Warfarin And Vitamin K Deficiency

Prothrombin (factor II) is a vitamin K-dependent coagulation factor, as are factors VII, IX, and X, protein C, and protein S. In the liver, reduced vitamin K is required as a cofactor for the carboxylation of glutamic acid residues in the precursors of these coagulation proteins. Deficiency of vitamin K or inhibition of this process by an antagonist such as warfarin results in decreased levels of these factors in the plasma. In the United States, all hospital-born infants are prophylactically treated with intramuscular vitamin K.,. Nutritional deficiency of vitamin K is rare in adults; however, it does occur as a result of poor nutrition and malabsorption in patients with liver disease.

Sodium warfarin, a vitamin K antagonist, is widely used as an oral anticoagulant. Even in those who are closely monitored, as many as 25 percent of patients taking warfarin develop hemorrhagic complications due to severe coagulation factor deficiencies. Routinely monitored by the prothrombin time (PT), large doses of warfarin also can cause prolongation of the activated partial thromboplastin time (aPTT). The treatment of overdosage of warfarin depends on the severity of clinical manifestations, not the degree of prolongation of the PT. If there is no evidence of bleeding, temporary discontinuation of the warfarin may be all that is needed. Warfarin has a half-life of 2.5 days in patients with normal hepatic function. Patients who manifest bleeding complications can be treated with fresh frozen plasma (FFP) or vitamin K, (intravenous, intramuscular, or subcutaneous)—each has advantages and disadvantages. Infusion of FFP can result in the rapid repletion of coagulation factors and control of hemorrhage. FFP, however, carries some risk of viral transmission and the risk of volume overload. Parenteral administration of vitamin K, will reverse the warfarin effect in 12 to 24 h. Some do not advise intravenous administration of vitamin K 1 because of the risk of hypersensitive anaphylactic reactions, although usually 1 mg can be given intravenously safely. Intramuscular or subcutaneous vitamin K 1 is typically given in doses of 5 to 10 mg daily in states of coagulation factor deficiency. The use of oral vitamin K1 for the treatment of acute bleeding is not recommended. Its absorption is erratic and the effect may not be observed for several days to weeks. In addition to the risk of intravenous administration of vitamin K ,, the major disadvantage to its use is that its effect may last up to 2 weeks, making it difficult or impossible to anticoagulate the patient using warfarin during that time.

Drug-induced deficiency of the vitamin K-dependent factors also can be seen in patients receiving some antibiotics, particularly the third-generation cephalosporins that contain the M-methylthiotetrazole side chain (moxalactam, cefamandole, cefotaxime, cefoperazone).

Warfarin has long been used as a rodenticide; however, resistance has developed in the animals, and new products known as superwarfarins are now used. Brodifacoum is the most widely available of these agents. Many case reports now in the literature describe intentional and accidental ingestion of these products. Such patients present with a severe coagulopathy; major mucosal bleeding and internal bleeding are common and can be fatal. Treatment with high doses of vitamin K,, up to 50 to 100 mg/day for several weeks, is often required to correct this coagulopathy because of the long half-life of these products.

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