Varicocelectomy – The Unkindest Cut of All

Varicocele is the price a man pays for his upright posture and scrotal testes. Animals do not develop varicocele. Varicosities also occur in ovarian veins, but fortunately, they are not visible to the naked eye and are, therefore, not implicated in any ovarian dysfunction.

In the year 1885, British surgeon Barwell opined that varicocele was a possible cause of male infertility.^[1] Tulloch, in 1953, operated on a patient and showed a rise in all semen parameters following varicocelectomy.^[2] Several decades later, we are still struggling to prove that varicocele is one of the causes of male infertility. This topic has given rise to many controversies. While varicocele is a routine finding in about 15% of the general male adult population, its incidence is higher in infertile men, 19%–40%.^[3,4]

Various theories are being offered as mechanisms for altered semen parameters with varicocele.

Rise in scrotal temperature: It was reported that the rise in temperature occurs due to pooling of venous blood.^[5] It is a widely held belief that the testes are placed in the scrotum for optimal spermatogenesis, as they need cooler temperatures than the core body temperature. It is interesting to note that only some mammals (like humans) have testes placed in the scrotum. The others, despite the abdominal location of the testes, continue to have normal spermatogenesis. Venous blood is cooler than arterial blood. Hence, pooling of venous blood in the scrotum due to varicocele should logically lead to cooler temperatures, conducive to optimal spermatogenesis. This internal contradiction within the ‘temperature hypothesis’ is often overlooked.

Reflux of blood from the left renal vein into the internal spermatic vein: It was postulated that refluxing venous blood from the left renal vein carried adrenocortical metabolites to the testes, which impaired spermatogenesis.^[6] This theory does not explain how static venous blood can perfuse into testicular tissue and affect spermatogenesis.

Increased spermatozoa Deoxyribo nucleic acid (DNA) fragmentation index (DFI): Varicocele is claimed to increase DFI.^[7] The concept of high DFI as a cause of male infertility is highly controversial.^[8] While some research groups advocate for DFI testing in specific subsets of infertile men (e.g., recurrent assisted reproductive technology (ART) failure), major guidelines like the American urology association / American society of reproductive medicine (AUA/ASRM) (2020/2024 amendment) generally do not recommend sperm DNA fragmentation analysis in the initial evaluation of the infertile couple, reserving it for specific circumstances like recurrent pregnancy loss.^[8] At best, DFI can be considered a useful research tool and is not meant for routine assessment of male infertility.

Stress pattern of semen parameters: Varicocele has been described to cause a stress pattern of semen analysis. Abnormal semen parameters like oligozoospermia, asthenozoospermia, and teratozoospermia have been attributed to this stress pattern.^[9] These definitions have often been reclassified in the last 44 years. Moreover, the semen picture is highly variable even in the same fertile male over different periods.^[10] WHO has been redefining the values for Oligozoospermia^[11] with the 6th edition of the WHO Manual for the Examination and Processing of Human Semen published in July 2021. Morphology assessment of the spermatozoa is highly subjective^[12] and semen parameters are highly variable biological measures, as noted by the AUA/ASRM.

Thus, we wonder whether varicocele is the cause of male infertility or whether it is an associated condition. It is debatable if any of the explanations offered for varicocele causing infertility is tenable, and they do not give us a clue to the actual mechanism.