Varicocele is a pathologic enlargement of the testicular veins that is associated with impaired spermatogenesis and infertility. In fact, varicocele is the most common correctable cause of male infertility. Varicoceles are found in up to 15% of the adult male population, but fortunately not all men with varicoceles are infertile. However, varicoceles are found in approximately 35% of men with primary infertility and up to 80% of men with secondary infertility (Wein AJ, Kavoussi LR, Partin AW, Peters CP, editors. Campbell-Walsh Urology. 11th ed. Philadelphia: Elsevier; 2016).
Varicoceles are diagnosed by physical exam and are graded I-III. Grade I varicocele is palpable only during the Valsalva maneuver; grade II varicocele is palpable in the standing position; and grade III varicocele is visible without palpation. The use of scrotal ultrasound in diagnosis should be restricted to men with a difficult physical exam, such as those with prior surgical history or challenging body habitus. It is important to distinguish a subclinical varicocele—a varicocele that is not visible on exam and detected only with ultrasound—because surgical correction has not been shown to improve semen parameters.
This article presents an overview of the pathophysiology of varicoceles and discusses indications for treatment, two primary repair techniques, and treatment outcomes.
Varicoceles form because of increased hydrostatic pressure in the internal spermatic veins, possibly because of incompetent or absent venous valves. Anatomic differences cause increased hydrostatic pressures, making varicoceles more common on the left (Asian J Androl 2015; 17:659-67). Therefore, isolated right-sided varicoceles are rare and, when identified, should prompt a workup for an ipsilateral pathologic retroperitoneal process with imaging.
Clinical varicoceles can negatively affect sperm concentration, motility, and morphology. The following five mechanisms contribute to the pathogenesis of impaired testicular function: hypoperfusion from retrograde flow leading to hypoxia, heat stress from impaired countercurrent heat exchange, oxidative stress from accumulation of reactive oxygen species, hormonal imbalances from abnormal Leydig cell function and decreased intra testicular testosterone, and accumulation of exogenous toxins. However, no single mechanism accounts for the observed impairment (J Assist Reprod Genet 2014; 31:521-6). Literature supports that grade of varicocele is associated with degree of spermatogenesis impairment and worse semen parameters.