warfarin and Afibrinogenemia

Topics: Afibrinogenemia; Anticoagulants; Blood Coagulation Tests; Codon, Nonsense; Fibrinogen; Genetic Predisposition to Disease; Genetic Testing; Humans; Male; Middle Aged; Recurrence; Thrombelastography; Venous Thrombosis; Warfarin

Topics: Adult; Afibrinogenemia; Fibrinolytic Agents; Hematoma, Subdural; Humans; Liver Transplantation; Male; Warfarin

The authors hypothesized that various hemostatic products may differently affect viscoelastic clot formation depending on their respective procoagulant activity and fibrinogen content.. In vitro coagulopathy modeling using warfarin-treated plasma (international normalized ratio, 2.8-3.8) and fibrinogen-deficient plasma evaluated by rotational thromboelastometry (ROTEM; Pentapharm, Munich, Germany).. A university laboratory.. Different volumes of cryoprecipitate, fresh frozen plasma (FFP), fibrinogen concentrate, and platelet concentrate were mixed with each abnormal plasma to simulate the in vivo transfusions of 250 mL to 1,000 mL. Three thromboelastometric variables that reflect the rate and extent of clot growth were measured: (1) coagulation time (CT), (2) angle, and (3) maximal clot firmness (MCF).. In warfarin-treated plasma, the addition of FFP, cryoprecipitate, and platelets led to a dose-dependent improvement of CT and angle, whereas MCF increased with cryoprecipitate or platelets only. The addition of fibrinogen concentrate improved MCF and angle but not CT. In fibrinogen-deficient plasma, the addition of cryoprecipitate, platelets, and fibrinogen concentrate led to a dose-dependent improvement of ROTEM variables, whereas the addition of FFP resulted in significantly longer CT and lower MCF values compared with other hemostatic products. The addition of platelets in the presence of cytochalasin D (a platelet inhibitor) resulted in improvements of ROTEM variables that were similar to when FFP was added to warfarin-treated and fibrinogen-deficient plasma.. Cryoprecipitate supports clot formation on ROTEM more efficiently than FFP because of the high fibrinogen content. Improved ROTEM variables after platelet addition are presumably caused by increased interaction among thrombin-activated platelets and fibrinogen.

Topics: Afibrinogenemia; Anticoagulants; Blood Coagulation; Blood Platelets; Data Interpretation, Statistical; Dose-Response Relationship, Drug; Hemostasis; Humans; In Vitro Techniques; Plasma; Prothrombin; Thrombelastography; Warfarin

The type of coagulation factors and proteins in cryoprecipitate determine the appropriate indications for its use. To determine the pattern of use at a tertiary care medical center, we performed a retrospective audit of cryoprecipitate utilization. A total of 51 patients received 88 pools of cryoprecipitate. In 39 patients, cryoprecipitate was transfused for appropriate indications: hypofibrinogenemia (n = 19), tissue plasminogen activator reversal (n = 1), management of massive transfusion (n = 7), correction of uremic bleeding (n = 2), and for making fibrin sealant (n = 10). Overall, these patients used approximately 80% of the cryoprecipitate transfused. In 12 other patients, cryoprecipitate was transfused inappropriately to attempt reversal of the anticoagulant effects of warfarin therapy (n = 6), to treat impaired surgical hemostasis in the absence of hypofibrinogenemia (n = 4), and to treat hepatic coagulopathy with multiple factor deficiencies (n = 2). The patterns of misuse, involving 24% of all cryoprecipitate orders, suggest a widespread misunderstanding and need for focused education about the coagulation factors and proteins present in cryoprecipitate and appropriate indications for its use.

Topics: Adult; Afibrinogenemia; Aged; Aged, 80 and over; Blood Loss, Surgical; Blood Transfusion; Factor VIII; Fibrin Tissue Adhesive; Fibrinogen; Hemorrhage; Humans; Liver Neoplasms; Medical Audit; Middle Aged; Retrospective Studies; Tissue Plasminogen Activator; Uremia; Warfarin

Afibrinogenemia, a rare coagulation disorder, has not been associated with vertebral artery dissections.. A 28-year-old woman with afibrinogenemia developed spontaneous neck pain followed by a right medullary infarction, and MR angiography showed extensive bilateral vertebral artery dissection. She was treated with fibrinogen replacement and anticoagulants and showed a favorable evolution, with only mild residual right upper arm incoordination.. In this patient spontaneous bilateral vertebral artery dissection complicated afibrinogenemia. Since anticoagulant therapy is usually indicated for arterial dissection, this association created a therapeutic problem. This patient received anticoagulants with fibrinogen replacement, which resulted in a favorable evolution.

Topics: Adult; Afibrinogenemia; Anticoagulants; Aortic Dissection; Contraindications; Female; Fibrinogen; Heparin; Humans; Intracranial Embolism and Thrombosis; Magnetic Resonance Imaging; Neck Pain; Vertebral Artery; Warfarin

A 57 year old man presented with apparently spontaneous lower extremity deep vein thrombosis and pulmonary embolism. He was treated in conventional fashion with intravenous heparin and oral warfarin. After 4 daily doses of warfarin the prothrombin and proconvertin (P+P) time was within therapeutic range, and heparin was stopped. Over the next six hours complete defibrination occurred, associated with severe bleeding complications. Functional protein C measured after normalization of routine coagulation tests averaged 40% of normal, and was only 3.5% of normal immediately prior to the episode of defibrination. We conclude that the very low functional protein C levels seen immediately prior to defibrination were caused by a combination of pre-existent protein C deficiency and warfarin therapy, and directly predisposed to defibrination once heparin was stopped, despite "therapeutic" warfarin anticoagulation. Exacerbation of intravascular coagulation should be considered a potential prothrombotic effect of warfarin therapy in protein C deficient individuals.

Topics: Afibrinogenemia; Disseminated Intravascular Coagulation; Glycoproteins; Heparin; Humans; Male; Middle Aged; Protein C; Pulmonary Embolism; Thrombophlebitis; Warfarin

Acetylsalicylic acid and phenylbutazone increased the bleeding significantly from standardized wounds in dogs defibrinogenated with Defibrase. Administration of dipyridamole and Xylocain had no effect. The results were the same in dogs treated with warfarin sodium. The results demonstrate the value of using laboratory animals with an induced coagulopathy when establishing the effect on the haemostasis exerted by drugs known in vitro to interfere with platelet functions. Acetylsalicylic acid and dipyridamole did not alter the activity of the K-vitamin-dependent coagulation factors, factors V, VIII, platelet count or fibrinogen concentration.

Topics: Afibrinogenemia; Animals; Aspirin; Batroxobin; Blood Coagulation; Blood Coagulation Disorders; Blood Platelets; Dogs; Hemostasis; Peptide Hydrolases; Phenylbutazone; Warfarin

Topics: Afibrinogenemia; Animals; Blood Coagulation Tests; Cyproheptadine; Dogs; Fibrinogen; Hematocrit; Histamine Release; Hypoprothrombinemias; Plasminogen; Prothrombin; Streptokinase; Vitamin K; Warfarin

Topics: Acid Phosphatase; Afibrinogenemia; Blood Coagulation Disorders; Blood Proteins; Bone Marrow Examination; Diethylstilbestrol; Factor V; Factor VIII; Fibrinogen; Humans; Male; Middle Aged; Prostatic Neoplasms; Warfarin

Topics: Afibrinogenemia; Blood Coagulation Tests; Colonic Neoplasms; Deoxyribonuclease I; Disseminated Intravascular Coagulation; Drug Therapy; Enzyme Inhibitors; Factor V; Factor VIII; Fibrinolysis; Heparin; Humans; Immunoelectrophoresis; Plasminogen; Streptodornase and Streptokinase; Streptokinase; Warfarin