Aetiology
The bell clapper deformity is the most common anatomical defect associated with the development of intra-vaginal testicular torsion.[3] Other causes include trauma.[3] The inciting event for this type of testicular torsion is usually unknown; however, trauma may be the cause in a minority of cases (4% to 8%).[13][14]
The exact aetiology of extra-vaginal torsion is unknown and an anatomical defect is not usually identified.[3]
Pathophysiology
Normally, the testicle descends through the inguinal canal covered by a layer of peritoneum. This layer, the tunica vaginalis, normally attaches to the posterior wall inferiorly near the inferior posterior testicle and superiorly at the superior testicular region. If both attachments of the tunica vaginalis occur superior to the testicle, the bell clapper deformity develops, which increases the likelihood of torsion because the testicle is freely mobile within the tunica. This abnormality has been reported in 12% of cases in an autopsy series and is frequently a bilateral phenomenon.[9]
Once torsion has occurred, time to de-torsion and restoration of the vascular supply will determine the extent of testicular viability. Humoral factors may play a role in the spermatogenesis of the unaffected, contralateral testicle as well.[3] The exact mechanism responsible for the effect of torsion/de-torsion injury on the contralateral testicle is unknown. Testicular germ cell death occurs secondary to decreased oxygen supply, cellular energy depletion, and toxic metabolite formation.[15] Mechanisms for ischaemia/reperfusion injury that can affect both testes have been suggested, including inflammatory mechanisms and/or free oxygen radical formation.[15]
Number of rotations, which can range from 180° to 1080°, and duration of ischaemia both determine the degree of tissue viability.[16][17][18] If de-torsion occurs within 4 to 6 hours after the onset of symptoms, then the affected testis will most likely remain viable. If the testes remain twisted for more than 10 to 12 hours, ischaemia and irreversible testicular damage are likely.[19] After 12 hours, necrosis has most likely occurred.
Classification
Intra-vaginal torsion
Intra-vaginal torsion is the most common type of testicular torsion. It occurs because of an abnormally high attachment of the tunica vaginalis to the spermatic cord, which allows rotation of the testicle within the sac. During normal anatomical development, the testicle descends through the inguinal canal covered by a layer of peritoneum. This layer, the tunica vaginalis, attaches to the posterior scrotal wall near the inferior posterior testicle and superiorly at the superior testicular region. If both attachments of the tunica vaginalis occur superior to the testicle, the bell clapper deformity is formed, which increases the likelihood of torsion because the testicle is freely mobile within the tunica.
Extra-vaginal torsion
Extra-vaginal torsion is a rare entity. It occurs during the perinatal period as the testicle descends and twists around the spermatic cord prior to attachment to the posterior scrotal wall.
Long mesorchium
The mesorchium is a dense band of connective tissue that attaches the efferent ductules of the epididymis to the posterolateral wall of the testes. If elongated, this may allow the testicles to twist and the epididymis to remain fixed.[2]
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