Ovarian Hyperstimulation Syndrome (OHSS)

DEFINTION:
Ovarian Hyperstimulation Syndrome (OHSS) is a clinical symptom complex associated with ovarian enlargement resulting from exogenous gonadotropin therapy.

PATHOPHYSIOLOGY:
The etiology of OHSS is complex, but hCG, either exogenous or endogenous (derived from a resulting pregnancy), is believed to be an early contributing factor. Development of OHSS involves increased vascular permeability and loss of fluid, protein, and electrolytes into the peritoneal cavity, which leads to hemoconcentration. Increased capillary permeability is felt to result from vasoactive substances produced by the corpus luteum. Vascular endothelial growth factor (VEGF) is believed to play a major role, and angiotensin II may also be involved. Hypercoagulability may be related to hyperviscosity following hemoconcentration. Alternatively, it may be secondary to the high estrogen levels present, and these high levels can increase coagulation factors. Predisposing factors for OHSS include multifollicular ovaries such as with PCOS, young age, high estradiol levels during ovulation induction and pregnancy.

CLINICAL PICTURE:
Symptoms may include abdominal pain and distension, ascites, gastrointestinal problems, respiratory compromise, oliguria, hemoconcentration, and thromboembolism. These symptoms may develop during ovulation induction or in early pregnancies that were conceived through exogenous ovarian stimulation.

DIAGNOSIS AND TREATMENT:

Abdominal pain is prominent and caused by ovarian enlargement together with accumulation of peritoneal fluid. Although sonographic examination of women with OHSS usually reveals enlarged ovaries with numerous follicular cysts and ascites, OHSS is a clinical diagnosis. Treatment of OHSS is generally supportive. Paracentesis is typically performed transvaginally as an outpatient and can ameliorate abdominal discomfort and relieve respiratory distress. Reaccumulation of ascites may prompt additional paracenteses or rarely placement of a percutaneous catheter for continuous drainage. Untreated hypovolemia can lead to renal, hepatic, or pulmonary end organ failure. Thus, fluid balance must be maintained by replacement with an isotonic fluid such as normal saline. Monitoring of electrolytes is critical. Because of hypercoagulability in these women, prophylaxis for thromboembolism should be strongly considered with severe OHSS.

PREVENTION:
Strategies to avoid OHSS during exogenous ovulation induction include: o Decreasing follicular stimulation coasting (withholding FSH administration for 1 or more days prior to the hCG trigger injection) and prophylactic treatment with volume expanders. o Substitution of hCG for FSH during the final days of ovarian stimulation. With this strategy, low-dose hCG administration can support maturation of larger ovarian follicles, but has been postulated to directly or indirectly increase atresia rates of small antral follicles and thereby lower rates of OHSS. o If concern of OHSS is present during induction, then the hCG trigger can be withheld, resulting in cycle cancellation. Alternatively, a single dose of GnRH agonist such as leuprolide acetate (Lupron) can be used in place of hCG. This results in an endogenous LH surge, which can bring about the final stages of follicle and oocyte maturation without significant risk of OHSS. o Prevention of pregnancy does not completely eliminate the risk of OHSS but certainly limit the duration of the symptoms. Thus, an additional option in ART cycles is to freeze all embryos and forgo embryo transfer that cycle.

REFERENCES:
Williams Gynecology second edition.

BY:
Mahmoud Ahmed Mahmoud 846