This chapter deals with the classification, pathophysiology, prediction, prevention, and treatment of ovarian hyperstimulation syndrome (OHSS). OHSS is characterized by bilateral cystic ovarian enlargement and third-space fluid shift resulting in ascites and pleural effusion. It may be moderate or severe in severity, early or late in onset, spontaneous or iatrogenic in etiology. Prediction of OHSS is the cornerstone of prevention. It is based on identifying the characteristics of the patients who would be high responders as well as the use of ultrasonography and estradiol assessment. The pathophysiology of OHSS suggests the involvement of an inflammatory mechanism during the development of the fluid leakage associated with OHSS. Therefore, investigators hypothesized that glucocorticoids could possibly prevent OHSS in patients at high risk. Laparoscopic ovarian drilling has been used successfully for prevention of OHSS in patients with polycystic ovaries. The medical treatment of OHSS consists of correction of circulatory volume and electrolyte imbalance.

This chapter focuses on the surgical management of polycystic ovary syndrome (PCOS). The mechanism of action of laparoscopic ovarian drilling (LOD) is unclear. Its beneficial effect is apparently due to destruction of the androgen-producing stroma. Patients who were resistant to clomiphene citrate (CC) may respond to this medication after the procedure. Sensitivity to exogenous gonadotrophin treatment is increased. Gonadotrophin treatment following LOD is associated with a lower duration of stimulation, lower total dose of gonadotrophins, and higher pregnancy rates. LOD and metformin therapy improve menstrual disturbances and ovulatory dysfunction to a similar extent. The pregnancy rates after both treatments are also similar, but the safety of metformin in pregnancy is unproven. The improvement in hyperandrogenism is thought to be secondary to the reduction in LH concentrations and the decreased androgen production by the ovarian stroma.