Ovarian Hyperstimulation Syndrome Medication

Updated: Apr 09, 2021
  • Author: Richard Scott Lucidi, MD, FACOG; Chief Editor: Richard Scott Lucidi, MD, FACOG  more...
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Medication

Medication Summary

Medical therapy is aimed at the correction of fluid and electrolyte balance. Normal saline is used to restore the patient’s intravascular and extravascular volume. In addition, albumin can be used to expand plasma volume, and dopamine can be employed to increase blood pressure.

Thrombosis can occur in the arteries (25%) and veins (75%). Therefore, the use of heparin, low molecular weight heparin (enoxaparin sodium [Lovenox] and others), antiembolism stockings, and sequential compression devices (boots) are all recommended as prophylaxis against thrombosis. Heparin prophylaxis is usually started in patients with a history of thrombosis, factor V Leiden deficiency, or other thrombophilic states before the induction of ovulation.

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Anticoagulants

Class Summary

These agents inhibit key factors involved in thrombogenesis.

Heparin

Heparin augments the activity of antithrombin III and prevents the conversion of fibrinogen to fibrin. It does not actively lyse, but heparin can inhibit further thrombogenesis, and it prevents reaccumulation of a clot after spontaneous fibrinolysis. To prevent thrombosis, subcutaneous heparin 5000-7500 U daily is begun on the first day of admission. It is stopped after adequate ambulation is achieved.

Enoxaparin (Lovenox)

Enoxaparin is a low-molecular-weight heparin (LMWH) produced by partial chemical or enzymatic depolymerization of unfractionated heparin (UFH). It binds to antithrombin III, enhancing its therapeutic effect. The heparin-antithrombin III complex binds to and inactivates activated factor X (Xa) and factor II (thrombin). LMWH differs from UFH by having a higher ratio of anti–factor Xa to anti–factor IIa.

Enoxaparin does not actively lyse thrombi but is able to inhibit further thrombogenesis. It prevents reaccumulation of clot after spontaneous fibrinolysis. Its advantages include intermittent dosing and a decreased requirement for monitoring. Heparin anti–factor Xa levels may be obtained if needed to establish adequate dosing. There is no point in checking the aPTT; the drug has a wide therapeutic window, and aPTT does not correlate with anticoagulant effect.

Desirudin (Iprivask)

Desirudin is a highly selective thrombin inhibitor. It inhibits fibrin formation, activation of coagulation factors, and thrombin-induced platelet aggregation. This results in prolongation of activated partial thromboplastin time.

Lepirudin (Refludan)

Lepirudin, a recombinant hirudin derived from yeast cells, is a highly specific direct thrombin inhibitor. It is indicated for anticoagulation in HIT and associated thromboembolic disease. Its action is independent of antithrombin III. Lepirudin blocks the thrombogenic activity of thrombin. It affects all thrombin-dependent coagulation assays (eg, aPTT values increase in a dose-dependent manner). Adjust the dose on the basis of aPTT ratios (target, 1.5-2.5 times normal) determined every 4 hours and then daily.

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Electrolyte Supplements, Parenteral

Class Summary

These are used to replenish intravascular and extravascular volume.

Normal saline

Normal saline is used to restore interstitial and intravascular volume.

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Blood Components

Class Summary

These agents are used to expand plasma volume.

Albumin (Albuminar, Albutein, Buminate, Plasbumin-25)

Albumin is a major plasma protein that is responsible for the colloid oncotic pressure of blood. It is pooled from blood, serum, plasma, or placenta from healthy donors. Albumin is administered in certain types of shock or impending shock. Use a 5% solution to expand plasma volume and maintain cardiac output. Use a 25% solution to raise oncotic pressure.

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Cardiovascular, Other

Class Summary

These agents increase blood pressure.

Dopamine

Dopamine is a naturally occurring, endogenous catecholamine that stimulates beta1-adrenergic, alpha1-adrenergic, and dopaminergic receptors in dose-dependent fashion; it stimulates the release of norepinephrine.

At low dosages (2-5 mcg/kg/min), dopamine acts on dopaminergic receptors in renal and splanchnic vascular beds, causing vasodilation-selective dilation of the renal vasculature, enhancing renal perfusion. It also reduces sodium absorption, decreasing the energy requirements of damaged tubules. This enhances urine flow, which, in turn, helps to prevent tubular cast obstruction. Most clinical studies have failed to establish this beneficial role for renal-dose dopamine infusion.

At midrange dosages (5-15 mcg/kg/min), dopamine acts on beta-adrenergic receptors to increase heart rate and contractility.

At high dosages (15-20 mcg/kg/min), the drug acts on alpha-adrenergic receptors to increase systemic vascular resistance and raise blood pressure.

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