Skip to main content Accessibility help

We use cookies to distinguish you from other users and to provide you with a better experience on our websites. Close this message to accept cookies or find out how to manage your cookie settings.

Close cookie message
×
Hostname: page-component-cd9895bd7-p9bg8 Total loading time: 0 Render date: 2024-12-26T16:20:11.652Z Has data issue: false hasContentIssue false

Chapter 17 - Ovarian Hyperstimulation Syndrome

from Section 3 - Reproductive Endocrinology and Infertility

Published online by Cambridge University Press:  24 November 2021

By
Tom Gunnar Tanbo
Edited by
Tahir Mahmood ,
Charles Savona-Ventura ,
Ioannis Messinis  and
Sambit Mukhopadhyay
Tahir Mahmood
Affiliation:
Victoria Hospital, Kirkcaldy
Charles Savona-Ventura
Affiliation:
University of Malta, Malta
Ioannis Messinis
Affiliation:
University of Thessaly, Greece
Sambit Mukhopadhyay
Affiliation:
Norfolk & Norwich University Hospital, UK
Get access

Summary

Ovarian hyperstimulation syndrome (OHSS) mostly occurs due to excessive FSH stimulation, with final follicle maturation by hCG for IVF. Symptoms usually start 2–4 days after oocyte retrieval; alternatively, endogenous hCG from an implanting embryo can initiate OHSS some days later. Luteinized follicles synthesize vascular endothelial growth factor (VEGF) which induces angiogenesis and increased capillary permeability by inhibition of the cell adhesion molecule vascular endothelial-cadherin (VE-cadherin). This causes fluid leakage from the vascular bed to the third space, resulting in enlarged lutein cysts and ascites. Initial symptoms are bloated abdomen with pain, and in more severe cases dyspnoea, decreased renal and hepatic function and thromboembolism. There is no causal treatment of established OHSS, but there are several prophylactic strategies based on risk evaluation of each patient. In established OHSS, treatment is mainly supportive, by correcting fluid, salt and protein deficits, and low molecular weight heparin for thrombosis prophylaxis.

Keywords

ovarian hyperstimulation syndromecontrolled ovarian stimulationgonadotrophinpolycystic ovary syndromedyspnoeavascular endothelial growth factor
Type
Chapter
Information
The EBCOG Postgraduate Textbook of Obstetrics & Gynaecology
Gynaecology
 , pp. 139 - 145
Publisher: Cambridge University Press
Print publication year: 2021

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

Delvigne, A. Symposium: update on prediction and management of OHSS: epidemiology of OHSS. Reprod Biomed Online 2009;19:8–13.Google Scholar
Bhide, P, Homburg, R. Anti-Müllerian hormone and polycystic ovary syndrome. Best Pract Res Clin Obstet Gynecol 2016;37:38–45.CrossRefGoogle ScholarPubMed
Blankstein, J, Shalev, J, Saadon, T, et al. Ovarian hyperstimulation syndrome: prediction by number and size of preovulatory ovarian follicles. Fertil Steril 1987;47:597–602.Google Scholar
De Leon, FD, Vijayakumar, R, Brown, M, et al. Peritoneal fluid volume, estrogen, progesterone, prostaglandin, and epidermal growth factor concentrations in patients with and without endometriosis. Obstet Gynecol 1986;68:189–194.Google ScholarPubMed
Herr, D, Bekes, I, Wulff, C. Regulation of endothelial permeability in the primate corpora lutea: implications for ovarian hyperstimulation syndrome. Reproduction 2015;149:R71–R79.CrossRefGoogle ScholarPubMed
Gómez, R, Simón, C, Remohí, J, Pellicer, A. Vascular endothelial growth factor receptor-2 activation induces vascular permeability in hyperstimulated rats, and this effect is prevented by receptor blockade. Endocrinology 2002;143:4339–4348.CrossRefGoogle ScholarPubMed
Abramov, Y, Barak, V, Nisman, B, Schenker, JG. Vascular endothelial growth factor plasma levels correlate to the clinical picture in severe ovarian hyperstimulation syndrome. Fertil Steril 1997;67:261–265.CrossRefGoogle Scholar
Rodewald, M, Herr, D, Duncan, WC, et al. Molecular mechanisms of ovarian hyperstimulation syndrome: paracrine reduction of endothelial claudin 5 by hCG in vitro is associated with increased endothelial permeability. Hum Reprod 2009;24:1191–1199.CrossRefGoogle ScholarPubMed
Gavard, J, Gutkind, JS. VEGF controls endothelial cell permeability by promoting the beta-arrestin-dependent endocytosis or VE-cadherin. Nat Cell Biol 2006;8:1223–1234.CrossRefGoogle ScholarPubMed
Villasante, A, Pacheco, A, Ruiz, A, Pellicer, A, Garcia-Velasco, YES. Vascular endothelial cadherin regulates vascular permeability: implications for ovarian hyperstimulation syndrome. J Clin Endocrinol Metab 2007;92:314–321.CrossRefGoogle ScholarPubMed
Polishuk, WZ, Schenker, JG. Ovarian overstimulation syndrome. Fertil Steril 1969;20:443–450.CrossRefGoogle ScholarPubMed
Lai-Fook, SJ, Houtz, PK, Jones, PD. Transdiaphragmatic transport or tracer albumin from peritoneal to pleural fluid measured in rats. J Appl Physiol 2005;99:2212–2221.CrossRefGoogle ScholarPubMed
Bishop, CV, Lee, DM, Slayden, OD, Li, X. Intravenous neutralization of vascular endothelial growth factor reduces vascular function/permeability of the ovary and prevents development of OHSS-like symptoms in rhesus monkeys. J Ovarian Res 2017;6:41.Google Scholar
Schenker, JG, Polishuk, WZ. The role of prostaglandins in ovarian hyperstimulation syndrome. Eur J Obstet Gynecol Reprod Biol 1976;6:47–52.Google Scholar
Navot, D, Margalioth, EJ, Laufer, N, et al. Direct correlation between plasma renin activity and severity of the ovarian hyperstimulation syndrome. Fertil Steril 1987;48:57–61.Google Scholar
Yayama, K, Okamoto, H. Angiotensin II-induced vasodilation via type 2 receptor: role of bradykinin and nitric oxide. Int Immunopharmacol 2008;8:312–318.CrossRefGoogle ScholarPubMed
Blumenfeld, Z. The ovarian hyperstimulation syndrome. Vitam Horm 2018;107:423–451.CrossRefGoogle ScholarPubMed
Grossman, LC, Michalakis, KG, Browne, H, Payson, MD, Segars, JH. The pathophysiology of ovarian hyperstimulation syndrome: an unrecognized compartment syndrome. Fertil Steril 2010;94:13928.Google Scholar
Evbuomwan, I. The role of osmoregulation in the pathophysiology and management of severe ovarian hyperstimulation syndrome. Hum Fertil (Camb) 2013;16:162–167.CrossRefGoogle ScholarPubMed
Ferraretti, AP, Gianaroli, L, Tarlatzis, BC Ovarian Hyperstimulation Syndrome. Rome: Serono, 1997, pp. 21–34.Google Scholar
D’Angelo, A, Amso, NN, Hassan, R. Coasting (withholding gonadotrophins) for the prevention of ovarian hyperstimulation syndrome. Cochrane Database Syst Rev 2017;5:CD002811.Google Scholar
Lambalk, CB, Banga, FR, Huirne, JA, et al. GnRH antagonist versus long agonist protocols in IVF: a systematic review and meta-analysis for patient type. Hum Reprod Update 2017;23:560–579.Google Scholar
Youssef, MA, Van der Veen, F, Alinany, HG, et al. Gonadotropin-releasing hormone agonist versus HCG for oocyte triggering in antagonist-assisted reproductive technology. Cochrane Database Syst Rev 2014;31:CD008046.Google Scholar
Tang, H, Mourad, S, Zhai, SD, Heart, RJ. Dopamine agonists for prevention of ovarian hyperstimulation syndrome. Cochrane Database Syst Rev 2016;11:CD008605.Google ScholarPubMed
Youssef, MA, Mourad, S. Volume expanders for the prevention of ovarian hyperstimulation syndrome. Cochrane Database Syst Rev 2016;8:CD001302.Google Scholar
Tso, LO, Costello, MF, Albuquerque, LE, Andriolo, RB, Macedo, CR. Metformin treatment before and during IVF or ICSI in women with polycystic ovary syndrome. Cochrane Database Syst Rev 2014;11:CD006105.Google Scholar
Guo, JL, Zhang, DD, Zhao, Y, et al. Pharmacologic interventions in preventing ovarian hyperstimulation syndrome: a systematic review and network meta-analysis. Sci Rep 2016;6:19093.CrossRefGoogle ScholarPubMed
Walls, ML, Hart, RJ. In vitro maturation. Best Pract Res Clin Obstet Gynaecol 2018;53:60–72.CrossRefGoogle ScholarPubMed
Sunkara, SK, Rittenberg, V, Raine-Fenning, N, et al. Association between the number of eggs and live birth in IVF treatment: an analysis of 400 135 treatment cycles. Hum Reprod 2011;26:1768–1774.Google Scholar
la Cour Freiesleben, N, Gerds, TA, Forman, JL, et al. Risk charts to identify low and excessive responders among first-cycle IVF/ICSI standard patients. Reprod Biomed Online 2011;22:50–58.CrossRefGoogle ScholarPubMed

Save book to Kindle

To save this book to your Kindle, first ensure no-reply@cambridge.org is added to your Approved Personal Document E-mail List under your Personal Document Settings on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part of your Kindle email address below. Find out more about saving to your Kindle.

Note you can select to save to either the @free.kindle.com or @kindle.com variations. ‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi. ‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.

Find out more about the Kindle Personal Document Service.

Available formats
×

Save book to Dropbox

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Dropbox.

Available formats
×

Save book to Google Drive

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Google Drive.

Available formats
×