Ovarian hyperstimulation syndrome - a complication of the past

Ovarian hyperstimulation syndrome (OHSS) occurs due to increased vascular permeability brought about by abundant vascular endothelial growth factor (VEGF) production by luteinized granulosa cells. The resultant haemoconcentration and hypercoagulability can lead to life-threating complications. The increased pool of granulosa cells and their prolonged stimulation by human chorionic gonadotrophin (HCG), either exogenous used for triggering ovulation or endogenous from a pregnancy occurring in the same cycle, are the two main drivers of OHSS. Substitution of the HCG trigger with a single dose of gonadotrophin-releasing hormone agonist (GnRHa) causes rapid luteolysis, and almost eliminates the risk of OHSS entirely. The advent of vitrification and cycle segmentation with a freeze-all approach following a GnRHa trigger enabled avoidance of the more severe, late form of OHSS. Complementary methods including GnRH antagonist and dopamine agonist administration in the luteal phase can decrease the risk of OHSS further by suppressing the endogenous LH concentration and inactivating VEGF receptors, respectively. After decades of research leading to the above-mentioned preventive methods, OHSS now occurs extremely rarely. Therefore, patients can be stimulated to realize their potential without the fear of this complication of the past.