Manual of Clinical Nutrition Management III- 3 Copyright © 2013 Compass Group, Inc.
ANTICOAGULANT THERAPY
Discussion
Oral anticoagulants are used to create a partial deficiency of the active form of vitamin K, which is responsible
for maintaining normal blood coagulation. By inhibiting the action of vitamin K, there is a reduced risk of
abnormal blood clotting.
Indications
Oral anticoagulants are typically prescribed for the primary and secondary prevention of the following
conditions:
venous thrombosis
pulmonary embolism
myocardial infarction
Persons with prosthetic heart valves, atrial fibrillation with embolization, or heredity disorders that result
in a hypercoagulant state may be treated with anticoagulants indefinitely (1,2).
A major complication of anticoagulant therapy is hemorrhage. The therapeutic index and safety of
anticoagulation therapy is assessed through the measurement of the prothrombin time (PT), which is
expressed as the international normalized ratio (INR) (2). An INR of 2.0 to 3.0 is generally considered in the
therapeutic range, and the risk of bleeding increases when the INR exceeds 4.0 (2).
Nutrition Implications of Anticoagulant Therapy
The goal of medical nutrition therapy for persons receiving anticoagulant therapy is to provide a consistent
intake of vitamin K. The Daily Value for vitamin K is 80 mcg for adults (3). The Daily Value can be used as an
appropriate goal for persons on anticoagulant therapy (3,4). The average dietary intake of vitamin K for adults
in the United States is estimated to be 90 to 118 mcg/day (5-7). Although most patients’ intake will fall into
this acceptable range, all patients should have their diets assessed for typical sources and patterns of foods
containing vitamin K. Persons who receive anticoagulant therapy should limit their consumption of foods
that have a high level of vitamin K.
The list of drugs that interact with vitamin K antagonists is constantly expanding (7). Drug-drug
interactions that increase or decrease the effect of anticoagulant therapy should be evaluated before
concluding that dietary intake is responsible for a change in the anticoagulant response (2,5,7). Drugs that
increase the anticoagulant effect are agents for gout treatment, anabolic steroids, antiarrhythmic agents,
antibiotics, antifungal agents, antihyperlipidemic agents, cimetidine, disulfiram, isoniazid, omeprazole,
sulfonylureas, and tamoxifen citrate. Drugs that decrease the anticoagulant effect are anticonvulsant agents,
cholestyramine, griseofulvin, oral contraceptives, rifampin, sucralfate, and vitamin K (5,8).
Nutrition Assessment and Diagnosis
The oral anticoagulant dose should be established based on the patient’s normal vitamin K intake. After the
dose is established, a reasonable goal is to maintain the daily vitamin K intake within 250 mcg of baseline (1,9).
If major changes in food intake occur, the anticoagulant level may need to be reestablished. Vitamin K intake
may increase when a patient starts a weight-reduction diet and includes a greater number of vegetables that
are high in vitamin K or begins a high-protein, low-carbohydrate diet (see discussion below). Other reasons
for an increased vitamin K intake may include an adjustment in diet because of hospitalization or a change in
seasonal eating patterns (1). Unlike other fat-soluble vitamins, stores of vitamin K are rapidly depleted if
intake is deficient (1). This information should be considered when assessing the vitamin K level of a patient
who has had a low intake of food for a week or longer, as may occur in the hospital setting.
Nutrition Intervention and Monitoring
Patients should be educated about the dietary changes that impact anticoagulant therapy. They also should
be informed of foods that are high in vitamin K (III‐3). Patients should be encouraged to keep their diet
consistent with their present pattern. However, if there is a change in diet that includes vitamin K–rich foods,
patients should contact their physician and have their INR/PT monitored.