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.

中文翻译：

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子宫复旧异常可能导致乏力和产后出血：一个假设，并对证据进行审查。

子宫复旧有两个主要组成部分——（1）血管复旧；(2)子宫肌层复旧。1945 年，卢瑟福 (Rutherford) 和赫蒂格 (Hertig) 提出了血管内卷化问题；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导致妊娠期肌细胞增生和肥大，子宫肌层急剧增大。分娩后，子宫重量迅速下降，子宫肌层发生生理性退化，并伴有子宫肌层组织的大量破坏。由此产生的组织病理学，有科学证据支持，可以被称为“产后子宫病”，并且可以解释产后月经期延迟直至复旧完成的原因。当子宫收缩乏力导致不受控制的出血时，产后子宫切除术检查可能由围产期病理学家负责。当婴儿分娩终止暴露于胎儿肾上腺皮质的激素影响时，可能会开始产后子宫切除术，并且当胎盘分娩终止暴露时，可能会加速产后子宫切除术检查人绒毛膜促性腺激素（HCG）。这一假设可以解释为什么第三产程延长和处理延迟是子宫收缩乏力导致严重出血的危险因素。