Ovarian hyperstimulation syndrome (OHSS) is the most serious iatrogenic complication of ovulation induction. The ovaries are noted to have a significant degree of stromal edema, interspersed with multiple hemorrhagic follicular and theca-lutein cysts, areas of cortical necrosis, and neovascularization. Mutations in follicle-stimulating hormone (FSH) receptors could be activating, resulting in OHSS, or inactivating, resulting in sterility. Bone morphogenic protein-15 (BMP-15) appears to be associated with mechanisms of infertility and superfertility in a dosage-sensitive manner. Human chorionic gonadotropin increases vascular endothelial growth factor (VEGF) production by granulosa cells and endothelial cells, which results in increased vascular permeability. Increased intraovarian blood flow and low intravascular ovarian resistance are correlated with the severity of OHSS in patients who develop the syndrome. The medical treatment of OHSS consists of correction of circulatory volume and electrolyte imbalance. Ultrasonographic guidance of transvaginal or transabdominal aspiration of ascites improves the symptoms of patients with OHSS.