Aetiology
Anatomical features, namely increased hydrostatic pressure in the left renal vein and incompetent or congenitally absent valves, are typically implicated as the primary causes of varicocele formation.
They are most commonly thought to be caused by incompetent valves within the left internal spermatic vein. In addition, the left pampiniform plexus is subjected to increased hydrostatic pressures due to the right-angle insertion of the vein into the left renal vein.[18] The left internal spermatic vein inserts into the left renal vein at a right angle, as opposed to the right internal spermatic vein, which joins the inferior vena cava at an oblique angle. In addition, the left internal spermatic vein is 8 to 10 cm longer, resulting in increased hydrostatic pressure transmission. Furthermore, a 'nutcracker' phenomenon may exist as the left renal vein traverses under the superior mesenteric artery.[19]
Varicoceles have been demonstrated in males with competent valves.[20] It is clear, therefore, that varicocele formation cannot be explained by a single theory and results from a combination of anatomical factors.
Rarely, varicocele can be caused by a retroperitoneal or abdominal compressive mass. This could cause a varicocele that does not diminish in the supine position or an isolated right-sided varicocele.[21]
Pathophysiology
Clinically detectable varicoceles can be associated with abnormal gonadotrophin levels, impaired spermatogenesis, histological changes to sperm, and infertility. The exact cause is not known, but most believe that a major contributor is thermal damage secondary to an impaired countercurrent mechanism that normally keeps intrascrotal temperatures 1°C to 2°C (2°F to 4°F) lower than normal body temperature.[22] Other theories cite inadequate elimination of reactive oxygen species due to impeded venous out-flow, impaired arterial in-flow resulting in hypoxia, and reflux of toxic adrenal and renal metabolites as causative factors.[19]
The presence of a varicocele has an impact on testicular development (in the adolescent) and fertility/semen parameters (in the adult). Seminiferous tubules and germinal cells make up 98% of testicular volume. A decrease in volume associated with an ipsilateral varicocele has been used as the primary indication for surgical correction in the adolescent. There is a positive correlation between increasing varicocele grade and volume loss among adolescents.[4] Decreased sperm motility and abnormal morphology has been documented in adolescents with varicoceles.[23]
Classification
Clinical classification[1]
Varicoceles may be graded based on their size.
Sub-clinical: varicocele detected only by Doppler ultrasound.
Grade I (small): varicocele palpable only with Valsalva manoeuvre.
Grade II (moderate): varicocele palpable without Valsalva manoeuvre.
Grade III (large): varicocele visible through the scrotal skin.
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