Whilst severe OHSS occurs in 2%‐6% of patients in an unselected population, 1, 13 certain patient groups, such as those with polycystic ovaries, are at five‐fold increased risk of OHSS. 12 Most classifications diagnose mild OHSS if symptoms alone are present with mild ovarian enlargement (ovarian diameter 5‐12 cm), moderate OHSS if ascites on ultrasound is additionally present and severe OHSS if marked clinically apparent ascites (grade 2), pleural effusions, biochemical evidence of haemoconcentration or intravascular depletion are also evident. This has led to the formation of an “OHSS working group” who have recently published an expert consensus statement on the definition and the classification of OHSS in clinical trials. 2, 3 However, due to a lack of objective normative data at OHSS screening, there has been a lack of consistency in the criteria used to diagnose OHSS. The most widely used criteria are those devised by Golan et al in 1989 with the updated classification by Navot et al in 1992. Several classifications have been proposed for the diagnosis of OHSS based on symptoms, sonographic and laboratory parameters. 9, 10, 11 To date, there has been no direct comparison of markers of early OHSS following these triggers of oocyte maturation.
The peak serum LH level following kisspeptin occurs at a similar interval to GnRHa (~4 hours following administration), but to a lower amplitude, as kisspeptin only stimulates the release of an endogenous pool of GnRH. 8 Kisspeptin acts to stimulate the release of endogenous GnRH from the hypothalamus. More recently, kisspeptin has been evaluated as a novel trigger of oocyte maturation. In women at high risk of OHSS, gonadotrophin‐releasing hormone agonist (GnRHa), which has a shorter duration of action than hCG, can be used as an alternative trigger of oocyte maturation. Whilst hCG is the most commonly used trigger of oocyte maturation, it is also the most frequent aetiological factor in the development of OHSS, due to its long duration of action (7‐10 days). Even so, 20% of IVF cycles started in Europe 6 and 28% of IVF cycles conducted in the US 7 necessitated segmentation to mitigate the risk of late OHSS. 5 The risk of early OHSS can more reliably be mitigated using alternative triggers of oocyte maturation to hCG. Cryopreservation of embryos with transfer in later cycles (segmentation) can be used to manage the risk of OHSS, although logically, segmentation can only mitigate the occurrence of late OHSS. 4 Consequently, early OHSS is regarded as predominantly trigger‐related, whereas late OHSS is regarded as predominantly pregnancy‐related. 4 By contrast, late OHSS occurs due to the production of endogenous hCG from a developing pregnancy. 4 Early OHSS results from excessive stimulation of the ovaries, usually due to the administration of hCG to trigger oocyte maturation.
Ovarian hyperstimulation syndrome can be further categorised as early (≤9 days following trigger administration) or late (≥10 days) OHSS, to reflect differences in pathophysiology. Thus, OHSS is characterised by ovarian enlargement, ascites, pleural effusion, oliguria, haemoconcentration and thromboembolic events. This leads to increased capillary permeability and fluid shifts from the intravascular compartment into the third space of the body. 1 Ovarian hyperstimulation syndrome results from the release of vasoactive substances from the ovary, such as vascular endothelial growth factor (VEGF A) due to excessive ovarian stimulation after triggering oocyte maturation during IVF treatment. 1 The hormone used to induce oocyte maturation plays a critical role in the risk of OHSS following IVF treatment, with exogenous human chorionic gonadotrophin (hCG) being the most frequent aetiological agent. Ovarian hyperstimulation syndrome (OHSS) is a largely iatrogenic condition that is associated with significant morbidity and even mortality in otherwise healthy women undergoing fertility treatment.
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