Kumar Pratap, Sait Sameer Farouk, Sharma Alok, Kumar Mukesh
Departments of Obstetrics and Gynecology, Kasturba Medical College, Manipal University, Manipal, Karnataka, India.
J Hum Reprod Sci. 2011 May;4(2):70-5. doi: 10.4103/0974-1208.86080.
Ovarian hyperstimulation syndrome (OHSS) is an iatrogenic complication of assisted reproduction technology. The syndrome is characterized by cystic enlargement of the ovaries and a fluid shift from the intravascular to the third space due to increased capillary permeability and ovarian neoangiogenesis. Its occurrence is dependent on the administration of human chorionic gonadotrophin (hCG). β-hCG and its analogs, estrogen, estradiol, prolactin, histamine and prostaglandins have all been implicated in OHSS but now it is increasingly better understood that the vasoactivesubstances such as interleukins, tumor necrosis factor-α, endothelin-1, and vascular endothelial growth factor (VEGF) secreted by the ovaries have been implicated in increasing vascular permeability. Enlargement of the ovaries causes abdominal pain, nausea and vomiting. Leakage of fluid from follicles, increased capillary permeability leading to third spacing (due to the release of vasoactive substances), or frank rupture of follicles can all cause ascites. Due to leakage of fluid through the impaired blood vessels both within and outside the ovary there is massive fluid-shift from the intra-vescular bed to the third compartment results in intravascular hypovolemia with concomitant development of edema, ascites, hydrothorax and/or hydropericardium. Low-dose gonadotrophin protocols have been implemented to reduce the risks of fertility treatment in polycystic ovary syndrome patients. Prophylactic albumin administration may interrupt the development of OHSS by increasing the plasma oncotic pressure and binding mediators of ovarian origin. OHSS is significantly lower in an antagonist protocol than in an agonist protocol. Cabergoline inhibits partially the VEGF receptor 2 phosphorylation levels and associated vascular permeability without affecting luteal angiogenesis reduces the 'early' (within the first 9 days after hCG) onset of OHSS. To prevent thrombosis, subcutaneous heparin 5000-7500 U/d is begun on the first day of admission. These patients need a hospital ward where the clinical picture is well understood and the personnel have expertise in its treatment and follow-up. Admission to an intensive care unit is necessary when critical OHSS develops.
卵巢过度刺激综合征（OHSS）是辅助生殖技术的一种医源性并发症。该综合征的特征是卵巢囊性增大，由于毛细血管通透性增加和卵巢新生血管形成，液体从血管内转移至第三间隙。其发生取决于人绒毛膜促性腺激素（hCG）的使用。β - hCG及其类似物、雌激素、雌二醇、催乳素、组胺和前列腺素都与OHSS有关，但现在人们越来越清楚地认识到，卵巢分泌的血管活性物质如白细胞介素、肿瘤坏死因子 - α、内皮素 - 1和血管内皮生长因子（VEGF）与血管通透性增加有关。卵巢增大可引起腹痛、恶心和呕吐。卵泡液渗漏、毛细血管通透性增加导致第三间隙形成（由于血管活性物质的释放）或卵泡破裂均可引起腹水。由于卵巢内外受损血管内的液体渗漏，大量液体从血管内床转移至第三间隙，导致血管内血容量减少，同时伴有水肿、腹水、胸腔积液和/或心包积液的形成。已采用低剂量促性腺激素方案来降低多囊卵巢综合征患者生育治疗的风险。预防性给予白蛋白可通过增加血浆胶体渗透压和结合卵巢来源的介质来阻断OHSS的发展。拮抗剂方案中OHSS的发生率明显低于激动剂方案。卡麦角林可部分抑制VEGF受体2的磷酸化水平及相关的血管通透性，而不影响黄体血管生成，从而减少OHSS的“早期”（hCG注射后9天内）发病。为预防血栓形成，入院第一天开始皮下注射肝素5000 - 7500 U/d。这些患者需要一个临床情况被充分了解且医护人员具备治疗和随访专业知识的医院病房。当发生严重OHSS时，有必要入住重症监护病房。
