Prevention and treatment of moderate and severe ovarian hyperstimulation syndrome: a guideline Practice Committee of the American Society for Reproductive Medicine American Society for Reproductive Medicine, Birmingham, Alabama Ovarian hyperstimulation syndrome (OHSS) is an uncommon but serious complication associated with assisted reproductive technology (ART). This systematic review aims to identify who is at high risk, how to prevent OHSS, and the treatment for existing OHSS. (Fertil Steril Ò 2016;106:1634–47. Ó2016 by American Society for Reproductive Medicine.) Earn online CME credit related to this document at www.asrm.org/elearn Discuss: You can discuss this article with its authors and with other ASRM members at https://www.fertstertdialog.com/users/ 16110-fertility-and-sterility/posts/12461-22981 INTRODUCTION Ovarian hyperstimulation syndrome (OHSS) is an uncommon but serious complication associated with controlled ovarian stimulation during assisted reproductive technology (ART). Mode- rate-to-severe OHSS occurs in approxi- mately 1%–5% of cycles (1–5). However, the true incidence is difficult to delineate as a strict, consensus definition is lacking. The traditional description of the syndrome generally includes a spectrum of findings, such as ovarian enlargement, ascites, hemo- concentration, hypercoagulability, and electrolyte imbalances. Symptoms are often qualified by their severity (mild, moderate, or severe) and by the timing of onset (early or late) (Table 1). Severe OHSS can lead to serious complications, including pleural effusion, acute renal insufficiency, and venous throm- boembolism. Because OHSS is the most serious consequence of controlled ovarian stimulation, every attempt should be made to identify patients who are at highest risk. Understanding the path- ophysiology of this condition may aid in identifying measures to prevent its development and treat assoc- iated symptoms. Classic physiologic changes of OHSS include arteriolar vasodilation and an increase in capil- lary permeability that results in fluid shifting from intravascular to extra- vascular spaces (6, 7). This fluid shift results in a state of hypovolemic hyponatremia. Vascular endothelial growth factor (VEGF) appears to be integral to the development of this condition and is involved in follicular growth, corpus luteum function, angiogenesis, and vascular endothelial stimulation (8–10). In response to human chorionic gona- dotropin (hCG), VEGF appears to mediate the vascular permeability of OHSS as systemic hCG levels positively correlate with severity of the disease (10–12). Other systemic and local vasoactive substances, including interleukin-6, interleukin- 1b, angiotensin II, insulin-like growth factor 1, transforming growth factor b, and the renin-angiotensin system are also directly and indirectly involved in the pathogenesis of OHSS symptoms (8,12–16). As understanding of stimulation tech- niques, disease pathophysiology, and monitoring technology improve, an objective of ovulation induction should be near-complete mitigation of the syndrome. The condition is self-limiting and, in patients who do not conceive, typically resolves at the time of the next menstrual period. In patients who do become pregnant, rising hCG levels continue to stimu- late the ovaries and symptoms may extend through the end of the first trimester. A systematic search of the litera- ture was performed in order to answer three questions about OHSS: who is at Received August 25, 2016; accepted August 25, 2016; published online September 24, 2016. Reprint requests: Practice Committee, American Society for Reproductive Medicine, 1209 Montgom- ery Hwy, Birmingham, Alabama 35216 (E-mail: [email protected]). Fertility and Sterility® Vol. 106, No. 7, December 2016 0015-0282/$36.00 Copyright ©2016 American Society for Reproductive Medicine, Published by Elsevier Inc. http://dx.doi.org/10.1016/j.fertnstert.2016.08.048 1634 VOL. 106 NO. 7 / DECEMBER 2016
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