///2009 Abstract Details
2009 Abstract Details2019-08-03T15:55:31+00:00

The Use of Recombinant Factor VIIa in the Management of a Parturient with Severe Factor VII Deficiency and Placenta Previa

Abstract Number: 189
Abstract Type: Case Report/Case Series

Brad M Taicher D.O., M.B.A.1 ; H. Jane Huffnagle D.O., F.A.O.C.A.2; Suzanne L Huffnagle D.O., F.A.O.C.A3; Brian Daniel D.O.4; Elia Elia M.D.5; Wlodzimierz Grodecki M.D.6

Introduction: Factor VII (FVII) deficiency presents a significant risk of postpartum hemorrhage. We present a case in which a parturient with severe FVII deficiency and a complete placenta previa was successfully managed with recombinant factor VIIa (rFVIIa).

Case Report: A 38 y/o female, G4P2112, presented to our hospital at 37 weeks gestation with a complete placenta previa for an elective C/S and PPTL. She had a PMH of asthma, diet controlled gestational DM and FVII deficiency diagnosed during her previous pregnancy. Her FVII level was 5% of normal on admission. After consultation with obstetrics and hematology, we developed a plan to treat the patient with rFVIIa 30 mcg/kg ten minutes prior to induction of GA for the C/S. Preoperatively, an arterial line and two large IVs were secured. An uneventful rapid sequence induction and intubation was performed using thiopental and succinylcholine, and she was maintained with sevoflorane in O2 and N2O. A healthy baby girl was delivered 9 minutes later and the placenta was completely extracted. Excellent hemostasis was achieved and the remainder of the case was uneventful, with an EBL of 870 mL. Repeat doses of 30 mcg/kg rFVIIa were administered at two and four hours after the initial dose. There was no significant post-partum bleeding and our patient was discharged on POD #4. Her baby was diagnosed with FVII deficiency.

Discussion: Congenital FVII deficiency is a rare autosomal recessive disorder with an incidence of about 1:500,000 and variable expression; heterozygotes have FVII levels of about 50% and homozygotes < 10% (1). While clinical bleeding does not always correlate with FVII levels, therapy is recommended for levels < 15% (2). rFVIIa is cloned from human FVIIa, expressed in baby hamster kidney cells, secreted into calf serum, collected, and then purified. It acts primarily through the extrinsic pathway by binding with exposed tissue factor at the site of injury to activate factor X to Xa. This initiates the conversion of prothrombin to thrombin in order to form a fibrin clot (3). The half-life of 2.5 hours necessitates dosing every 2 hours. There is a risk of thrombo-embolic complications, either from binding with circulating tissue factor or from direct activation of factor X at pharmacologic plasma levels (feedback loop activates the intrinsic pathway) (4). This risk must be weighed against the benefit of the drug. Although the FVII level required to prevent bleeding in our patient was unknown, her treatment was adequate. In the future, we may be able to decrease the dose of rFVIIa or consider a smaller bolus with infusion, potentially minimizing the risk of adverse events such as alloantibody formation or thrombosis.

References:

1. Eskandari, et al. Obstet Gynecol. 2002; 99: 935-7.

2. Jimenez-Yuste, et al. Haemophilia 2000, 6:588-90.

3. Novoseven Package Insert

4. Yusim, et al. J of Clin Anes 2006, 7:545-51.

SOAP 2009