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314 S. I. Wahl, M. B. Rubin, and C. W. Bakal
https://t.me/med1917
FIGURE 26-1. Aberrant origin of the left cavernosal artery
curved arrow
(
penis (
arrowhead
). Sonographic evaluation at the base of the
) may lead to misinterpretation.
limitations decrease the accuracy of ultrasound. Thus,
ultrasound is used most frequently as a screening tool,
and many urologic surgeons will proceed to pudendal
arteriography to confirm the presence of arterial occlusive disease and plan intervention.
■ Pudendal Arteriography
Pudendal arteriography is an anatomic rather than a
functional study, which we consider necessary in any potential candidate for penile arterial reconstruction.
High-quality selective bilateral penile pharmacoarteriography is necessary to appreciate the type and frequency
of anatomic variance, site of obstruction, and potential
collateral routes in patients suspected of having arterial
occlusions.
Impotence
We generally perform arteriography on an outpatient basis with the patient under mild conscious sedation. Multiplanar pelvic arteriography is performed to exclude the
possibility of significant proximal lesions in the common
and internal iliac arteries and to identify any anomalous
origins of the penile arteries. This study usually is performed from the right common femoral artery with a 4- or
5-Fr pigtail catheter. We then proceed to selective left internal iliac artery catheterization with a 4- or 5-French
Cobra 2 catheter. Superselective catheterization of the anterior division is often necessary to demonstrate thevascular anatomy adequately. The internal pudendal artery is
identified by its characteristic course across the middle of
the obturator foramen in the ipsilateral anterior oblique
position. We routinely use an intracavernosal injection of
60 mg ofpapaverine for optimal visualization of thepenile
vascular anatomy, especially if superselective catheterization of the internal pudendal artery is not possible. Some
authors have foundthat vasodilatation with direct intrapudendal arterial injections of vasoactive drugs, such as nitroglycerin or papaverine, can overcome the vasoconstriction in the small or medium-sized arteries and consequent
poor visualization of these vessels.
19
Others have found
that intracavernosal papaverine–phentolamine combinations are helpful.
18
After completion of the left-sided
study, it is usually possible to use the same cobra-shaped
catheter to perform the ipsilateral,right-sided catheterization; in a few instances, a recurvant catheter, such as a
Sos-1 catheter (Angiodynamics, Queensbury, NY), may be
needed. We routinely use low osmolar contrast, filming in
the ipsilateral anterior oblique projection. The penis is
generally draped across the contralateral thigh in a profile
position so that the cavernosal and dorsal arteries are not
superimposed.
It is imperative that pudendal arteriography include
visualization of both inferior epigastric arteries, because
these arteries are the preferred donor vessels when planning penile revascularization surgery. There is no single
type of revascularization surgery that fits every case;
therefore, a pudendal arteriogram is also necessary for
selection of the recipient vessel. Connecting the donor
artery to a branch of the dorsal penile artery in an endto-side fashion or, when possible, with an end-to-end anastomosis that allows the most efficient runoff is the preferred method of surgical revascularization. This method
is possible if the dorsal penile artery has clearly demonstrated good branches to the cavernosal artery on the
arteriogram. In the event that no such branches exist or
no suitable dorsal arteries are available, revascularization
of an isolated segment of deep dorsal vein with good
communicators to the intracavernous tissue is the choice
for the recipient vessel.
20,21
The classic angiography pattern of penile anatomy
demonstrates bilateral symmetry with a single pudendal
artery on each side that gives rise to scrotal branches,
where it becomes the common penile artery. The common penile artery divides into one dorsal penile artery,
one cavernosal artery, and one bulbar artery (Fig. 26-
22,23
2).
Generally, transverse root collaterals, a single
spongiosal artery, and perforating arteries between the
dorsal penile and cavernosal arteries also are seen. These
vascular patterns are highly variable, and potent men may
exhibit anatomy that differs from the classic pattern
which actually may be found only in a minority of patients. Occasionally, normal variance of penile anatomy
may be confused with arterial occlusive disease when
there is a unilateral origin of all cavernosal branches,
unilateral hypoplasia of a dorsal penile artery, and aberrant origins of bulbar or cavernosal arteries (Table 26-1).
24
➘
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FIGURE 26-2. The classic penile arterial anatomy. The internal pudendal artery (
small arrow
(
). The common penile artery divides into the dorsal penile
head
D
) and cavernosal artery (C) and the bulbar arteries (B).
(
), becoming the common penile artery (
large arrow
) gives rise to a scrotal branch
arrow-
Pudendal Arteriography 315
FIGURE 26-3. Right pudendal arteriogram demonstrating dif-
fuse atherosclerotic changes (
arrows
).
In most patients who have arteriogenic impotence, the
impaired penile perfusion is a component of generalized
atherosclerosis (Fig. 26-3). Common risk factors associated with penile arterial insufficiency include hypertension, hyperlipidemia, diabetes mellitus, and cigarette
smoking. Blunt perineal or pelvic trauma and pelvic irradiation are also well-known causes of insufficient penile
blood flow.
7,25,26
It is clinically important to be able to differentiate the
cavernosal artery from the deep penile artery. Careful
evaluation of the film and attention to technique usually
will allow this differentiation.
17
Collateral roots that may
assume functional impotence in patients with intrapenile
occlusive disease include collateral communication from
one side to another (for example, cavernosal artery to
cavernosal artery through transverse communicators at
the penile root) and communication between the dorsal
and penile cavernosal arteries through perforating
branches.
TABLE 26-1.
Variant (n
Dorsal penile-cavernosal perforators 29% 91%
Accessory cavernosal branches 29% 57%
Bilateral cavernosals arising from one
penile artery 41% 13%
Bilateral absence of cavernosals 2% 4%
Aberrant origin of cavernosal artery 12% 9%
Penile Arterial Anatomic Variations
Jarow Bookstein
et al. (5) and Lang (19)
⫽
42) (n⫽23)
Priapism
On pudendal arteriography, only the dorsal penile and
bulbar arteries are well visualized in low-flow priapism.
Classically, the cavernosal arteries are not seen. Cavernosography will confirm the angiographic findings by
demonstrating delayed venous drainage by as much as 15
minutes. In high-flow priapism resulting from trauma,
abnormal rapid antegrade flow through the internal pudendal and penile arteries is seen, often with pooling of
contrast in the corpus cavernosum from a ruptured cavernosal artery. Cavernosal artery to corpora cavernosal
fistulae may be evident in an intense contrast blush at the
base of the penis, frequently associated with rapid early
filling of venous channels seen in the late arterial phase
of filming.
High-flow priapism often is treated effectively by using
intracavernous vasoconstrictive agents or by surgical procedures designed to shunt blood away from the corpus
cavernosum to the corpus spongiosum.
of internal pudendal branch arteries also has been successful.
zation of the pudendal artery and its branches has been
performed using autologous blood clot, absorbable gelatin sponge, and N-butyl-cyanoacrylate.
cently, superselective embolization using platinum microcoils has been described.
REFERENCES
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Perlmutter AD, Stanley TA, eds. Campbell’s urology. Philadelphia: WB
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2. Melman A. The evaluation of erectile dysfunction. Urol Radiol
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4. Lue TF, Hricek H, Marich KW, et al. Vasculogenic impotence evaluated by high-resolution, ultrasonography and pulsed Doppler
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5. Jarow JP, Pugh VW, Routh WD, et al. Comparison of penile arterial
anatomy affects interpretation of Doppler ultrasonography and
pulsed Doppler spectrum analysis. Invest Radiol 1993;28:806– 810.
6. Wahl SI, Rubin MB, Bakal CW. Radiologic evaluation of penile
arterial anatomy in arteriogenic impotence. Int J Impot Res 1997;
9:93–97.
7. Levine FJ, Greenfield AJ, Goldstein I. Arteriographically determined occlusive disease within the hypogastric-cavernous bed in
impotent patients following blunt perineal and pelvic trauma. J Urol
1990;144:1147–1153.
8. Witt MA, Goldstein I, Saenz de Tejada I, et al. Traumatic laceration
of intracavernosal arteries: the pathophysiology of nonischemic,
high flow, arterial priapism. J Urol 1990;143:129–132.
9. Hauri D, Spycher M, Bruhlmann W. Erection and priapism: a new
physiologic concept. Urol Int 1983;38:138.
10. Ricciardi R Jr, Bhatt GM, Cynamon J, et al. Delayed high flow
priapism: pathophysiology and management. J Urol 1993;
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11. Walker TG, Grant PW, Goldstein I, et al. “High-flow” priapism:
treatment with superselective transcatheter embolization. Radiology
1990;174:1053–1057.
12. Lue TF, Hricek H, Marich KW, et al. Vasculogenic impotence evaluated by high-resolution ultrasonography and pulsed Doppler analysis. Radiology 1985;155:777.
13. Benson CB, Vickers MA. Sexual impotence caused by vascular disease: diagnosis by using duplex sonography. AJR Am J Roentgenol
1989;153:1149–1153.
14. Collins JP, LewandowskiBJ. Experience with intracorporal injection
of papaverine and duplex ultrasound scanning for assessment of
arteriogenic impotence. Br J Urol 1987;59:84–88.
15. Mellinger BC, Fried JT, Vaughn ED. Papaverine-induced penile
blood flow acceleration in impotent men measured by duplex scanning. J Urol 1990; 144:827.
16. Rajfer J, Canan V, Dorey FJ, et al. Correlation between penile
angiography and duplex scanning of cavernous arteries in impotent men. J Urol 1990; 143:1128.
17. 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.
18. Chiang PH, Chiang CP, Wu CC, et al. Colour duplex sonography in
the assessment of impotence. Br J Urol 1991;68:181–186.
19. Bahren W, Gall H, Scherb C, et al. Arterial anatomy and arteriographic diagnosis of arteriogenic impotence. Cardiovasc Intervt Radiol
1988;11:195–210.
20. Hatzichristou D, Goldstein I. Penile microvascular and arterial bypass surgery. Urol Clin North Am 1993;1:39–60.
21. Hawatmeh IS, Houttuin E, Gregory JG, et al. Vascular surger y for
the treatment of the impotent male. In: Krane RJ, Siroky MB,
Goldstein I, eds. Male sexual dysfunction. Boston: Little, Brown,
1983:683–690.
22. Ferner H, Straubesand J, eds. Sobotta atlas of human anatomy, vol 2,
10th ed. Baltimore: Urban & Schwartzberg, 1983:200–201.
23. Kadir S. Atlas of normal and variant angiographic anatomy. Philadelphia: WB Saunders, 1991:227–293.
24. Bookstein JJ, Lang EV. Penile magnification pharmacoarteriography: details of intrapenile arterial anatomy. AJR Am J Roentgenol
1987;146:883–888.
25. Goldstein I, Feldman MI, Deckers PJ, et al. Radiation-associated
impotence: a clinical study of its mechanism. JAMA 198
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26. Rosen
27. Steers WD, Selby JB. Use of methylene blue and selective emboliza-
28. Bertram RA, Webster GD, Carson CC III. Priapism: etiology, treat-
29. Alvarez Gonzalez E, Pamplona M, et al. High flow priapism after
30. Numan F, Cakirer S, Islak C, et al. Post-traumatic high-flow priapism
31. Kerlan RK, Gordon RL, LaBerge J, et al. Superselective microcoil
MP, Greenfield AJ, Walker TG, et al. Arteriogenic impotence:
findings in 195 impotent men examined with selective internal
pudendal angiography. Radiology 1990;151:80–90.
tion of the pudendal artery for high flow priapism refractory to
medical and surgical treatments. J Urol 1991;146:1361–1363.
ment, and results in series of 35 presentations. Urology 1985;26:
229–235.
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4;251:259–
M.Rosenblatt and K. W. DickeyVaricoceleand Female Infertility
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27
Varicocele and Female Infertility
MELVIN ROSENBLATT and KEVIN W. DICKEY
Since the beginning of recorded history, humans have
placed an emphasis on fertility. In many cultures, childlessness is viewed as a deficiency on the part of both male
and female partners. Even in today’s modern society,
procreation is considered a basic human right, and infertile couples must cope with difficult psychological and
social problems. Unfortunately, the incidence of infertility in newly married couples is on the rise. In industrialized countries, the incidence of infertility has increased
from 7 to 8% in 1960 up to 20 to 35% today.
to the growing problem, new medical therapies have
been advanced both to diagnose and to treat the wide
variety of disorders that can cause infertility. Over the past
two decades, advances in fluoroscopically guided catheter
techniques have helped to treat some of these disorders.
This chapter reviews these techniques as they pertain to
the treatment of varicoceles, fallopian tube occlusions,
and cervical stenosis.
■ Varicoceles
Varicocele, defined as abnormal distention of veins in the
pampiniform plexus, has long been recognized to be
associated with testicular dysfunction (Fig. 27-1). As early
as the first century AD, Celsus described the association
between swollen veins over the testes and testicular atro-
2
phy.
The realization that varicocele ablation can restore
testicular function was made in the late 1800s when Barwell described the restoration of testicular function with
subsequent conception after varicocele occlusion.
though the association with testicular dysfunction was
recognized, treatment was primarily directed toward the
1
In response
3
Al-
relief of painful symptoms. The procedure was not used
to repair varicoceles in infertile males. It was not until
1952, when Tuloch reported the restoration of fertility in
an azospermic male, that varicocele ligation as a treatment for infertility gained widespread acceptance.
then, varicocelectomy has become the most common operation performed for male infertility.
The importance of the varicocele and its role in infertility lies in its common occurrence in the general population. Among young men, the reported incidence of
varicoceles in the literature ranges from 5 to 26% with a
mean incidence of approximately 15%.
among infertile men is much higher, occurring in approximately 40% of patients.
Treatment for this disorder has focused on the ligation
of the spermatic vein, and various surgical techniques
have been described in the literature.
carino described a percutaneous technique for radiologically sclerosing the spermatic vein.
tion, technical enhancement and the development of
newer embolic agents has made this a safe, effective, and
relatively simple procedure.
12,13
5
6–11
The incidence
14–17
18
Since its introduc-
4
Since
In 1977, Iac-
Anatomy
The veins of the spermatic cord emerge from the mediastinum of the testicle to form the pampiniform plexus,
which consists of three groups of freely anastomosing
veins: the anterior, middle, and posterior. The external
spermatic vein and the cremasteric veins constitute the
posterior group. These veins course posterior to the spermatic cord and drain into the inferior epigastric veins at
the level of the external inguinal ring. The middle group
317
318 M. Rosenblatt and K. W. Dickey
https://t.me/med1917
ISV, are present in 14% of patients (Fig. 27-3).
23
Capsular
collaterals arise from intrarenal or capsular veins and
pursue a tortuous course before joining the ISV. Retroperitoneal collaterals, which are present in 40% of patients, provide communications between the upper ISV
and lumbar veins (Fig. 27-4).
24
Communications occur
frequently between the colic veins, the inferior mesenteric vein on the left, and the superior mesenteric vein on
the right.
24
These vessels usually contain valves and join
with the ISV at the level of the iliac crest. Bridging collaterals, draining directly into the IVC, also occur but involve the right ISV far more often than the left.
24
All these
collateral pathways, when present, can permit venous
reflux by bypassing competent ISV valves.
Collaterals that anastomose with the lower portion of
the ISV include parallel channels and venous communications to the internal iliac and inferior epigastric veins.
Parallel channels are fine, multiple, threadlike veins that
originate and terminate in the ISV (Fig. 27-5). If left
unoccluded, these seemingly insignificant vessels can, in
time, enlarge and reconstitute the ISV. Collaterals to the
internal iliac and inferior epigastric veins are infrequent;
for example, internal iliac vein anastomoses were found
to be present in only 2% of cases.
24
FIGURE 27-1. Internal spermatic vein (ISV) venogram demonstrating the reflux of contrast material into the dilated veins
of a left varicocele. This image normally should not be obtained
because the scrotum should be shielded from radiation exposure during venography.
courses medially along the vas deferens and drains into
the internal iliac veins. The anterior group, or the internal spermatic vein (ISV), accompanies the spermatic artery as it courses through the retroperitonium. On the
left side, the ISV drains into the left renal vein. On the
right, the ISV usually enters the inferior vena cava (IVC)
just below the origin of the right renal vein (Fig. 27-2).
Drainage of the right ISV into the right renal vein has
been noted in 10% of cases.
19
In most instances, the ISV
contains valves that are normally located within one centimeter of the vein opening.
20
The anatomy of the ISV is highly variable, and multiple
collateral pathways exist. Knowledge of these pathways
offers insight into the pathogenesis of varicoceles and is
important in providing effective treatment.
21,22
Several
collateral pathways anastomose with the upper portion of
the ISV. These pathways include hilar, capsular, intrarenal, retroperitoneal and colonic communications
(see Fig. 27-2). Hilar collaterals, which emanate from the
hilar portion of the renal vein and anastomose with the
Etiology
Varicoceles can be primary or secondary. Secondar y
varicoceles usually occur in older patients and result from
spermatic or renal vein obstruction by tumor or massive
hydronephrosis.
common type, is most prevalent in adolescent males and
occurs on the left side in approximately 90% of cases.
is bilateral in 8 to 9% and is right-sided in 1 to 2%.
Several hypotheses have been advanced to explain this
asymmetric presentation. Incomplete or absent valves,
which occur more frequently on the left side, have been
cited as one possible explanation (Fig. 27-6). Ahlberg et
al. found absent valves in 40% of left spermatic veins
examined at autopsy compared with 23% on the right.
Unfortunately, the frequent occurrence of valvular abnormalities is inconsistent with the relatively low 15%
incidence of varicoceles in the general population. Additionally, several investigators have noted varicoceles in
patients with competent ISV valves.
such as the vertical course and perpendicular insertion of
the left spermatic vein
non, have been proposed. The nutcracker phenomenon is
compression of the left renal vein between the aorta and
the superior mesenteric artery in the upright posi-
31–33
tion.
leads to increased hydrostatic pressure in the left ISV and
formation of the varicocele. More recently, a developmental etiology has been advanced. The embryogenesis
of the left venous system is more complex than the right,
25,26
Primary varicocele, by far the more
27
29
Other hypotheses,
30
and the nutcracker phenome-
The physiologic obstruction of the renal vein
It
28
19
Varicocele and Female Infertility 319
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FIGURE 27-2. Venous anatomy of the internal spermatic veins.
and developmental anomalies are common. Disordered
involution of the cardinal veins during development results in persistent intercardinal vein anastomoses. These
collaterals permit retrograde flow in the ISV and varicocele formation.
Pathophysiology
There is great debate about whether and how varicoceles
effect spermatogenesis. Some investigators claim that the
relationship, if any, is coincidental.
onstrated significant alterations in sperm density motility
and morphology in association with varicoceles.
35, 36
How
the varicocele, which is predominantly a unilateral process, causes bilateral testicular dysfunction is obscure. Sev-
29
eral hypotheses, including scrotal hyperthermia,
grade flow of toxic metabolite such as prostaglandin’s E
and F2a
advanced.
38,39
and hypoxia due to venous stasis, have been
40
It is possible that many of these factors act
37
retro-
2
in conjunction to cause impaired spermatogenesis. This
damage, once begun, progresses over time and results
34
Others have dem-
in testicular atrophy and irreversible cellular damage.
320 M. Rosenblatt and K. W. Dickey
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FIGURE 27-3. Left internal spermatic vein (ISV) venogram
demonstrating an atypical origin of the ISV from the superior
aspect of the left renal vein (
and smaller renal vein (RV) collateral. RVC, renal vein collateral; HC, hilar collateral.
arrowhead
) as well as a large hilar
Diagnosis
Varicoceles are diagnosed most often on clinical examination and are described by their size. A grade 1 varicocele is small and can be palpated only while the patient
performs a valsalva maneuver. Grade 2 varicoceles are
easily palpable but are not visible, whereas grade 3 varicoceles can be detected by visual scrutiny alone.
coceles that cannot be detected by careful clinical examination have been termed subclinical varicoceles, which are
defined as reflux in the ISV without palpable distention
of the pampiniform plexus.
42
The significance of the
subclinical varicocele, as it relates to infertility, is a subject
of ongoing debate. A recent review by Marshman et al.
discovered that most investigators believe this type of
varicocele can cause infertility and they argue in the favor
of treatment.
43
These arguments are based on observed
improvement in fertility after subclinical varicocelec-
44
tomy
and degree of infertility.
and the lack of correlation between varicocele size
45,46
Several noninvasive diagnostic modalities are used to
detect subclinical varicoceles; including thermography,
Doppler ultrasound,48radionuclide imaging,49and realtime ultrasound,
ity and specificity.
46
which have varying degrees of sensitiv-
50,51
At present, real-time scrotal ultrasound is the preferred noninvasive imaging modality used
to detect subclinical venous dilatation and reflux. The
presence of a varicocele is confirmed by the visualization
of two to three dilated venous channels with diameters
larger than 3 mm that increase in size in the erect position
or with a valsalva maneuver.
46
Using these criteria, Hamm
41
Vari-
FIGURE 27-4. Left internal spermatic vein (ISV) venogram
demonstrating multiple retroperitoneal collaterals (RC).
et al. reported a sensitivity of 92.2% and a specificity of
52
100%.
Spermatic venography was considered the most accu-
47
rate means by which venous reflux could be demonstrated.
19
Recently, the value of venography has been
questioned. Netto et al. demonstrated reflux in normal
subjects and showed no correlation between the presence
of reflux and alteration in spermatogenesis.
53
of this study is that the venograms were performed with
the catheter tip in the spermatic vein orifice, which can
bypass a proximal valve and artificially demonstrates reflux. Considering the controversial value of venography
and its invasive nature, this procedure should be reserved
A criticism
Varicocele and Female Infertility 321
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FIGURE 27-5. Left spermatic venogram demonstrating multiple threadlike parallel veins as well as a small retroperitoneal
collateral (RC). IVC, internal spermatic vein; PC, parallel collaterals.
for the determination of venous anatomy just prior to
percutaneous occlusion.
Treatment
Indications
Indications for therapeutic varicocele occlusion include
pain, disfigurement, male-factor infertility, and, in the
adolescent, early evidence of testicular dysfunction. Although discomfort and disfigurement are straightforward
FIGURE 27-6. Left renal venogram demonstrating an incompetent proximal internal spermatic vein (ISV) valve with retrograde filling of the ISV. RV, renal vein.
indications for treatment, infertility is not. In the infertile
couple, the presence of a varicocele in the male partner,
although known to cause progressive deterioration in
spermatogenesis, is not indicative of oligospermia. In fact,
a majority of patients with varicoceles have sperm counts
well above the accepted lower limits of normal. These
limits, established by the World Health Organization
(WHO), are 20 millionsperm per milliliter, with a progressive motility of 40 to 60%.
54
Hargreave reported a 20%
incidence of varicoceles among the men seen in his infertility clinic: however, only 6.4% had a varicocele associated
with sperm densities lower than 20 million per milliliter.
To confuse the issue further, many men with oligospermia
have been able to father children. In 1993 Hargreave et al.
reported that in the absence of other factors, the future
chances of pregnancy decrease only when the motile
sperm concentration (percent motility ⫻ sperm density)
falls below 2 million per milliliter, which is well below the
WHO lower limits of normal.
2
In this same study, an in-
verse relationship was shownto exist between the duration
2
322
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M. Rosenblatt and K. W. Dickey
of involuntary infertility and the likelihood of future pregnancy. Thus, the longer a couple has been trying, the less
likely they are to conceive without therapeutic intervention. Taking these issues into consideration, our current
indication for therapeutic varicocele occlusion as a treatment for male infertility is the lack of conception after 12
months of unprotected intercourse in association with a
sperm motile density below WHO lower limits.
In the adolescent, an asymptomatic varicocele is cause
for concern because of potential future deleterious effects on fertility. The progressive, time-dependent, spermatotoxic effects of varicoceles have been demonstrated
in both animal and human studies.
35,55,56
There is a large
difference in the incidence of palpable varicoceles between men of couples who have never been able to produce children (primary infertility) and men of couples who
have produced children in the past but are currently infertile (secondary infertility).
57
This difference, 35% versus
81%, respectively, strongly suggests that infertility is acquired from the presence of a long-standing varicocele.
Cheval and Purcell demonstrated a time-dependent decline in sperm density and motility in a group of men with
varicoceles who initially had normal semen parameters.
The difficulty is that not all varicoceles will cause clinically
relevant future testicular damage. Therapy based on the
presence of a varicocele alone could result in substantial
overtreatment. Therefore, specific features need to be
identified that will indicate which patients are at higher
risk for future infertility. The most commonly used indicators are based on sperm parameters, testicular volume
measurements, and endocrine assessment.
In the older teenager, semen samples are often not
difficult to obtain. An abnormal result in a teenager with
a varicocele is an indication for treatment. In an adolescent in whom it is not possible to obtain a semen specimen, loss of testicular volume ipsilateral to the varicocele
indicating testicular growth arrest is considered to be the
primary indication for treatment.
can be measured by careful physical examination
60
ultrasonography.
Typically, there should be no more
59,60
Testicular volume
61
or by
than a 2-mL difference between testes. When the volume
difference exceeds 3 mL, varicocele occlusion should be
performed.
56
In the absence of discernible testicular volume loss, the gonadotropin releasing hormone stimulation test (Gn/RH) can help to identify men who show
early evidence of testicular injury. A supranormal leuteinizing hormone and follicle stimulating hormone response to intravenous Gn/RH indicates Leydig’s cell and
seminiferous tubule dysfunction.
56,59
This type of response, if noted in an adolescent with a varicocele, is an
indication for therapy.
Surgical treatment
The surgical approach to the treatment of varicoceles can
be low (inguinal) or high (retroperitoneal) ligation of the
ISVs. The inguinal approach, or modified Ivanissevich proce-
dure, involves making a small incision over the inguinal
canal to expose the spermatic and cremasteric veins.
These veins are dissected free of the surrounding structures (vas deferens and testicular artery) and ligated.
The retroperitoneal approach, or modified Palomo proce-
dure, exposes the ISV within the retroperitoneum after it
exits the inguinal canal
17
To accomplish this, a small abdominal incision is made at the level of the internal inguinal ring. The fibers of the external oblique faschia and
internal oblique muscle are divided to expose the dilated
ISVs. Once identified, the veins are ligated and divided.
Recently, laparoscopic ligation of the ISVs has become
popular. This technique requires three intraperitoneal
entry points for placement of the laparoscope and operative instruments.
62
With the laparoscope, the inner surface of the abdominal wall can be visualized, revealing
either the right or left ISV coursing through the retroperitoneum just above the internal inguinal ring. To access
these veins, the parietal peritoneum is incised and the
veins are isolated and ligated. Proponents of this technique have demonstrated its safety and efficacy.
58
ics argue that the laparoscopic approach transforms a
simple extraperitoneal procedure performed through a
single incision with local anesthesia into an intraabdominal procedure requiring three separate incisions and general anesthesia.
65,66
Percutaneous occlusion
Approach
A method for selectively catheterizing the ISV from a
femoral vein approach was first described in 1976;
one year later, this approach was used to occlude a refluxing ISV percutaneous.
18,68
Today, femoral vein catheterization is the most commonly used approach for embolization of spermatic veins.
69,70
From the right common
femoral vein, the left ISV can be catheterized with a 7.3 Fr
Hopkins curved catheter (Cordis Corp., Miami, FL) (Fig.
27-7). This catheter is placed in the distal left renal vein
and is gently pulled back to engage the orifice of the left
ISV (Fig. 27-8A). The right ISV, arising from IVC, can be
catheterized with a 6 or 7 Fr Simmons-shaped catheter
(Fig. 27-8B). The acute angle at which the right ISV arises
from the IVC makes catheterization from the femoral
route more difficult. Great care must be taken to avoid
inadvertent dissection of the vein orifice with the catheter
tip. After engaging the ISV orifice, subselective catheterization is often required to deliver the embolic agent,
which can be difficult from a femoral approach because
the direction of catheter tiptravel isopposite the direction
of applied force. The use of a 7 or 8 Fr Hopkins curved
guiding catheter permits coaxial catheterization of the
ISV and remedies this problem.
71
The difficulties associated with the catheterization of
63,64
67
16
Crit-
just
Varicocele and Female Infertility 323
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accomplished by vigorously injecting 10 to 20 mL of contrast material into the vein orifice while the patient performs a valsalva maneuver. Alternatively, if a tilt table is
available, the contrast can be injected with the patient in
reverse Trendelenberg position. The resulting images can
be recorded digitally or on a series of cut-film radiographs. The purpose of the venogram is to confirm the
presence of venous reflux and to delineate the highly
variable anatomy of the ISV. The anatomic information
helps determine which embolic agent will best provide
effective occlusion. On occasion, even with a clinically
obvious varicocele, a competent ISV valve is present and
no refluxcan be demonstrated. In this setting,anastomosing bypass channels to the distal renal vein, capsular veins,
or retroperitoneal veins must be present.
23,76,77
A renal
venogram sometimes can help to identify these collaterals. Unfortunately, the collateral branches are often small
and tortuous and will not fill from an injection into the
main renal vein. Furthermore, many of the collateral
branches responsible for retrograde flow in the ISV do
not drain into the renal vein. To demonstrate these collaterals more reliably, a venogram should be performed
after catheterizing across the competent valve. This approach not only better defines the anatomy of the ISV it
also allows an embolic agent to be deposited below the
insertion of these collaterals, thus permanently preventing reflux into the veins of the pampiniform plexus (Fig.
78
27-9).
FIGURE 27-7. A 7.3 Fr Hopkins curved catheter (Cook, Bloomington, IN).
the ISV from the femoral vein prompted other investigators to advocate an internal jugular or basilic vein approach.
72–75
From the internal jugular vein, a modified 7
Fr headhunter catheter can be used to select the origin
of the right or left ISV.
73,74
From this route, catheter
travel and applied force are in alignment, thus facilitating
deep catheterization of the vein. Additionally, the recovery period required after catheterization of the internal
jugular vein is somewhat shorter than the recovery period
required after femoral vein catheterization.
Venography
Irrespective of the route used, once the origin of the ISV
is catheterized, a venogram must be performed. This is
Embolotherapy
The goal of percutaneous therapy is to eliminate congestion in the veins of the pampiniform plexus by occluding
the refluxing ISV and all its collateral tributaries. Sclerosing agents, tissue adhesives (histoacryl), stainless steel
coils, and detachable balloons all have been used to accomplish this task. Of these, no single agent has proved
to be clearly superior. Each agent possesses its unique
advantages and disadvantages.
Sclerotherapy
Several different sclerosing agents are used for the treatment of varicoceles. Aethoxysklerol (polidocanol),
Sotradecol (sodium, tetradecyl, sulfate),80Varicocid (sodium, morrhuate, benzyl alcohol),
ing contrast
83
all have proved effective. Aethoxysklerol
and Varicocid are not approved by the U.S. Food and
Drug Administration (FDA) and therefore not available
in the United States. Sclerosants are easily delivered by
directly injecting them into the proximal ISV. Effectiveness depends on the amount injected and the length of
time the sclerosant remains in contact with the veins.
Ideally, the entire ISV and all its parallel collaterals
should be filled with sclerosant medium for several minutes. For this reason, relative stasis in the ISV should be
81
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