Type of test Blood

Normal findings

 (These depend on reagents used for PT.)

 11.0-12.5 seconds; 85%-100%

Full anticoagulant therapy: > 1.5-2 times control value; 20%-30%

INR: 0.8-1.1

Possible critical values

 20 seconds

 INR: > 5.5

Test explanation and related physiology

The PT is used to evaluate the adequacy of the extrinsic system and common pathway in the clotting mechanism. The PT measures the clotting ability of factors I (fibrinogen), II (pro thrombin), V, VII, and X. When these clotting factors exist in deficient quantities, PT is prolonged. Many diseases and drugs are associated with decreased levels of these factors. These include the following:

 • Hepatocellular liver disease (e.g., cirrhosis, hepatitis, and neoplastic invasive processes). Factors I, II, V, VII, IX, and X are produced in the liver. With severe hepatocellular dysfunction, synthesis of these factors will not occur.

• Obstructive biliary disease (e.g., bile duct obstruction secondary to tumor or gallstones or intrahepatic cholestasis secondary to sepsis or drugs). As a result of the biliary obstruction, the bile necessary for fat absorption fails to enter the gut, and fat malabsorption results. Vitamins A, D, E, and K are fat soluble and also are not absorbed. Because the synthesis of factors II, VII, IX, and X depends on vitamin K, these factors will not be adequately produced and serum concentrations will fall.

• Parenchymal (hepatocellular) liver disease can be differentiated from obstructive biliary disease by determination of the patient’s response to parenteral vitamin K administration. If PT returns to normal after 1 to 3 days of vitamin K administration (10 mg intramuscularly twice a day), one can safely assume that the patient has obstructive biliary disease that is causing vitamin K malabsorption. If, on the other hand, PT does not return to normal with the vitamin K injections, one can assume that severe hepatocellular disease exists and that the liver cells are incapable of synthesizing the clotting factors no matter how much vitamin K is available.

 • Oral anticoagulant administration. The coumarin derivatives dicumarol and warfarin (Coumadin, Panwarfin) are used to prevent coagulation in patients with thromboembolic disease. These drugs interfere with the production of vitamin K–dependent clotting factors, which results in a prolongation of PT, as previously described. The adequacy of coumarin therapy can be monitored by following the patient’s PT. The ideal INR must be individualized for each patient (Table 1).

Table1. Preferred international normalized ratio (INR) according to indication for anticoagulation

 PT test results are usually given in seconds, along with a control value. The control value usually varies somewhat from day to day because the reagents used may vary. The patient’s PT should be approximately equal to the control value. Some laboratories report PT values as percentages of normal activity, because the patient’s results are compared with a curve representing normal clotting time. Normally, the patient’s PT is 85% to 100%.

To have uniform PT results for physicians in different parts of the country and the world, the World Health Organization has recommended that PT results include the use of the INR value. The reported INR results are independent of the reagents or methods used. Most hospitals are now reporting PT times in both absolute and INR numbers.

Such factors as weight, body mass index, age, diet, and con current medications are known to affect warfarin dose requirements during anticoagulation therapy. Warfarin interferes with the regeneration of reduced vitamin K from oxidized vitamin K in the vitamin K oxidoreductase (VKOR) complex. A recently identified gene for the major subunit of VKOR, called VKORC1, has been identified and may explain up to 44% of the variance in warfarin dose requirements. Furthermore, warfarin is metabolized in part by the cytochrome P-450 enzyme CYP2C9. The CYP2C9∗2 and CYP2C9∗3 genetic mutations have been shown to decrease the enzyme activity of these metabolizing enzymes, which has led to warfarin sensitivity and, in serious cases, bleeding complications. A warfarin pharmacogenomic test panel is available that can identify any mutations in the VKORC1-1639, CYP2C9∗2, or CYP2C9∗3 genes. The warfarin pharmacogenomic test can be used as part of an algorithm to determine the best initial warfarin dose and does not replace the need for routine PT testing for the calculation of the INR.

Point-of-care home testing is now available for patients who require long-term anticoagulation with warfarin. Like glucose monitoring, a finger stick is performed. A drop of blood is placed on the testing strip and inserted into the handheld testing device. The PT and INR are provided in a few minutes. The treating physician is notified by phone and any therapeutic changes can be instigated the same day.

Interfering factors

• Alcohol intake can increase PT levels.

 • A high-fat diet may decrease PT levels.

* Drugs that may cause increased levels include allopurinol, aminosalicylic acid, barbiturates, beta-lactam antibiotics, cephalosporins, cholestyramine, chloral hydrate, chlorpromazine, cimetidine, clofibrate, colestipol, ethyl alcohol, glucagon, heparin, methyldopa, neomycin, oral anticoagulants, propylthiouracil, quinidine, sulfonamides. quinine, salicylates, and Drugs that may cause decreased levels include anabolic steroids, barbiturates, chloral hydrate, digitalis, diphenhydramine, estro gens, griseofulvin, oral contraceptives, and vitamin K.

 Procedure and patient care

• See inside front cover for Routine Blood Testing.

• Fasting: no

• Blood tube commonly used: light blue

• Obtain the blood specimen before the patient is given the daily dose of warfarin.

• Remember, hemostasis will be delayed if the patient is taking warfarin or if the patient has any coagulopathies.

• Patients taking warfarin will have their doses regulated by PT and INR values.

• If the PT is greatly prolonged, evaluate the patient for bleeding tendencies.

* Teach patients on warfarin to check themselves for bleeding.

• The anticoagulant effect of warfarin can be reversed by the slow parenteral administration of vitamin K.

* Instruct patients on warfarin therapy not to take any other medications unless approved by their physician.

 Abnormal findings

 Increased levels

- Cirrhosis

- Hepatitis

- Vitamin K deficiency

- Salicylate intoxication

- Bile duct obstruction

- Coumarin ingestion

- DIC

- Massive blood transfusion

- Hereditary factor deficiency

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