Stagnation of Blood in the Microvasculature of the Affected and Contralateral Testes of Men with Short‐term Torsion of the Spermatic Cord

Abstract

Bilateral testicular biopsies from four men with a short duration (3 hours 10 minutes to 4 hours 30 minutes) of unilateral spermatic cord torsion and testicular biopsies from six men with irreversible brain death were used for the present investigation. Extensive light and electron microscopic studies and quantitative analyses of all biopsy materials were performed. The torsioned testes revealed variable degrees of damage to the seminiferous tubules, including germ cell disorganization and sloughing of immature germ cells. Ninety‐five percent of the blood vessels from the biopsied tissue specimens were clogged with blood cells. The seminiferous tubules of the contralateral testis had normal germ cell arrangements and counts. However, 88% of the microvessels from the tissue biopsied from the contralateral testes were packed with blood cells, whereas only 10% of the blood vessels in the control biopsy specimen were clogged with blood cells. At the electron microscopic level, fewer tight junctions and enlarged pores were found between the endothelial cells of the affected vessels, and microvilli were completely absent from these endothelial cells. The clogging caused by blood cells in the affected vessels was so severe that no space was found between the membrane of the endothelial cell and the membrane of the blood cells. It has been suggested that local clogging by blood is responsible for the initiation of degenerative changes in the testes of men with unilateral torsion of the spermatic cord.

The value of serum mean platelet volume in testicular torsion

“…26,27 Studies have shown that testicular venous congestion causes formation of vascular microthrombi that induce the intrinsic coagulation pathway. 27,28 Furthermore, hypoxia has been shown to increase the formation of microthrombi and production of endothelin-1. 29,30 Endothelin-1 is a vasoconstricting factor that acts via endothelin-A receptors.…”

“…30 These published findings suggest that the MPV is elevated in testicular torsion because this condition causes vascular pathology. [26][27][28] Erythrocyte sedimentation rate and C-reactive protein, which are acute-phase markers, have been shown to be elevated during the clinical examination leading to a diagnosis of testicular torsion. 3,31 The MPV was shown to be significantly higher in patients with acute pancreatitis compared with control subjects, 32 but a significantly lower MPV was detected in paediatric patients with acute appendicitis.…”

Bidirectional Flow Within the Intratesticular Arteries Caused by Microvenous Thrombosis Secondary to Testicular Torsion

“…12 Venous congestion within the testis results in clogging of the microvessels with red blood cells. 13 Microthrombus formation is initiated via the intrinsic coagulation pathway secondary to venous stasis and has been documented in torsed testes. 13 Hypoxic ischemia then initiates a complex biochemical process contributing to a procoagulative state, including up-regulation of P-selectin and factor III, which influences both the intrinsic and extrinsic coagulation pathways, resulting in further microthrombus formation.…”

“…13 Microthrombus formation is initiated via the intrinsic coagulation pathway secondary to venous stasis and has been documented in torsed testes. 13 Hypoxic ischemia then initiates a complex biochemical process contributing to a procoagulative state, including up-regulation of P-selectin and factor III, which influences both the intrinsic and extrinsic coagulation pathways, resulting in further microthrombus formation. 14 The combination of severe reduction of the intratesticular venous flow and the subsequent compression of the arterial system would be expected to increase resistance to intratesticular arterial perfusion.…”

Experimental testicular torsion: time course of the effect on the contralateral testicular histology

“…Early changes on the contralateral side can be explained not only by an immunologic response, but also by other mechanisms such as stress [1] and stagnation of blood in the microvasculature [6]. On the one hand, complete regeneration may occur after an early change, and on the other, damage may develop slowly.…”