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Can Urol Assoc J. 2007 September; 1(3): 277278.

PMCID: PMC2422961

Varicocelectomy: microsurgical inguinal varicocelectomy is thetreatment of choice

Saleh Binsaleh,MD andKirk C Lo,MD

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Introduction

Varicocelectomy is by far the most commonly performed operation for the treatment ofmale infertility. The goal of treatment of the varicocele is to obstruct the refluxing venousdrainage to the testis while maintaining arterial inflow and lymphatic drainage.

In principle, repair of varicocele should halt any further damage to testicular function,1andin a large percentage of men, results in improved spermatogenesis2as well as enhancedLeydig cell function.3Urologists, therefore, have a potentially important role in preventingfuture infertility, which underscores the importance of using a varicocelectomy techniquethat minimizes the risk of complications and recurrence.4

A variety of surgical and nonsurgical approaches have been advocated for varicocelectomy.They include minimally invasive procedures, such as laparoscopic varicocelectomy andtransvenous percutaneous embolization, and the traditional open surgical approach(retroperitoneal, inguinal and subinguinal). The current standard of care is to perform opensurgical varicocele repair with microscopic assistance to minimize possible complications.

In this section, we discuss the microsurgical inguinal approach as the treatment of choicefor varicocele ligation.

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Inguinal microsurgical approach

Inguinal approach is the modification of the technique described by Ivanissevich andGregorini in 1918. The inguinal approach involves a 35-cm incision over the inguinal canal,the opening of the external oblique aponeurosis and the delivery of the spermatic cord. Thecord is elevated and any external spermatic veins that are running parallel to the spermaticcord or perforating the floor of the inguinal canal are identified and ligated. All internalspermatic veins are identified and dissected under microscopy and then ligated with suturesor surgical clips. The vas deferens, vasal vessels, testicular artery (or arteries) and as manylymphatic channels as possible are preserved. Postoperatively, testicular venous return is

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via the vasal veins, which drain into the internal pudendal system and usually havecompetent valves.4

Compared with inguinal approach, the use of subinguinal approach is associated with agreater number of internal spermatic veins and arteries requiring attention. Hopps andcolleagues5confirmed this microanatomy variation and its impact on the surgical technique.

The primary branch point for the testicular artery occurred most commonly during itscourse through the inguinal canal. Internal spermatic arteries at the subinguinal level weremore than 3 times as likely to be surrounded by a dense network of adherent veins than

when they were identified at the inguinal level. Taken together, these data suggest thatmicroscopic dissection is more difficult with a subinguinal incision. Similarly, identificationof testicular artery pulsation can be difficult in the subinguinal approach owing to arterialcompression by the edge of the external ring against elevated cord, compared with when theexternal oblique aponeurosis is opened.6Artery identification is crucial in every patient, andeven more so in children or prepubertal adolescents in whom the artery is very small andsystemic blood pressure is low. Inguinal approach should also be the first choice in men

with a solitary testis in whom preservation of the artery is critical.6

Delivery of the testis for direct visual access to all possible avenues of testicular venousdrainage (scrotal or gubernacular collaterals) or for concomitant diagnostic testicular biopsyis possible through a small inguinal incision4;however, others found that varicocelectomy

without testicular delivery has equal or greater beneficial effects on semen parameterswithout affecting varicocele recurrence rates or pregnancy rates after varicocelectomy.7

There are few studies that compare head to head the 2 open approaches using microsurgicaltechnique. A group of researchers from Italy8compared the intraoperative results ofinguinal versus subinguinal varicocelectomy using a magnifying loupe under localanesthesia. The inguinal approach to the spermatic cord showed a trend toward an easierpreservation of the artery and a reduced incidence of recurrence, while postoperative pain

was significantly lower in the subinguinal group. Orhan and colleagues9retrospectively

evaluated 82 microsurgical inguinal varicocelectomies and 65 subinguinal cases. There wasno significant difference between the 2 groups in operative time, semen improvement orpregnancy rate, although the number of veins and arteries was higher in the subinguinalgroup.

Finally, open microsurgical varicocelectomy has a lower recurrence rate and fewercomplications, compared with laparoscopic varicocelectomy or retroperitoneal high-openligation.1012

In conclusion, inguinal varicocelectomy is the original approach and the standard againstwhich others should be compared. Except in limited situations, such as previous inguinalsurgery or marked obesity that hinders dissection, microsurgical inguinal varicocelectomyshould be the treatment of choice.

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Rev Urol. 2001 Summer; 3(3): 120133.

PMCID: PMC1476052

Current Management of Adolescent Varicocele

Darius A Paduch,MD andSteven J Skoog,MD, FAAP, FACS

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Abstract

The finding of varicocele in an adolescent male is common. Varicocele rarely causessymptoms and is often diagnosed on the routine physical examination. There is clearassociation between varicocele and male factor infertility; however, there is debate about

whether, when, and whom to treat when present in adult or adolescent males. This review ofthe epidemiology, etiology, pathophysiology, and treatment of the adolescent with

varicocele will provide the reader with tools to make appropriate decisions in dealing withthis condition.

Key words:Varicocele, Varicocelectomy, Testicular growth arrest, Male infertility,Retroperitoneal ligation, Microsurgical inguinal repair

Avaricocele can be defined as an abnormal tortuosity and dilation of the veins of thepampiniform plexus (PP). Idiopathic varicocele is usually asymptomatic. It is noticed as anasymmetry in scrotal size, and presents as heaviness in the scrotum, or, rarely, withtesticular pain. In most cases, the adolescent is unaware of the varicocele, and it isdiscovered during a regular physical examination or examination for military service.14

The incidence of high-grade varicocele is approximately 5% throughout theworld.5Varicocele is associated with a time-dependent growth arrest in adolescents andadult males.6There is a clear association between varicocele, infertility, and testicular

growth arrest.79It is also known that varicocelectomy can reverse growth arrest inadolescents.1013This knowledge has raised the question of how best to manage adolescents

with varicocele.

Adolescents do not present with infertility, and thus should prophylactic repair beperformed to prevent infertility in the future? Who would benefit the most from

varicocelectomy: adolescents with testicular growth arrest or any adolescent withvaricocele? Is it better to wait for a semen analysis or offer earlier treatment based on

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testicular growth arrest? These questions can be only answered when we have a betterunderstanding of the pathophysiology of varicocele.

This review presents the current literature on adolescent varicocele and provides guidelinesto the clinician on how to manage adolescents with varicocele.

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Epidemiology

In the general population of healthy males, the overall incidence of varicocele (all grades) is10% to 15%.4,5,14,15Approximately 30% to 50% of males with primary infertility have

varicocele.1619Varicocele is most common on the left side. It appears at early puberty, butcan occasionally be found in preadolescent boys.2,20The incidence in older adolescents

varies from 12.4% to 17.8%, with an average of 14.7% (Table 1), similar to the incidence inadult males.

Table 1Incidence of Varicocele in General Population of Healthy Adolescents

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Anatomy

The arterial blood supply to the testicle comes from the testicular artery, vasal artery, andcremasteric artery. At the level of the testis, all three arteries anastomose to allow adequate

blood supply, even with the division of the testicular artery.21,22

Venous drainage (Figure 1)is more complicated, with many individual variations. Above thetestis is a network of communicated veins called the pampiniform plexus, which drains viathe testicular vein trunci, pudendal veins, and cremasteric veins.23,24In most cases, thetesticular vein trunci form a single testicular vein entering the renal vein on the left and theinferior vena cava on the right. Venographic studies have demonstrated that the lefttesticular vein can rarely enter the inferior vena cava, and there are communications

between the testicular vein and the inferior vena cava below the level of the renal veins.2527There is also cross-communication between the left and right testicular venous systems(Figure 2).26,2830

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Figure 1Anatomy of venous drainage from left testis. For abbreviations, see accompanying list.

Figure 2Intraoperative venogram showing left to right cross-communicating veins. CC, cross-communications; PP, pampiniform plexus veins.

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Etiology

The predominance of left-side varicocele and the unique anatomy of the left testicular veinare the basis for several theories explaining the etiology of varicocele. The presence of

venous valves was long believed to be a mechanism guarding against developing varicocele,and incompetence of the venous valve system was thought to be responsible for varicoceledevelopment. However, it was shown that there are males without varicocele who have anincompetent venous valve system and males with varicocele who have competent venous

valves.29

Hydrostatic pressure difference could be a factor causing a left varicocele. Although the lefttesticular vein is longer than the right, the simple difference in hydrostatic pressure of astanding column of blood cannot be the only reason for development of varicocele, because

all males would be affected.

The nutcracker effect is thought to occur when the testicular vein is compressed betweenthe superior mesenteric artery and aorta. The increase in hydrostatic pressure results in

varicocele formation. Although a high left renal vein to vena cava pressure gradient is notedin patients with varicocele, it is not a consistent feature.31,32

More recently, it has been hypothesized that increased arterial blood flow to the testis atpuberty exceeds venous capacity, resulting in venous dilatation and varicocele.33,34Theresults of animal studies to support this interesting theory are conflicting, and confirmationin humans will be necessary.35

The finding of elevated nitric oxide, a potent vasodilator, in the PP of males with varicocele

raises another potential cause for the etiology of varicocele in the adolescent.36

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Pathophysiology

The pathophysiology of varicocele can be studied in animal models by partial ligation of theleft renal vein.37Many features of the human condition, such as increased temperature of

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the affected testis, increased arterial blood flow, and histopathologic changes, can bereplicated in animal models.38

The following theories attempt to explain the deleterious effect of the varicocele ontesticular function:

Hyperthermia. The presence of varicocele is associated with elevated scrotal andtesticular temperature and altered spermatogenesis.39Experimental studies have shownthat spermatogenesis occurs optimally at temperatures lower than body temperature. Manyof the enzymes responsible for optimal DNA synthesis in the testis are temperature-dependent.40,41The scrotal position of the testis and the countercurrent cooling systemprovided by the PP surrounding the testicular artery allow for heat exchange and areresponsible for regulating optimal temperature for spermatogenesis.42Stasis of blood in the

varicocele with resultant increased temperature may be responsible for the deleteriouseffect of varicocele on spermatogenesis.43Increased temperature is associated withdecreased number of spermatogonia (SP) and increased apoptosis of germinal epitheliumcells.44

Abnormal blood flow. A current hypothesis assumes that increased blood flow throughthe testis can affect spermatogenesis.45,46An increase in hydrostatic pressure with a changein filtration pressure could considerably alter the composition of the interstitial fluid.47Thisconceivably could alter the intimate paracrine communications between the Leydig cells(LCs), peritubular myoid cells, and Sertoli cells (SCs), ultimately affectingspermatogenesis.1The myoid cells and capillary epithelium undergo pathological changes inassociation with varicocele that may effect transmembrane transport of substrates to thegerminal epithelium.48

Hypoxia and adrenal reflux.Stasis of blood in the PP could affect partial oxygenpressure and change aerobic metabolism in the testis. However, hypoxia has not beendemonstrated in testicular venous blood sampling in humans or experimentalanimals.49,50Reflux of blood down the testicular vein has been demonstrated in patients with

varicocele.5153Therefore, exposure of the testis to adrenal or renal metabolites ishypothesized to be a cause for testicular damage. However, adrenal or renal metabolites atthe level of the testis have not been documented.37,54Adrenalectomy in rats withexperimental varicocele did not diminish the effects of the varicocele.55,56Thus theadrenal/renal reflux theory does not appear to be responsible for the testicular damageassociated with varicocele.55,57

Endocrine imbalance. Puberty, spermatogenesis, and testicular development areregulated by the hypothalamic-pituitary-testicular axis. There is a wide array of endocrineabnormalities associated with varicocele. LCs are under the control of luteinizing hormone(LH) and are responsible for testosterone (T) production. Some studies have shown that theserum T level may be affected by varicocele; however, it is intratesticular testosterone that isimportant in the regulation of spermatogenesis.58,59In experimental animal models,

varicocele can result in a decreased intratesticular testosterone level.60The results of humanstudies are mixed. Ando and colleagues found reduced serum T level in males with

varicocele and increased serum T level after repair of the varicocele.6165Swerdloff andWalsh, however, showed that there was no difference in testosterone level between maleswith and without a varicocele.66

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Increased LH serum levels and an abnormal response to gonadotropin-releasing hormone(GnRH) could implicate a compromise of the hypothalamic-pituitary-gonadal axis involvedin the control of T and spermatogenesis, a pattern similar to hypergonadotropichypogonadism.67,68Increased LH level results in LC hyperplasia, a known histologic findingin varicocele testicular biopsies.6971

SC responsiveness to follicle-stimulating hormone (FSH) may be diminished in varicocelepatients. Stimulation of SCs with FSH reversed spermatogenesis arrest in experimentalanimal models.72Varicocelectomy restored normal levels of FSH.73Altered levels of seruminhibin found in patients with varicocele may reflect altered function of SCs.74Cameron andassociates noticed that Sertoli-germ cell junctional complexes appeared to be structurallyabnormal in patients with varicocele.75They concluded that testicular disruption associated

with varicocele is a phenomenon of the adluminal compartment, and that SCs are moresensitive to perturbation of the testicular environment than are germ cells. SCs may be theprimary intratubular site of alteration leading secondarily to spermatogenicdisruption.76Histologic studies of the testis from patients with varicocele showed absentgerm cells or altered spermatogonia to SC ratio, signs often associated with SCdysfunction.77In addition to measuring circulating hormone levels, screening for point

mutations in the circulating hormones, receptors, and secondary signaling systems may givemore precise insight into male infertility and allow for patient stratification.78

Paracrine regulation of the testis. Insight into the detailed mechanism ofspermatogenesis is even more complicated because it is also regulated by complexinteractions and signals at the cellular level in the testis (Figure 3).1,79

Figure 3Endocrine regulation of spermatogenesis. Sertoli cells under the influence of follicle-stimulating hormone regulate spermatogenesis by activin, androgen binding protein, anddirect interactions with spermatogonia and spermatids. Leydig cells (LCs) regulate ...

Both SCs and LCs regulate spermatogenesis by steroidogenesis and growth factorproduction.80,81SCs tightly regulate germ cell proliferation and differentiation and areimplicated in the control of germ cell apoptosis. Fas (APO-1, CD95), a transmembranereceptor protein expressed by germ cells, transmits an apoptotic signal within cells when

bound by Fas ligand (FasL) produced by SCs. The Fas system has been implicated in

regulation of apoptosis in germ cells.82SCs stimulated by FSH produce inhibin (In) andactivin (Ac).83Inhibin has negative feedback control on the pituitary and FSH secretion. Italso binds to LCs regulating T production. Activin binds to round spermatids andspermatogonia (SP), affecting spermatogenesis. SP are known to stimulate transferrinproduction by SCs by an unidentified protein substance.84

LCs control spermatogenesis not only by steroid production but also by epidermal growthfactors (EGFs) that bind to SP and spermatids regulating cell divisions.85Receptors for

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transforming growth factor (TGF), one of the EGFs produced by LCs, are found inperitubular myoid cells (PC). PCs secrete peritubular myoid cell substance (PmodS) thatstimulates SCs. LCs control adluminal tubular compartment and transport of nutrients fromthe vascular space to germinal epithelium by vascular endothelial growth factor (VEGF).

VEGF is of particular interest in varicocele, because it regulates endothelial permeabilityand is an angioproliferative factor.86

Locally produced neurotropins play their distinct role in spermatogenesisregulation.87Opioid receptors are found on LCs. During stress, release of endorphinsstimulates opioid receptors and decreases testosterone production. Blocking opioidreceptors by naloxone restores testosterone production to normal.88Naloxone did notchange the serum concentration of LH, FSH, or T when given to patients with varicocele.89

Free radicals may also be considered paracrine substances, because they are produced andact locally. There is strong evidence that varicocele is associated with increasedconcentration of free radicals in semen. Free radical concentrations normalize after

varicocelectomy.90,91

With each discovery of a new paracrine substance and a better understanding of themolecular mechanisms controlling spermatogenesis, we will better define thepathophysiologic mechanisms responsible for growth arrest and deleterious effects onspermatogenesis. The ability to measure these substances may allow us to predict whichadolescent and/or adult with varicocele requires surgical intervention.

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Pathology

Testicular hypotrophy. The testicular function most affected by varicocele isspermatogenesis.92The most common findings on semen analysis are increased number ofpathologic sperm forms, decreased motility, and decreased sperm density.8,93,94Spermanalysis in adolescents with varicocele shows decreased sperm density, increased number ofpathological forms, and decreased motility; however, there are no established norms foradolescent semen analysis.93Varicocele is also associated with testicular growth arrest inadolescents.10,12Testicular growth arrest may be considered the hallmark of testiculardamage in adolescent varicocele. Significant volume loss in adolescents with varicocele has

been noted in 77% of boys, 10% of whom had a left testis one fourth the size of the righttestis.95Testicular hypotrophy is time-dependent.96,97

Testicular volume during preadolescence is constant, and at the onset of puberty the testissuddenly increases in size even prior to other pubertal changes. In adolescents with

varicocele, the rapid growth of the testis between the ages of 11 and 16 is affected byvaricocele and results in a volume discrepancy between the right and left testis. The

hypothesis that there is a negative correlation between testicular volume and sperm density,motility, and number of pathologic forms is well supported in the literature.8,98,99

Histopathology. Testicular biopsy in males with varicocele shows a wide array ofabnormalities. The most common findings are LC hyperplasia, decreased number of SP pertubule, spermatogenesis arrest, and sloughing of germinal epithelium.99103A thickened

basement membrane of seminiferous tubules and proliferative lesions of endoepitheliumare often demonstrated and may affect transport of oxygen and glucose through these

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structures.104,105The damage to the basement membrane seems to be time-dependent, asshown by ultrastructural and immunohistochemical observations that highlighted focaldamage at the level of the peritubular basal lamina in pubertal boys with varicocele, but thisdamage was not as severe as that described in adult varicocele.106Myofibroblasts obtainedfrom pubertal males with varicocele showed no evidence of transformation into fibroblastsother than increased presence of extracellular matrix. In adult males, myofibroblaststransform into fibroblasts, with varicocele causing peritubular fibrosis. This can explain whythe varicocelectomy in adolescents is able to reverse growth arrest and restore normalarchitecture of the testis, while the same procedure in adults with varicocele does not alwaysaffect testicular atrophy, although it may improve the semen characteristics.107,108

Peritubular fibrosis and increased thickness of basal membrane correlate negatively withsperm density and number of pathologic forms.109The longitudinal smooth muscle fibers in

vein walls are hypertrophied in high-grade varicocele; however, it is not yet clear whetherthis is a cause or a consequence of varicocele. One can stipulate that vein wall hypertrophymay be the result of a high volume of blood flowing through the vessels or increasedhydrostatic pressure.110

Go to:

Diagnosis

The adolescent with varicocele is often asymptomatic, and the varicocele is detected onroutine physical exam. The patient should be examined standing in a warm room to relaxthe scrotum and allow easier examination of the spermatic cord. The scrotum is first visuallyinspected for any obvious distention around the spermatic cord; a visible varicocele isconsidered a large or grade 3 varicocele. The scrotum, testes, and cord structures are thengently palpated. A palpable varicocele has been described as feeling like a bag of worms or asquishy tube. More subtle varicoceles may feel like a thickened, asymmetric cord. Thenonvisible but palpable varicocele is considered to be moderate in size (grade 2). If a

varicocele is not palpable, but the patient performs a Valsalva maneuver that distends thePP of veins, a small (grade 1) varicocele is present.

After examining the patient in the standing position, the patient should be examined supine.Idiopathic varicocele is more prominent in the upright position and disappears in the supineposition. A thickened cord due to a varicocele should resolve in the supine position, whereasa thickened cord due to a lipoma will not change when the patient is supine. Secondary

varicocele, especially on the right side, can be caused by serious conditions such asretroperitoneal tumors, kidney tumors, or lymphadenopathy.111A secondary varicocele doesnot change its size so dramatically in the supine position.

Testicular size needs to be measured to determine whether the varicocele is adversely

affecting the growth of the testis. The volume of a normal testis measures 1 cc to 2 cc in theprepubertal male. Because of extensive individual variation in normal growth anddevelopment, testicular size is correlated with Tanner stage, growth velocity, and bone agerather than chronological age.

A number of methods have been used to measure the size of the testis. These include visualcomparison, rulers, calipers, comparative ovoids (Prader orchidometer), punched-outelliptical rings (Takahara orchidometer), and ultrasound. A high correlation (r= .992)

between ultrasound and actual volume was noted and was shown to be highly

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reproducible.112The Prader orchidometer was shown to correlate with ultrasoundmeasurement in 256 patients (r= .91), although the degree of correlation was dependent onthe investigators clinical experience. In a clinical study of 22 male adolescents with a

varicocele, 24% of patients with growth arrest would have been missed if measured byPrader orchidometer alone, and 3 patients felt to have a significant size discrepancy (>2 mL)

by Prader orchidometer measurements were found to be normal by ultrasound volumeestimate. These findings indicate that clinical estimates of testicular size by the Praderorchidometer are not as accurate or reproducible as those determined by ultrasound.

Accurate measurement is important because operative decisions rest in the balance.113Thisfinding was recently confirmed by Diamond and colleagues who recommend annualultrasound assessment of testicular volume in adolescents with varicocele.114

There is considerable disagreement as to what constitutes a significant size discrepancyjustifying surgical intervention. Testicular ultrasound is the most accurate and reproduciblemethod to assess testicular volume and significant testicular size variations. A volumedifference of less than 2 mL can be due to the measurement technique alone. Therefore, size

variation of more than 2 mL by ultrasound is currently the best indicator of testiculardamage and should serve as the minimal requirement for surgical repair of the adolescent

varicocele.1Surgical intervention reverses testicular growth arrest, and assessment oftesticular volume postoperatively predicts resolution of the varicocele.12,11

Go to:

Management

There are some cardinal questions to be answered regarding management of adolescentvaricocele:

Once a varicocele has been found, what information needs to be given to thepatient and his parents?A number of psychological reactions (anxiety, depressed mood)

were experienced in approximately 30% of boys who were informed aboutvaricocele.116Because the word infertilityis often associated with sexual impairment, webelieve that during discussion with the patient and his parents, the only fact that should bestressed is that varicocele may result in a decrease in testicular volume that can be reversed

by surgical treatment. However, it is hard to discount the association between varicoceleand infertility in this era of common accessibility to the medical literature on the Internet(we found 1743 Web pages in searching for the term varicocele; many included the

word infertilityin the text). Because there are studies that demonstrate an abnormal semenanalysis in adolescents, it seems advisable to discuss all findings first with the parents whocan be helpful in presenting the problem to the child.117,118

Once diagnosed, whom should we treat?Varicocele is the most common correctable

cause of male infertility.119

Two thirds of patients will have improvement in semen analysisafter varicocele repair, and 40% of partners will become pregnant.16Historically, adolescentvaricocele was left untreated because its relationship to infertility was not well established.Subsequently, Kass and Belman showed that testicular growth arrest could be reversed by

varicocelectomy in adolescents.120Repair of varicocele not only reversed growth arrest butalso improved semen analysis in adolescents and young males.118,121,122

There is good evidence that, if left untreated, with time the varicocele will continue to affecttesticular growth with loss of volume and progressive deterioration in semen

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analysis.6,123Goldstein and Gorelick suggest that varicocele causes a progressive decline infertility and that prior fertility in men with varicocele does not predict resistance to

varicocele-induced infertility in the future, so-calledsecondary infertility.6However, Lundand Larsen followed 39 men with varicocele for 8 years and were not able to showprogressive decline in semen analysis results compared with healthy subjects.124

The association between varicocele and infertility is well established.7The most difficultquestion is which clinical test should we use to establish the indications for surgicaltreatment in an adolescent with varicocele?

Currently, the clinical tests used to establish criteria for varicocele repair are:

1. Grade of varicocele2. Measurement of testicular volume to assess testicular growth arrest3. GnRH stimulation test4. Measurement of PP vein diameter5. Serum LH, FSH, and inhibin levels6. Semen analysis

1. Varicocele grade. Varicocele grade does not correlate well with abnormal semenanalysis or infertility in adults.125There are varying opinions regarding correlation betweengrade of varicocele and degree of testicular hypotrophy in adolescents. Lyon and associatesfound no correlation of varicocele grade and testicular size in 30 adolescents.95In contrast,Skoog, Steeno, and Paduch all independently noticed that boys with severe varicocele have asmaller ipsilateral testicle.10,113,116It was also noticed that the smaller the testis, the worse thesemen analysis results.8,93However, grade of varicocele by itself should not be the soleindication for treatment.

2. Testicular volume. There is an abundance of literature confirming that varicocele isassociated with testicular growth arrest in adolescents, and varicocele repair results in

testicular catch-up growth.10,118,121,122Testicular growth arrest with a volume difference ofmore than 2 mL assessed by ultrasonography is the most common indication fortreatment.1,10The development of secondary infertility is another strong argument for early

varicocele repair because, if left untreated, varicocele can not only affect testicular volumebut also spermatogenesis.6A decrease in testicular volume is the best indicator for surgicalcorrection of varicocele. However, not every boy with varicocele and testicular growth arrest

will be infertile, and there is still a need to search for a test that would better distinguishbetween adolescents with a varicocele who will develop infertility and those who will remainfertile. In adult males, the situation is a little simpler because the indications for surgery areusually established after 12 months of infertility confirmed by abnormal semen analysis andthe presence of varicocele. Obtaining a semen sample in adolescents is possible but difficult.

3. GnRH stimulation test. Damage to germinal epithelium results in compensatorystimulation of the pituitary gland and subsequent increase in FSH and LH production bygonadotrophs.126Intravenous administration of GnRH stimulates the pituitary gland torelease FSH and LH. FSH levels are elevated in any condition (like varicocele) affecting theintegrity of germinal epithelium.127In theory, the GnRH stimulation test could distinguish

between adolescents with varicocele who have abnormal testicular functions and those whohave normal spermatogenesis.11However, in clinical practice, the GnRH stimulation test isexpensive, requires multiple serum samples, and lacks an association between abnormal

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results, growth arrest, and infertility.128130An abnormal GnRH stimulation test was found in30% of adolescents with varicocele and was not correlated with atrophy orinfertility.131Currently, it seems that the GnRH stimulation test has a limited role in theclinical evaluation of adolescents with varicocele in the United States, but is still used inclinical trials in Europe.132

4. PP vein diameter. Ultrasonographic measurement of PP vein diameter (PPVD) hasbeen used to look for subclinical varicocele in the adult infertile population when thephysical exam is inconclusive and to follow persistent varicocele, but PPVD measurementsare not useful in adolescents.133,134

5a. Inhibin level. Serum inhibin levels reflect the integrity of the seminiferous tubule andfunction of the SCs. Inhibin measurement in serum does not add any diagnostic informationnot found by FSH measurement. Inhibin B levels after dynamic GnRH stimulation failed toaid in stratification of adolescents with varicocele.136At present, there are not enough data tosupport the use of serum In levels in making clinical decisions.74,83,137139

5b. FSH stimulation. FSH has been utilized as an adjuvant therapy after varicocelectomy

in adult infertile patients; however, it also can be used in adolescents with varicocele.Radicioni and Schwarzenberg postulate that more than 50% of improvement in semenanalysis in males treated with a 3-month course of FSH indicates a better outcome after

varicocelectomy.140However, at present there isnt enough evidence to advocate FSHstimulation prior to varicocelectomy in adolescents.

6. Semen analysis. Increased number of pathologic forms, decreased progressivemotility, and decreased sperm density are the most common abnormalities found on semenanalysis in men with varicocele-related infertility. Varicocele is associated with impaireddisposal of residual sperm cytoplasm in the testis and epididymis.141The retained spermcytoplasm causes release of free radicals and infertility. Varicocelectomy was shown to lowerthe number of sperm with retained cytoplasm.142It is concluded that varicocele may causedeleterious alterations in early spermatid head differentiation during spermiogenesis andthat varicocele patients with a high incidence of sperm acrosome and nucleusmalformations are appropriate candidates for varicocele correction.143By applying strictmorphologic criteria to semen analysis, it was shown that varicocele repair improves themorphologic abnormalities of the sperm head found on preoperative semenanalysis.144Because there is good correlation among sperm morphology, fertility index, andresults from artificial reproductive techniques (ART), it is prudent to offer varicocelectomyto men with abnormal sperm morphology even with normal testicular size.145,146

Management summary. Currently, prophylactic surgery for every adolescent withvaricocele is not advised because it would result in the treatment of 15% of adolescents.However, it appears that treatment should be offered to:

1. Adolescents with testicular growth arrest (2 SD from normal testicular growthcurves, more than 2 mL of difference between left and right testicles)

2. Adolescents with abnormal semen analysis with high-grade varicocele3. Adolescents with symptoms: pain, heaviness, swelling4. Adolescents with bilateral varicoceles

Go to:

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Treatment Options

Treatment options in the management of adolescents with varicocele originated from thepractice in adult male infertility.

Surgical ligation and division of the testicular veins or intravenous embolization of the

testicular veins accomplish varicocele repair.Three open surgical approaches are currently used: subinguinal (Marmar), inguinal(Ivanissevich), and retroperitoneal (Palomo). Laparoscopic varicocele ligation is often usedin adults. Embolization techniques, regardless of embolizing material, can be classified asantegrade (infusion through scrotal part of the PP veins) and retrograde (catheter placedthrough femoral vein puncture) techniques.

Failure rate, frequency of complications, cost, and outcome are important factors that needto be evaluated in choosing the preferable treatment option in adolescent patients (Table 2).It is important to remember that most studies on varicocele repair concern adult infertilemales with varicocele and not adolescents.

Table 2Surgical Approach, Complications, and Relative Costs of Varicocele Repair

Failure rate. Recurrence of the varicocele after the repair can occur in 9% to 16% of

adolescents. It was shown by Lund and our group that persistence of varicocele should beassessed by performing an ultrasound 6 months after surgery.148Persistence of the

varicocele results in lack of catch-up testicular growth.12Most authors attribute the highpersistence rate to missed venous collaterals that run parallel to the main testicular vein.The collaterals can be quite difficult to identify and ligate separately from the testicularartery. The reported persistence rate using the artery-sparing retroperitoneal approachranges from 3% to 11%.12,147,149,150Ligation of both testicular vein trunci and the artery has theadvantage of a decreased persistence rate and does not result in testicular atrophy, becausethe testis has collateral arterial blood supply from the cremasteric and deferentialarteries.12,21Atassi and colleagues achieved a persistence rate below 2% in adolescentstreated by high retroperitoneal ligation with testicular artery ligation.12Artery and veinligation using laparoscopy was also shown to result in similar catchup growth of the testis inadolescents and a low persistence rate.151There is, however, some objection to simultaneousligation of the testicular artery in men with previous inguinal surgery, as there may be acompromised blood supply from the cremasteric and deferential arteries. Interruption ofthe testicular artery in these patients creates a high probability of developing testicularatrophy. Subsequent vasectomy in patients with testicular artery division should be avoided

because ligation of the vasal artery could result in testicular atrophy.

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Nagar recently reported a low persistence rate after varicocelectomy, if patients werestratified using color Doppler ultrasound.152A high ligation was performed only whenreverse blood flow was demonstrable in the varicocele during a Valsalva maneuver, and alow approach was utilized when this finding was absent. One can hypothesize that pelviccollateral and cross-communicating veins were responsible for the varicocele in patients

who showed lack of reverse blood flow through the PP on ultrasound. Obviously, outcome inthis group would be unsuccessful if managed by a high retroperitoneal approach. The highincidence of pelvic splanchnic veins communicating with the internal spermatic vein foundduring embolization confirms Nagars hypothesis.153We previously showed the importanceof cross-communicating veins and pelvic veins in the persistence of varicocele; these resultsand Nagars observations are opening a whole new area for future study.154

The high varicocele persistence rate and postoperative hydrocele rate led to thedevelopment of microsurgical varicocelectomy. Both subinguinal and inguinal microsurgicalrepair are used quite often in adults with varicocele and indeed offer lower persistence ratesand a low incidence of postoperative hydrocele.155157The low persistence rate using themicrosurgical inguinal repair is attributed to ligation of all distended veins and collaterals atthe level of the internal inguinal ring.155,156Because more pediatric urologists and surgeons

are gaining experience in microsurgical inguinal varicocele repair, we may see thisprocedure becoming a surgery of choice for adolescents.158,159Reports by Minevitch andGoldstein demonstrated a significantly lower rate of persistence and postoperativehydrocele in adolescent patients.158,160,161The microscopic approach allows one to ligate onlythe veins, leaving the lymphatic vessels intact and decreasing the postoperative hydrocelerate to less than 1%.156,157These encouraging reports were recently confirmed by aprospective study by Cayan and associates, who treated 468 patients by either highretroperitoneal ligation or inguinal microsurgical repair. Microsurgical varicocelectomyresulted in fewer cases of postoperative hydrocele and recurrences.162

Laparoscopic varicocele repair with and without artery-sparing modifications are suitablesurgical techniques.163165The testicular vein and artery can be divided with hemostatic clips

or coagulated with bipolar electrode.166Laparoscopic varicocele ligation can be employed inadolescents.167169Laparoscopic surgery in the pediatric population bares the risk ofsignificant complications like bowel perforation, major vascular injury, pneumothorax, andincisional hernia. Laparoscopic varicocele ligation is more expensive, takes longer, andoffers no benefits of pain management or earlier return to daily activities as compared withthe microvascular inguinal approach.170In a prospective, randomized study to comparelaparoscopy versus open repair for varicocele in adult males with infertility (160 patients inthe laparoscopy arm and 120 in the inguinal arm), laparoscopy was shown to be moreexpensive and to lack any advantages over the inguinal approach.171We are also concernedabout the much higher cost of laparoscopy and its potential risks. In our opinion,laparoscopic varicocelectomy should not be used in adolescents. A retroperitoneal approach

or microsurgical inguinal repair is preferred.Retrograde embolization, unfortunately is associated with an unacceptable high rate ofpersistence and is the most expensive of treatment techniques.1A possible explanation ofsuch a high persistence rate of varicocele after embolization is the highly variable anatomyof the testicular venous drainage and technical difficulties.172Because the embolization isperformed in otherwise healthy young males with approximately 70 more years of life, oneshould also be concerned about radiation exposure during embolization, with a subsequent

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