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Title: 周産期雌馬における致死的な子宮広間膜血腫に関する病理学的研究
Other Titles: Pathology of Lethal Peripartum Broad Ligament Hematoma in Mares
Authors: 上野, 孝範1 Browse this author
Authors(alt): Ueno, Takanori1
Issue Date: 25-Mar-2010
Abstract: The broad ligament is a double peritoneal membrane connecting the abdominal wall and the uterus, and the blood vessels pass through the broad ligament to supply the uterus. In aged mares, broad ligament hematoma that often leads to the death by blood loss can occur in perinatal period. It is difficult to arrest hemorrhage by surgical procedure and to estimate and prevent the broad ligament hematoma, because there are few case reports on the sites of arterial rupture, etiology and pathogenesis of the broad ligament hematoma in pregnant mares. The present study purposes elucidating 1) clinical findings of broad ligament hematoma by hearing investigation for owners and clinical veterinarians, 2) preferential rupture sites of blood vessels by necropsy, 3) mechanisms of the arterial ruptures by histopathological examination, and 4) aging changes of the arteries predisposed to the broad ligament hematoma. In the first chapter, the breeding site of 36 Thoroughbred mares died of broad ligament hematoma in perinatal period was identified by necropsy. I also interviewed owners and clinical veterinarians treated the horses. The mean age of the affected mares was 17.15 ± 3.43 years (S. D.), and the parity was 9.86 ± 2.85 times (S. D.). Thirty mares showed clinical signs after delivery, and 18 of the 19 mares in which the time course between delivery and death could be specified, died within 24 hours after delivery. At necropsy, rupture sites were identified in 31 of 36 mares, and the sites were located in the uterine artery (24 mares), internal pudendal artery (5 mares), caudal mesenteric artery (1 mare), and internal iliac artery (1 mare). Among these, the proximal uterine artery that lies near the bifurcation from the iliac artery was the most frequent site of rupture. The arterial ruptures occurred 4 times more frequently at the left side than the right. The rupture at uterine artery tended to occur in aged mare. The arterial ruptures preferably occurred at arterial bifurcations subjected to severe hemodynamic stress. Most of the ruptures were a tear in the arterial wall, but in other cases, the arteries were completely transected. The broad ligament hematoma usually occurred in mares older than 14 years. The proximal part of uterine artery that is the preferential site for rupture can be monitored by transrectal echography. Therefore, the proximal part of uterine artery should be check primarily using transrectal echography in the mares suspected of broad ligament hematoma. The antemortem identification of rupture sites may enable the arrest of hemorrhage by surgical procedure. In the second chapter, I pathologically examined 31 mares in which the rupture sites were macroscopically identified and investigated the mechanisms of the arterial ruptures. The morphology of the ruptures was classified into three types: rupture with longitudinal fissures, rupture without longitudinal fissures, and transection. The arterial ruptures with fissures occurred only in the proximal uterine artery, and transections mainly occurred in the internal pudendal artery. Histologically, fibrosis of the tunica media and thickened tunica intima were observed adjacent to the arterial ruptures, and these changes were observed commonly on both sides of the ruptured and apparently intact arterial walls. Therefore, these arterial change might be related with aging and multiparity. The lumen of some proximal uterine artery without rupture was partially dilated with thin arterial wall, forming small aneurism. These changes might be the result of hemodynamic stress to the arterial wall and similar lesions were observed in distal uterine artery forming spiral shape. The middle to distal uterine artery had abundant longitudinal smooth muscle fasicles in the tunica adventitia, and the luminal surface of these area formed circumferential ridges and grooves. These structures might make the middle to distal uterine artery more resistant to mechanical forces such as tugging and increased blood pressure, and might contribute to lower incidence of arterial ruptures in those areas in compare with that of proximal uterine artery. Coagulative necrosis and infiltration of inflammatory cells were observed at the rupture sites of the internal pudendal artery. These changes were not observed in other arteries. The internal pudendal artery runs between the uterus and pelvis, and the artery may be injured due to being caught between them during pregnancy or parturition. Therefore, the cause of internal pudendal artery rupture may be physical injury by the external forces. At the ruptured edge of internal iliac artery, circular smooth muscles of the tunica media were crossed with longitudinal smooth muscle bundles and collagen fibers. Due to its structure, the artery might be poorly dilative and increased blood pressure may cause arterial rupture. The caudal mesenteric artery of one mare was transected, and blood cells flooded among smooth muscle cells in tunica media at elongated edge of transected artery. Since this mare suffered dystocia due to an excessively-sized fetus, arterial rupture might occur at parturition by vigorous traction of caudal mesenterium, small colon and rectum. The present study revealed that broad ligament hematoma in mares had preferential site for arterial rupture, the proximal uterine artery, but the rupture may also occur in other arteries with different mechanisms. Therefore, ruptured sites should be sought at necropsy and therapy considering the age of mare, number of delivery, extent of dytocia and size of fetus. In the third chapter, the uterine artery and external iliac artery of mares of variable ages without broad ligament hematoma were histologically examined to determine whether the histological lesions of arteries described in the former chapter at non-rupture sites were the specific change for mares with broad ligament hematoma or aging changes common for mares. The mares had the same arterial changes in uterine artery as observed in the mare with broad ligament hematoma and they were congruent with aging changes of arteries in humans and rats. The aging changes included an atrophy of smooth muscle cells with medial fibrosis. The fibrotic area of the uterine artery appeared irregularly-shaped thick bands in the proximal part and regular thin bands in middle and distal uterine artery. The other aging changes were the disruption of internal elastic lamina and thickening of tunica intima due to an increase of collagenous stroma and proliferation of smooth muscle cells. Tunica intima of the proximal uterine artery was thicker than those of middle and proximal arteries, reflecting the different magnitude of hemodynamic stress on the uterine artery. The results of morphometrical analysis confirmed the aging changes of arterial walls. In the tunica media of external iliac artery, a decrease of elastin and an increase of collagen with aging were detected by routine histopathology, but the age-dependency was not substantiated by the morphometrical analysis. The result of this chapter indicates the histological changes of arteries described in the chapter 2 was aging change common to mares and the degree of the aging changes differed among arteries and areas of arteries. These changes were more prominent at the proximal part of uterine artery, the most frequent site of arterial rupture in aged mares, thus the aging change were considered to be one of the predisposing lesions for the arterial rupture resulting in broad ligament hematoma. Arterial lesions with aging may elevate systolic pressure of arteries and increase the risk of arterial rupture. Therefore, daily monitoring of blood pressure might be helpful in evaluating the risk of broad ligament hematoma in aged mares at perinatal period.
Conffering University: 北海道大学
Degree Report Number: 甲第9481号
Degree Level: 博士
Degree Discipline: 獣医学
Type: theses (doctoral)
Appears in Collections:学位論文 (Theses) > 博士 (獣医学)

Submitter: 上野 孝範

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