Fostering Fertility: despite ovarian hyperstimulation

The goal of treatment for severe OHSS is restoring intravascular volume to reverse hemoconcentration and maintain urine output over 30 cc per hour. Normal saline is the crystalloid solution of choice for correcting hypovolemia, as more of it remains in the vascular space.^4,15 It also contains no potassium. (Patients with hyperkalemia may require treatment with cation exchange resins.) Unfortunately, expanding the intravascular compartment with crystalloids may exacerbate the ascites, as only 20% of the infused volume remains in the intravascular space after 1 hour.^4,15,20

The underlying pathogenic mechanism of OHSS is increased vascular permeability with hypoproteinemia and a loss of fluid into the third space.

When crystalloids alone are unable to reverse the oliguria, colloid solutions should be administered. Albumin is the preferred colloid, as it is the protein lost in OHSS and is associated with fewer risks than fresh frozen plasma or dextran.²⁰ Fifty to 100 g of albumin may be administered every 2 to 12 hours as needed to restore urine output.² A 50-g dose draws approximately 900 mL of extracellular fluid into the vascular compartment within 15 minutes.¹⁶ Unfortunately, albumin’s oncotic effect is lost within 36 hours when it leaves the vascular space, which may worsen the OHSS.

Diuretics may be used if oliguria persists after restoring the intravascular volume, provided the patient is not hemoconcentrated or hypotensive.² In general, however, diuretics should be avoided in OHSS, as they may further shrink an already contracted intravascular volume.^4,15

Surgery is indicated only in the presence of ovarian torsion, ectopic pregnancy, or cyst rupture.

In some cases, oliguria may persist even after hemoconcentration has been corrected. This generally is the result of tense ascites, which reduces renal blood flow by compressing the renal vessels and decreasing cardiac output. In these cases, paracentesis often brings prompt symptomatic relief and diuresis.^20,21 Paracentesis also is indicated for respiratory compromise, rising creatinine or falling creatinine clearance, and hemoconcentration unresponsive to fluid therapy.² However, the removal of large volumes of fluid may lead to rapid reaccumulation with further intravascular volume depletion. Paracentesis should be performed using aseptic technique under ultrasound guidance to avoid intraperitoneal hemorrhage from puncture of the ovarian cysts.^2,4 It may be accomplished abdominally or transvaginally.²⁰

While most experts would perform paracentesis for tense ascites for the indications mentioned earlier, there is no consensus as to whether patients should be subjected to paracentesis for less severe cases of ascites. Some physicians advise against routine paracentesis due to the risk of rapid fluid shifts, fistula formation, and infection, while others claim that it hastens the resolution of OHSS.

Renal-dose dopamine may be useful in prerenal failure unresponsive to fluid therapy and paracentesis. It may enhance urine output and prevent acute tubular necrosis and frank renal failure requiring hemodialysis.² Dopamine increases renal blood flow and glomerular filtration by dilating the renal vascular bed without affecting heart rate or blood pressure (BP). Patients administered dopamine should be managed in an ICU with CVP or Swan-Ganz monitoring.

Surgical treatment for OHSS is indicated only in the presence of ovarian torsion, ectopic pregnancy, or cyst rupture.^2,3 (Intraperitoneal bleeding from ruptured ovarian cysts typically is accompanied by abdominal pain and a falling hematocrit in the absence of diuresis.⁴) Surgery should be as conservative as possible and limited to the complication at hand, as ovarian changes in the syndrome are self-limited.

T ABLE 2

Management of moderate OHSS

TABLE 3

Admission orders for severe OHSS