation of the internal pudendal or
cavernosal artery is often the first-line management of non-ischaemic arterial priapism.40,41
corpora cavernosa but a soft glans and is a urological emergency
that requires prompt treatment. The diagnosis is usually clinical.
Aspiration of the cavernosal blood is both therapeutic and diagnostic. Ischaemic priapism is confirmed by the presence of deoxygenated blood and a low pH. A low pH indicates a severe degree of
ischaemia and compounds the risk of corporal fibrosis with concomitant loss of erectile function. Imaging is not usually required
before therapeutic intervention but may have a role if first-line
measures including aspiration of cavernosal blood and phenylephrine injection fail to significantly improve blood flow.7
On B-mode imaging there is engorgement of the cavernosal sinusoids as seen in a physiological erection. Due to sedimentation of
the corpuscular component of blood a fluid–fluid level within the
corpora cavernosa is visible on ultrasound of the penis if the patient
is left supine for a few minutes with no penile manipulation.38
Colour Doppler ultrasound findings are of low or absent diastolic
flow with variable, but usually not high, arterial inflow consistent
with a high resistance vascular bed.18
Priapism
Non-ischaemic:
• High PO2; oxygenated corporal blood on aspiration.
• Spectral Doppler waveforms show continuous increased systolic
and diastolic flow with a low resistance pattern.
• In the post-traumatic patient AV fistula may be identified and can
guide therapy.
Ischaemic:
• Low PO2; deoxygenated corporal blood on aspiration.
• Spectral Doppler waveforms show low or absent diastolic flow
with a high resistance pattern.
• Oedema.
Differentiation is necessary as ischaemic priapism requires urgent
treatment.
Ischaemic priapism
Ischaemic or low-flow priapism is a compartment syndrome caused
by veno-occlusive problems such as sickle cell disease, or by intracavernosal injection of vasoactive agents (Fig. 32.12). Ischaemic
priapism presents with a painful persistent tumescence of the
Figure 32.12 Ischaemic priapism. In this patient with sickle cell
disease, there is engorgement of the corpora cavernosa (short
arrows) and oedema of the overlying tissue (long arrow).
PEYRONIE’S DISEASE
Peyronie’s disease is defined as a combination of penile pain and
deformity with or without palpable penile plaques. The lack of a
consensus definition is reflected in the range of reported incidence
(1–10% of the adult male population).42 The incidence is highest in
the 40–60-year-old group. Peyronie’s disease is characterised by
formation of plaques in the tunica albuginea of the penis. Peyronie’s
disease most commonly presents with a dorsal curvature of the
penis. However, other malformations including penile shortening,
bottle-neck deformities (due to annular plaques) and indentations,
may all occur. Erectile dysfunction is a common association found
in 20–40% of such patients. Fibrotic plaque formation results from
vascular inflammation but the aetiology is controversial. Evidence
does not corroborate the long-held belief that trauma is a primary
cause.43 Peyronie’s disease may be associated with Dupuytren’s
contracture.
On ultrasound plaques are most commonly identified peripherally over the dorsum of the penis (Fig. 32.13). Imaging in the region
of maximal deformity or at the site of a palpable lesion will invariably demonstrate an abnormality. Recent work suggests that the
fibrotic lesions may be classified into three groups: firstly, hyperechoic foci with no acoustic shadow (Fig. 32.14); secondly, those
lesions with an acoustic shadow; and thirdly, calcified lesions.
Abnormalities are rarely hypoechoic.44 It has been suggested that
the first group represents active fibrotic foci which frequently
resolve spontaneously. The presence of calcified plaques is consistent with established, non-reversible disease.45 Abnormal plaques
627
CHAPTER 32 • Ultrasound of the penis
Figure 32.13 Peyronie’s disease. Linear calcification (arrows) in
the corpora cavernosa, causing acoustic shadowing; likely
Peyronie’s disease.
Figure 32.15 Malignant tumour of the penis. A poorly
vascularised mass (arrow) in the distal shaft of the penis; a
squamous cell carcinoma.
plaque may encase the cavernosal arteries and cause arterial erectile
dysfunction.48 Furthermore, there is also an increased incidence of
arterial and mixed vascular abnormalities.49 B-mode assessment of
calcification allows patient selection for lithotripsy therapy, and
CDUS examination is important prior to possible corrective surgery,
to ascertain the course of the cavernosal arteries in relation to
plaques.50
PENILE FIBROSIS
Figure 32.14 Peyronie’s disease. Focal area of altered reflectivity
(arrows) in the corpora cavernosa; likely Peyronie’s disease.
Peyronie’s disease
• Plaques may or may not be calcified.
• In the flaccid state plaques can be difficult to visualise, but may
become apparent during tumescence; image at the site of
maximal curvature.
• Both arterial and venous diseases are more common in
Peyronie’s disease – mixed aetiology is often present requiring
careful assessment to guide therapy.
• Plaques and/or fibrosis may occur following treatment with
PGE-1 and can necessitate cessation of treatment.
may extend beyond those that are palpable to involve the corporal
tissue or the inter-cavernosal septum and these may be visible on
ultrasound.46 Focal or diffuse thickening of the tunica (which
becomes more apparent following pharmacological stimulation)
may be the only ultrasound feature.47
Distortion of the tunica albuginea results in a higher incidence of
venous erectile dysfunction than in the general population. Rarely,
628
Penile fibrosis may result from a number of causes. Without prompt
treatment ischaemic priapism will cause fibrosis of the cavernosal
tissue, producing diffuse cavernosal fibrosis. On ultrasound this is
recognisable as replacement of normal sinusoidal tissue in the
corpora cavernosa by ill-defined hyperechoic regions. Regular selfinjection with intra-cavernosal stimulation therapy for erectile dysfunction, in particular papaverine, may cause focal areas of penile
fibrosis to develop.51 Ultrasound examination can delineate areas of
fibrosis allowing follow-up and guiding decisions on therapy.52 In
some patients there may be intra-corporal calcification without any
associated plaque and this is thought to result from regions of focal
fibrosis or possibly previous trauma.53
PENILE MASSES
Primary penile malignancies are rare. Squamous cell carcinoma
accounts for up to 95% of malignancies of the penis and is most
commonly located at the glans (Fig. 32.15). Squamous cell carcinoma is associated with human papilloma virus (types 16 and 18)
and is more common in the developing world. Other primary
malignancies include melanomas, basal cell carcinoma and lymphoma.54 Metastatic spread of malignancy to the penis may be
either haematogenous or lymphatic. Metastases should be suspected in patients with a known primary malignancy and new
onset priapism. Ultrasound is the preferred imaging modality for
penile malignancy.21,55 Ideally, it should be performed following
injection of PGE-1. Ultrasound can assist in identifying the depth
of tumour invasion and, specifically, allows evaluation of corpora
cavernosal infiltration. It has been shown to be more accurate than
clinical examination in determining the extent and size of the
References
Figure 32.16 Penile prosthesis. The low reflective area (arrow)
within the shaft of the penis is clearly of an artificial nature.
tumour.56 Detection of local lymph nodes is readily performed
using ultrasound; however, assessment of microscopic infiltration
is not possible.21,55
On ultrasound squamous cell carcinoma tends to be hypoechoic,
relatively heterogeneous and typically poorly vascularised on
CDUS. Interruption of the echogenic tunica albuginea indicates
malignant infiltration.57 Ultrasound is of limited value in large
tumours and MR imaging is generally indicated in this context. The
appearances of secondary disease are similar to those of primary
penile cancer involving the corpora.58
Other masses occurring in the penis include those found in the
skin and subcutaneous tissues elsewhere including cysts, lipomas
and neurofibromas. A further unusual ‘mass’ which may be encountered is a penile prosthesis, easily identifiable by parallel highly reflective walls and the ‘man-made’ symmetrical structure (Fig. 32.16).
PENILE TRAUMA
Blunt trauma to the flaccid penis rarely causes a fracture, but may
result in extra-tunica or cavernosal haematoma formation. Penile
fractures most commonly occur as a result of compression of the
erect penile shaft against the pubic symphysis during sexual intercourse. Presentation is usually acute with a history of pain, swelling
and sudden loss of tumescence during intercourse.43 The principal
role of ultrasound in the acute setting is to identify defects in the
tunica albuginea and to allow assessment of the extent of acute
haematoma formation (Fig. 32.17). Ultrasound aids diagnosis in
cases where the history or clinical findings are atypical. Identification of a tunica defect should prompt immediate surgical repair as
delay in treatment of over 24 hours following the initial injury
significantly increases the risk of long-term sequelae.59
Complications of penile fracture include corporal fibrosis with or
without plaque formation, disruption of the tunica albuginea and
urethral disruption.59,60 Urethral injury may be present in up to 20%
of cases.61 If there is clinical concern about a urethral injury then
formal urethrography is required. Erectile dysfunction due to
impairment of the veno-occlusive mechanism may also occur.62
Figure 32.17 Penile fracture. A transverse image through the
penis demonstrating a haematoma (short arrows) displacing the
normal structures of the penis (long arrow) as a consequence of a
fracture.
Urethrography involves ionising radiation, whilst urethroscopy is
invasive and may introduce infection. Ultrasound allows visualisation of the structures around the urethra whilst these other techniques essentially provide luminal views. Some practitioners have
advocated the use of ultrasound for evaluating the urethra. Using
high-frequency linear probes the normal anterior (bulbar and
penile) urethra is visualised when distended with fluid. Lidocaine
gel or normal saline may be used to obtain urethral distension in a
retrograde direction via the urethral meatus in a manner analogous
to conventional urethrography. Alternatively, antegrade passage of
urine with constriction of outflow at the glans by means of a clamp
or the patient’s fingers during the ultrasound examination may be
utilised. Images are acquired in longitudinal and transverse planes.
Imaging of the posterior urethra is more problematic but may be
performed with a transrectal probe. Micturating images of the posterior urethra with the probe in situ allow high-resolution images
of the posterior urethra. However, the self-evident problems of
micturition with the probe in place limit the value of this
technique.
The anterior (bulbar and penile) urethra is of relatively uniform
diameter and measures up to 1.0 cm across. The walls are smooth
and highly reflective. Strictures, intra-luminal masses and calculi
are well visualised.
Ultrasound of the urethra serves as an important adjunct to other
imaging modalities in the evaluation of stricturing disease. In particular, bulbar urethral strictures, which tend to be focal, benefit
from ultrasound evaluation in order to determine the best treatment. The presence of abnormal peri-urethral tissue, which measures more than 3 mm, is predictive of poor outcome unless surgical
resection is performed.63 Ultrasound has been shown to be more
accurate in the measurement of the length of strictures in the bulbar
urethra than conventional urethrography.64 Accurate evaluation of
stricture length is important as it in part determines the decision to
graft or excise a stricture.63
REFERENCES
URETHRAL ULTRASOUND
Formal urethrography supplemented by urethroscopy remains the
imaging modality of choice for the assessment of the male urethra.
1. Williams PL, Warwick R, Dyson M, Bannister LH. Splanchnology. In:
Williams PL, Warwick R, Dyson M, Bannister LH, editors. Gray’s
anatomy. 37th edn. London: Churchill Livingstone; 1989. p. 1432–1433.
2. Bella AJ, Brant WO, Lue TF. Penile anatomy. In: Bertolotto M, editor.
Color Doppler US of the penis. Berlin: Springer; 2008. p. 11–14.
629
CHAPTER 32 • Ultrasound of the penis
3. Wilkins CJ, Sidhu PS. Diseases of the penis with functional evaluation.
In: Baxter GM, Sidhu PS, editors. Ultrasound of the urogenital system.
Stuttgart: Thieme; 2006. p. 181–192.
4. Feldman HA, Goldstein I, Hatzichristou DG, et al. Impotence and its
medical and psychosocial correlates: results of the Massachusetts Male
Aging Study. J Urol 1994;151:54–61.
5. Benet AE, Melman A. The epidemiology of erectile dysfunction. Urol
Clin North Am 1995;22:699–709.
6. Virag R. Intracavernous injection of papaverine for erectile failure.
Lancet 1982;2(8304):938.
7. Montague DK, Jarow J, Broderick GA, et al. American Urological
Association guideline on the management of priapism. J Urol
2003;170:1318–1324.
8. Montague DK, Jarow JP, Broderick GA, et al. Chapter 1: The
management of erectile dysfunction: an AUA update. J Urol
2005;174:230–239.
9. Golijanin D, Singer E, Davis R, et al. Doppler evaluation of erectile
dysfunction – part 1. Int J Impot Res 2007;19:37–42.
10. Montorsi P, Ravagnani PM, Galli S, et al. Association between erectile
dysfunction and coronary artery disease: matching the right target
with the right test in the right patient. Eur Urol 2006;50:721–731.
11. Gontero P, Sriprasad S, Wilkins CJ, et al. Phentolamine re-dosing
during penile dynamic colour Doppler ultrasound: a practical method
to abolish a false diagnosis of venous leakage in patients with erectile
dysfunction. Br J Radiol 2004;77:922–926.
12. Lomas GM, Jarow JP. Risk factors for papaverine-induced priapism.
J Urol 1992;147:1280–1281.
13. Cormio L, Bettocchi C, Ricapito V, et al. Resistance index as a
prognostic factor for prolonged erection after penile dynamic colour
Doppler ultrasonography. Eur Urol 1998;33:94–97.
14. Shamloul R, Ghanem HM, Salem A, et al. The value of penile duplex
in the prediction of intracavernous drug-induced priapism. Int J Impot
Res 2004;16:78–79.
15. Govier FE, Asase D, Hefty TR, et al. Timing of penile color flow
duplex ultrasonography using a triple drug mixture. J Urol
1995;153:1472–1475.
16. Kim SH, Paick JS, Lee SE, et al. Doppler sonography of deep
cavernosal artery of the penis: variation of peak systolic velocity
according to sampling location. J Ultrasound Med 1994;13:591–594.
17. Mihmanli I, Kantarci M. Erectile dysfunction. Semin Ultrasound CT
MRI 2007;28:274–286.
18. Wilkins CJ, Sriprasad S, Sidhu PS. Colour Doppler ultrasound of the
penis. Clin Radiol 2003;58:514–523.
19. Bertolotto M, Lissiani A, Pizzolato R, Fute MD. US anatomy of the
penis: common findings and anatomical variations. In: Bertolotto M,
editor. Color Doppler US of the penis. Berlin: Springer; 2008.
p. 25–38.
20. Jarrow JP, Pugh VW, Routh WD, Dyer RB. Comparison of penile
duplex ultrasonography to pudendal arteriography. Variant penile
arterial anatomy affects interpretation of duplex ultrasonography.
Invest Radiol 1993;28:806–810.
21. Mancini M, Bartolini M, Maggi M, et al. The presence of arterial
anatomical variations can affect the results of duplex sonographic
evaluation of penile vessels in impotent patients. J Urol 1996;155:
1919–1923.
22. Schwartz AN, Wang KY, Mack LA, et al. Evaluation of normal erectile
function with color flow Doppler sonography. AJR Am J Roentgenol
1989;153:1155–1160.
23. Chiou RK, Alberts GL, Pomeroy BD, et al. Study of cavernosal arterial
anatomy using color and power Doppler sonography: impact on
hemodynamic parameter measurement. J Urol 1999;162:358–360.
24. Golijanin D, Singer E, Davis R, et al. Doppler evaluation of erectile
dysfunction – part 2. Int J Impot Res 2007;19:43–48.
25. Benson CB, Aruny JE, Vickers MA. Correlation of duplex sonography
with arteriography in patients with erectile dysfunction. AJR Am J
Roentgenol 1993;160:71–73.
26. Roy C, Saussine C, Tuchmann C, et al. Duplex Doppler sonography of
the flaccid penis: potential role in the evaluation of impotence. J Clin
Ultrasound 2000;28:290–294.
27. Patel U, Lees WR. Penile sonography. In: Solibiati L, Rizzatto G,
editors. Ultrasound of superficial structures. London: Churchill
Livingstone; 1995. p. 229–242.
28. Quam JP, King BF, James EM, et al. Duplex and color Doppler
sonographic evaluation of vasculogenic impotence. AJR Am J
Roentgenol 1989;153:1141–1147.
29. Bassiouny HS, Levine LA. Penile duplex sonography in the diagnosis
of venogenic impotence. J Vasc Surg 1991;13:75–82.
630
30. Kassouf W, Carrier S. A comparison of the International Index of
Erectile Function and erectile dysfunction studies. BJU Int
2003;91:667–669.
31. Lue TF, Hricak H, Schmidt RA, Tanagho EA. Functional evaluation of
penile veins by cavernosgraphy in papaverine-induced erection. J Urol
1986;135:479–482.
32. Fowlis GA, Sidhu PS, Jager HR, et al. Preliminary report: combined
surgical and radiological penile vein occlusion for the management of
impotence caused by venous-sinusoidal incompetence. Br J Urol
1994;74:492–496.
33. Aversa A, Rocchietti-March M, Caprio M, et al. Anxiety-induced
failure in erectile response to intracorporeal prostaglandin-E1 in
non-organic male impotence: a new diagnostic approach. Int J Androl
1996;19:307–313.
34. Goldstein I. Oral phentolamine: an alpha-1, alpha-2 adrenergic
antagonist for the treatment of erectile dysfunction. Int J Impot Res
2000;12(Suppl. 1):S75–S80.
35. Wespes E, Rondeux C, Schulmann CC. Effect of phentolamine on
venous return in human erection. Br J Urol 1989;63:95–97.
36. Muneer A, Minhas S, Arya M, Ralph DJ. Stuttering priapism – a
review of the therapeutic options. Int J Clin Pract 2008;62:1265–1270.
37. Gordon S, Marsh P, Day A, Chappell B. Priapism as the presenting
symptom of an aortocaval fistula. Emerg Med J 2004;21:265.
38. Bertolotto M, Mucelli FP, Liguori G, Sanabor D. Imaging priapism: the
diagnostic role of color Doppler US. Color Doppler US of the penis.
Berlin: Springer; 2008. p. 79–88.
39. Bertolotto M, Mucelli RP. Nonpenetrating penile traumas: sonographic
and Doppler features. AJR Am J Roentgenol 2004;183:1085–1089.
40. Walker TG, Grant PW, Goldstein I, et al. ‘High-flow’ priapism:
treatment with superselective transcatheter embolization. Radiology
1990;174:1053–1054.
41. Kang BC, Lee DY, Byun JY, et al. Post-traumatic arterial priapism:
colour Doppler examination and superselective arterial embolization.
Clin Radiol 1998;53:830–834.
42. Brant WO, Bella AJ, Lue TF. Peyronie’s disease: etiology and
treatment. In: Bertolotto M, editor. Color Doppler US of the penis.
Berlin: Springer; 2008. p. 55–60.
43. Zargooshi J. Penile fracture in Kermanshah, Iran: report of 172 cases.
J Urol 2000;164:364–366.
44. Bertolotto M, Coss M, Neumaier CE. US evaluation of patients with
Peyronie’s disease. In: Bertolotto M, editor. Color Doppler US of the
penis. Berlin: Springer; 2008. p. 61–70.
45. Bekos A, Arvaniti M, Hatzimouratidis K, et al. The natural history of
Peyronie’s disease: an ultrasonography-based study. Eur Urol
2008;53:644–650.
46. Brant WO, Bella AJ, Garcia MM, et al. Isolated septal fibrosis or
hematoma – atypical Peyronie’s disease? Eur Urol 2007;177:179–182.
47. Brock G, Hsu GL, Nunes L, et al. The anatomy of the tunica albuginea
in the normal penis and Peyronie’s disease. J Urol 1997;157:276–281.
48. Bertolotto M, de Stefani S, Martinoli C, et al. Color Doppler
appearance of penile cavernosal-spongiosal communications in
patients with severe Peyronie’s disease. Eur Radiol 2002;12:
2525–2531.
49. Kadioglu A, Tefekli A, Erol H, et al. Color Doppler ultrasound
assessment of penile vascular system in men with Peyronie’s disease.
Int J Impot Res 2000;12:263–267.
50. Levine LA, Coogan CL. Penile vascular assessment using color duplex
sonography in men with Peyronie’s disease. J Urol 1996;155:
1270–1273.
51. Pery M, Rosenberger A, Kaftori JK, Vardi Y. Intracorporeal
calcifications after self-injection of papaverine. Radiology 1990;176:
81–83.
52. Chew KK, Stuckey BG, Earle CM, et al. Penile fibrosis in
intracavernosal prostaglandin E1 injection therapy for erectile
dysfunction. Int J Impot Res 1997;9:225–229.
53. Doubilet PM, Benson CB, Silverman SG, Gluck CD. The penis. Semin
Ultrasound, CT, MRI 1991;12:157–175.
54. Kayes O, Ahmed HU, Arya M, Minhas S. Molecular and genetic
pathways in penile cancer. Lancet Oncol 2007;8:420–429.
55. Algaba A, Horenblas S, Pizzocaro-Luigi PG, et al. EAU guidelines on
penile cancer. Eur Urol 2002;42:199–293.
56. Agrawal A, Pai D, Ananthakrishnan N, et al. Clinical and sonographic
findings in carcinoma of the penis. J Clin Ultrasound 2000;28:
399–406.
57. Bertolotto M, Serafini G, Dogliotti L, et al. Primary and secondary
malignancies of the penis: ultrasound features. Abdom Imaging
2005;30:108–112.
References
58. Vapnek JM, Hricak H, Carroll PR. Recent advances in imaging studies
for staging of penile and urethral carcinoma. Urol Clin North Am
1992;19:257–266.
59. El Bahnasawy MS, Gomha MA. Penile fractures: the successful
outcome of immediate surgical intervention. Int J Impot Res
2000;12:273–277.
60. Asgari MA, Hosseini SY, Safarinejad MR, et al. Penile fractures:
evaluation, therapeutic approaches and long-term results. J Urol
1996;155:148–149.
61. Fergany AF, Angermeier KW, Montague DK. Review of Cleveland
Clinic experience with penile fracture. Urology 1999;54:352–355.
62. Gontero P, Sidhu PS, Muir GH. Penile fracture repair: assessment of
early results and complications using color Doppler ultrasound. Int J
Impot Res 2000;12:125–129.
63. Morey AF, McAninch JW. Sonographic staging of anterior urethral
strictures. J Urol 2000;163:1070–1075.
64. Nash PA, McAnich JW, Bruce JE, Hanks DK. Sono-urethrography in
the evaluation of anterior urethral strictures. J Urol 1995;154:72–76.
631