Factor V Treatment & Management

  • Author: Olga Kozyreva, MD; Chief Editor: Emmanuel C Besa, MD   more...
 
Updated: Jan 10, 2012
 

Medical Care

No concentrates of factor V are commercially available, so fresh plasma or fresh frozen plasma (FFP) infusions are used to correct the deficiency temporarily and should be given daily during a bleeding episode. The loading dose of FFP is 15-20 mL/kg and then 3-6 mL/kg daily. Subsequent dosages depend on monitoring the factor V level by obtaining peak and trough factor V level assays. The half-life ranges from 24-36 hours, with the aim being a factor V level of 25%. Fluid overload and viral transmission may be a complication of plasma therapy.

  • Preoperative and postoperative care when patients with factor V deficiency require surgery include the following:
    • In pregnant women, considerable bleeding can occur at the time of delivery; however, the administration of FFP can properly control bleeding, with excellent fetal outcome.
    • The safe level of factor V for adequate surgical hemostasis is 25% of the activity of factor V in normal control plasma.
    • Postoperatively, FFP should be administered for 3-10 days, with careful observation of wound bleeding.
    • Tooth extraction in a patient with factor V hereditary deficiency is safely performed with both supplementation of FFP and application of local hemostasis.
  • Patients with factor V deficiency can be given oral contraceptives to decrease menometrorrhagias, thereby improving anemia and decreasing transfusion needs.
  • The optimal treatment of patients with factor V inhibitors is uncertain. Fu et al were successful in using a combination of factor replacement, chemotherapy, and plasmapheresis in a patient with spontaneous, life-threatening intracranial bleeding caused by a factor V inhibitor. The patient deteriorated after initial treatment with FFP and platelet transfusions. He was subsequently treated with a combination of plasma exchange and chemotherapy, and he completely recovered.[8] The experience of Fu et al shows that combinations of therapies may be needed in patients with serious hemorrhage caused by acquired factor V deficiency.
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Consultations

Consultations may include hematologists, blood bank specialists, pathologists, and others as indicated based on hemorrhagic complications.

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Contributor Information and Disclosures
Author

Olga Kozyreva, MD  Attending Physician, Division of Hematology-Oncology, St Elizabeth's Medical Center; Assistant Professor, Tufts University School of Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Sarah K May, MD  Consulting Staff, Department of Hematology-Oncology, Caritas Carney Hospital, Commonwealth Hematology-Oncology PC

Disclosure: Nothing to disclose.

Karl J D'Silva  MD, Assistant Clinical Professor of Medicine, Department of Hematology/Oncology, Lahey Clinic, Sophia Gordon Cancer Center

Karl J D'Silva is a member of the following medical societies: Massachusetts Medical Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Paul Schick, MD  Emeritus Professor, Department of Internal Medicine, Jefferson Medical College of Thomas Jefferson University; Research Professor, Department of Internal Medicine, Drexel University College of Medicine; Adjunct Professor of Medicine, Lankenau Hospital

Paul Schick, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Society of Hematology, International Society on Thrombosis and Haemostasis, and New York Academy of Sciences

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Ronald A Sacher, MB, BCh, MD, FRCPC  Professor, Internal Medicine and Pathology, Director, Hoxworth Blood Center, University of Cincinnati Academic Health Center

Ronald A Sacher, MB, BCh, MD, FRCPC is a member of the following medical societies: American Association for the Advancement of Science, American Association of Blood Banks, American Clinical and Climatological Association, American Society for Clinical Pathology, American Society of Hematology, College of American Pathologists, International Society of Blood Transfusion, International Society on Thrombosis and Haemostasis, and Royal College of Physicians and Surgeons of Canada

Disclosure: Glaxo Smith Kline Honoraria Speaking and teaching; Talecris Honoraria Board membership

Rebecca J Schmidt, DO, FACP, FASN  Professor of Medicine, Section Chief, Department of Medicine, Section of Nephrology, West Virginia University School of Medicine

Rebecca J Schmidt, DO, FACP, FASN is a member of the following medical societies: American College of Physicians, American Medical Association, American Society of Nephrology, International Society of Nephrology, National Kidney Foundation, Renal Physicians Association, and West Virginia State Medical Association

Disclosure: Renal Ventures Ownership interest Other

Chief Editor

Emmanuel C Besa, MD  Professor, Department of Medicine, Division of Hematologic Malignancies, Kimmel Cancer Center, Jefferson Medical College of Thomas Jefferson University

Emmanuel C Besa, MD is a member of the following medical societies: American Association for Cancer Education, American College of Clinical Pharmacology, American Federation for Medical Research, American Society of Clinical Oncology, American Society of Hematology, and New York Academy of Sciences

Disclosure: Nothing to disclose.

References
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Antithrombin sites of action.
Cell surface-directed hemostasis. Initially, a small amount of thrombin is generated on the surface of the tissue factor (TF)–bearing cell. Following amplification, the second burst generates a larger amount of thrombin, leading to fibrin (clot) formation. Adapted from Hoffman and Monroe, Thromb Haemost 2001, 85(6): 958-65.
 
 
 
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