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异常的子宫复旧可能导致宫缩乏力和产后出血:假说与证据回顾。

Abnormal Uterine Involution May Lead to Atony and Postpartum Hemorrhage: A Hypothesis, With Review of the Evidence.

机构信息

Department of Pathology, Rutgers New Jersey Medical School, Newark, NJ, USA.

Department of Pathology, Highland Hospital and Rochester General Hospital, University of Rochester School of Medicine, Rochester, NY, USA.

出版信息

Pediatr Dev Pathol. 2023 Sep-Oct;26(5):429-436. doi: 10.1177/10935266231194698. Epub 2023 Sep 6.

DOI:10.1177/10935266231194698
PMID:37672676
Abstract

Uterine involution has 2 major components-(1) involution of vessels; and (2) involution of myometrium. Involution of vessels was addressed by Rutherford and Hertig in 1945; however, involution of myometrium has received little attention in the modern literature. We suggest that the pathophysiology of myometrial involution may lead to uterine atony and postpartum hemorrhage. The myometrium dramatically enlarges due to gestational hyperplasia and hypertrophy of myocytes, caused by hormonal influences of the fetal adrenal cortex and the placenta. After delivery, uterine weight drops rapidly, with physiologic involution of myometrium associated with massive destruction of myometrial tissue. The resulting histopathology, supported by scientific evidence, may be termed "postpartum metropathy," and may explain the delay of postpartum menstrual periods until the completion of involution. When uterine atony causes uncontrolled hemorrhage, postpartum hysterectomy examination may be the responsibility of the perinatal pathologist.Postpartum metropathy may be initiated when delivery of the baby terminates exposure to the hormonal influence of the fetal adrenal cortex, and may be accelerated when placental delivery terminates exposure to human chorionic gonadotrophin (HCG). This hypothesis may explain why a prolonged third stage of labor, and delays in management, are risk factors for severe hemorrhage due to uterine atony.

摘要

子宫复旧有两个主要部分-(1)血管的复旧;(2)子宫肌层的复旧。血管的复旧是由 Rutherford 和 Hertig 在 1945 年提出的;然而,子宫肌层的复旧在现代文献中很少受到关注。我们认为,子宫肌层复旧的病理生理学可能导致子宫收缩乏力和产后出血。由于胎儿肾上腺皮质和胎盘的激素影响,肌细胞的妊娠增生和肥大,使子宫肌层显著增大。分娩后,子宫重量迅速下降,伴随着与大量子宫组织破坏相关的生理性子宫肌层复旧。由此产生的组织病理学,有科学证据支持,可能被称为“产后子宫病”,并可能解释产后月经周期延迟到复旧完成。当子宫收缩乏力导致无法控制的出血时,产后子宫切除术检查可能是围产期病理学家的责任。产后子宫病可能在分娩结束时胎儿肾上腺皮质的激素影响终止时开始,并可能在胎盘娩出结束时人绒毛膜促性腺激素(HCG)的暴露终止时加速。这一假说可以解释为什么第三产程延长和处理延迟是由于子宫收缩乏力导致严重出血的危险因素。

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Abnormal Uterine Involution May Lead to Atony and Postpartum Hemorrhage: A Hypothesis, With Review of the Evidence.异常的子宫复旧可能导致宫缩乏力和产后出血:假说与证据回顾。
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