Journal of Human Reproductive Science
Home Ahead of Print Current Issue Archives
   Bookmark this page Print this page Email this page Small font sizeDefault font size Increase font size    Users online: 1527


 
REVIEW ARTICLE Table of Contents   
Year : 2011  |  Volume : 4  |  Issue : 2  |  Page : 70-75
Ovarian hyperstimulation syndrome


1 Departments of Obstetrics and Gynecology, Kasturba Medical College, Manipal University, Manipal, Karnataka, India
2 Departments of Obstetrics and Gynecology, Deen Dayal Upadhyay Hospital, Shimla, Himachal Pradesh, India
3 Department of Pharmacy Practice, Manipal College of Pharmaceutical Sciences, Manipal University, Manipal, Karnataka, India

Correspondence Address:
Pratap Kumar
Department of Obstetrics and Gynecology, Kasturba Medical College, Manipal University, Manipal-576 104, Karnataka
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0974-1208.86080

Rights and Permissions

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.


[FULL TEXT] [PDF]*
Print this article  Email this article
    

  Similar in PUBMED
    Search Pubmed for
    Search in Google Scholar for
  Related articles
   Citation Manager
  Access Statistics
   Reader Comments
   Email Alert *
   Add to My List *
 * Requires registration (Free)
 

 Article Access Statistics
    Viewed7240    
    Printed268    
    Emailed0    
    PDF Downloaded384    
    Comments [Add]    
    Cited by others 14    

Recommend this journal