<unk> S has been characterized by the presence of multiple luteinized cysts within the ovaries leading to<unk>  enlargement and secondary complications, but that definition includes almost all women undergoing<unk>  stimulation. The central feature of clinically significant<unk> S is the development of vascular hyperpermeability and the resulting shift of fluids into the third space. As hCG causes the ovary to undergo extensive luteinization, large amounts of estrogens, progesterone, and local cytokines are released. It is almost certain that vascular endothelial growth factor (VEGF) is a key substance that induces vascular hyperpermeability, making local capillaries "leaky", leading to a shift of fluids from the intravascular system to the abdominal and pleural cavity. Supraphysiologic production of VEGF from many follicles under the prolonged effect of hCG appears to be the specific key process underlying<unk> S. Thus, while the woman accumulates fluid in the third space, primarily in the form of ascites, she actually becomes hypovolemic and is at risk for respiratory, circulatory (such as arterial thromboembolism since blood is now thicker), and renal problems. Women who are pregnant sustain the<unk>  luteinization process through the production of hCG. Avoiding<unk> S typically requires interrupting the pathological sequence, such as avoiding the use of hCG. One alternative is to use a GnRH agonist instead of hCG. While this has been repeatedly shown to "virtually eliminate"<unk> S risk, there is some controversy regarding the effect on pregnancy rates if a fresh non-donor embryo transfer is attempted, almost certainly due to a luteal phase defect. There is no dispute that the GnRH agonist trigger is effective for oocyte donors and for embryo banking (cryopreservation) cycles. Classification<unk> S is divided into the categories mild, moderate, severe, and critical. In mild forms of<unk> S the ovaries are enlarged (5–12 cm) and there may be additional accumulation of ascites with mild abdominal distension, abdominal pain, nausea, and diarrhea. In severe forms of<unk> S there may be hemoconcentration, thrombosis, distension, oliguria (decreased urine production), pleural effusion, and respiratory distress. Early<unk> S develops before pregnancy testing and late<unk> S is seen in early pregnancy. Criteria for severe<unk> S include enlarged ovary, ascites, hematocrit > 45%, WBC > 15,000, oliguria, creatinine 1.0-1.5 mg/dl, creatinine clearance > 50 ml/min, liver dysfunction, and anasarca. Critical<unk> S includes enlarged ovary, tense ascites with hydrothorax and pericardial effusion, hematocrit > 55%, WBC > 25,000, oligoanuria, creatinine > 1.6 mg/dl, creatinine clearance < 50 ml/min, kidney failure, thromboembolic phenomena, and ARDS. 240px 430px Vaginal ultrasonography in the sagittal plane in a woman with mild<unk> S, showing a 33 mm wide anechogenic area behind the uterus in the recto-uterine pouch, which means there was ascites, that is, free fluid in the peritoneal cavity. Normally, there is up to 5 ml of fluid in the recto-uterine pouch, corresponding approximately to an area up to 10 mm wide. The ovary measured up to 6.5 cm in diameter.
Ovarian hyperstimulation syndrome
Gonadotropin-resistant ovary syndrome
Postpartum physiological changes
Obstetric transition
Anovulation
Puppy pregnancy syndrome
Cryptic pregnancy
Lactational amenorrhea