Ovarian hyperstimulation syndrome (OHSS) is a potential iatrogenic life-threatening situation. It is difficult to decipher OHSS pathophysiology. 1 The occurrence is directly proportional to estradiol in blood, follicle number, and human chorionic gonadotropin (hCG) with more chances of happening in polycystic ovarian disease. Complete prevention of OHSS is never possible, but endocrine profile and ultrasonographic follicular monitoring are the mainstay of its prediction. Complications such as hemoconcentration, hypovolemia, and thromboembolism can occur. Withholding hCG, continuation of gonadotropin-releasing hormone analogs, coasting, agonist trigger, intravenous albumin, dopamine agonists, and cryopreservation of embryos are cornerstones of OHSS prevention. 2 Mild OHSS usually requires no active therapy. Moderate and severe cases have to be treated. Surgery may be needed in ruptured ovarian cysts, torsion, or concomitant ectopic pregnancy. Transvaginal paracentesis is recommended in cases of severe ascites. Inpatient management is typically based on preventing complications such as derangement of kidney and liver functions, thrombosis, and severe respiratory depression. Recent ART treatment protocols behold more patient-friendly mild ovarian stimulation regimes that are individualized depending on patient's ovarian reserve. 3