Please print and use the Specimen Collection Bulletin as a tube-filling guide.

Requirements for patients receiving heparin are different: If testing cannot be performed within 1 hour of collection, frozen plasma must be submitted. Specimens should be centrifuged for at least 15 minutes at 1500xg to produce platelet-poor plasma, and the plasma quick frozen and maintained in this condition until tested.

A large number of conditions can complicate the use of the aPTT in monitoring UFH therapy,⁷ The College of American Pathologists (CAP) divided these factors into three groups.⁷ The first group of complicating factors encompasses those that affect the bioavailability of heparin. Aging, obesity, changes in heparin binding proteins, hepatic disease, renal disease, and heparin resistance fall under this heading. The second group of complicating factors includes those that alter the aPTT dose response to heparin.

Increased factor VIII or fibrinogen levels, decreased antithrombin levels, or a mild reduction in multiple factors (as might be seen in the early stages of a consumptive coagulopathy or in oral anticoagulant therapy) are examples of this type of complicating factor. Lastly, those factors that tend to cause a prolonged aPTT in the absence of heparin therapy should be considered. Lupus anticoagulants or deficiency in contact factors can produce an extended baseline aPTT. In all of these cases, the heparin anti-Xa assay may be more appropriate for monitoring heparin therapy. The aPTT should not be used for therapeutic monitoring of low molecular weight heparin or danaparoid.^7,8

An extended aPTT can be seen in acquired deficiencies of intrinsic factors II, IX, and X that result from vitamin K deficiency or the use of oral anticoagulants that block vitamin K-dependent production of procoagulant factors. These conditions also affect the level of factor VII, an extrinsic pathway factor. Since factor VII has a short half-life relative to the vitamin K-dependent factors of the intrinsic pathway, nutritional or therapeutic vitamin K-dependent factor deficiency can sometimes result in an extended PT with a normal aPTT. Consumption coagulopathies, such as disseminated intravascular coagulation (DIC), can produce an extended aPTT due to depletion of intrinsic factors. The aPTT can also be extended in conditions that reduce the production of procoagulant factors (ie, severe liver disease or malnutrition). Inhibitors, both factor specific and nonspecific, can also prolong the aPTT. A description of the many potential causes of an extended aPTT is described in more detail in the Coagulation Appendix.

Unfractionated heparin is commonly used to limit fibrin clot formation in individuals with increased risk of venous or arterial thrombosis.¹² Overdosing with heparin can increase the risk of hemorrhage and inadequate dosing decreases the efficacy of anticoagulation. Heparin works as an anticoagulant by enhancing the ability of plasma antithrombin to bind and inactivate the serine proteases XII, XI, IX, X, and thrombin. Therapeutic monitoring with the aPTT is commonly used because of the wide interindividual variation in response to this therapy. However, this application of the aPTT test can be less than optimal in a number of clinical circumstances (see Limitations).