Abstract
For the past two decades, significant advances have been made in the treatment of anovulation. The use of therapeutic agents for induction of ovulation, however, has given rise to several adverse reactions, the most important and serious of such complications being the ovarian hyperstimulation syndrome (OHSS), which can be fatal. It is characterized by gross ovarian enlargement, ascites, pleural effusion, hemoconcentration and thromboembolic disorder, which are potentially lethal conditions. The main pathogenic mechanism is considered to be increased capillary permeability, especially of the ovarian vessels, causing acute body fluid shift from the intravascular compartment to the peritoneal and pleural cavities. An experimental model of OHSS suggests that prostaglandins mediate this increased capillary permeability and transudation. Management is based on the concept of the pathogenic mechanism and includes maintenance of intravascular volume by plasma volume expanders, reduction of capillary permeability and prevention of thromboembolic complications. Surgical intervention is indicated only in cases of ovarian torsion or rupture and should be as conservative as possible.
Key Words: