Reflects all the classical clotting factors in the intrinsic and common coagulation pathways except factor VII.
Measures the activity of the intrinsic factors VIII, IX, XI, and XII and common coagulation pathways.
Developed to evaluate patients with hemorrhagic problems such as spontaneous bleeding, or bleeding after minor trauma or surgery, but is also used to monitor anticoagulants such as the unfractionated heparin and parenteral direct from being inhibitors, and to recognize inhibitors of coagulation factors like lupus anticoagulants.
The activated partial thromboplastin time is used to monitor unfractionated heparin anticoagulation when heparin is administered intravenously to achieve a target therapeutic range of 0.2 to 0.8 international units per milliliter for the treatment to a prevention of thrombosis.
Different therapeutic ranges for patients with acute coronary syndromes and those with venous thromboembolism exist.
Citrated patient plasma is re-calcified, phospholipid is added and the sample is incubated with the contact factor activator.
The time from re-calcification to clot formation is measured in seconds.
Most aPTT assays rely on optical density to detect fibrin clot formation.
Sensitivities of various reagents are highly variable to factor deficiencies, heparin and lupus anticoagulants.
Can be elevated when coagulation factor deficiency in common pathway of coagulation cascade is present and includes: fibrinogen, factor II, factor V or factor X.
Unfractionated heparin and low molecular weight heparin exert effect by antithrombin mediated inhibition of thrombin (Factor II) in the final common pathway, resulting in a prolongation of the activated PTT (APTT).
The test is performed by mixing the patient’s plasma with phospholipid calcium and an activator which leads to activation of the clotting factors in the intrinsic pathway, with that time to form a clot as the PTT result.
The PTT result varies with various instruments and reagents in each laboratory, and each laboratory has its own reference range.
Patients should have a PTT prior to initiation of anticoagulant therapy, such as unfractionated heparin or a parenteral direct thrombin inhibitor to get a baseline result.
Patients with venous or arterial thrombosis should have an initial PTT test to screen for possible lupus anticoagulants.
An elevated PTT suggests the presence of any coagulation factor deficiency state or presence of an inhibitor.
Acquired prolonged aPTT has four possibilities: therapeutic anticoagulation, lupus anticoagulant, acquired from Willebrand factor deficiency, and acquired inhibitor of factor VIII, IX, or XII.
The only way to differentiate between a factor deficiency or the presence of an inhibitor with a prolonged PTT is to perform a mixing study.
A mixing study refers to mixing the study plasma with a one-to-one ratio of normal pooled plasma and the PTT test is repeated- if the test results corrects it is suggested that there is a clotting factor deficiency.
Factor deficiencies can be subsequently identified on the basis of a normal prothrombin time with the most likely factors being deficient in the intrinsic pathway-factors VIII, IX, XI, and XII.
Factor deficiencies can be identified if both PT and PTT are prolonged deficiencies in the intrinsic and extrinsic pathways or a deficiency in the final common pathway can be present.
A mixing study that does not correct suggests the presence of an inhibitor.
Three categories of inhibitors are present that increase the PTT: 1-drugs that act as inhibitors including heparin and direct thrombin inhibitors such as lepirudin, argatroban, and the oral agent dagibatran, 2-Inhibitors directed against blood clotting factors such as factor VIII, and spontaneous development of inhibitor of factor VIII, a the autoimmune hemophilia A inhibitor, and 3-nonspecific inhibitors such as lupus anticoagulants.
Artifactual causes of prolongation of the PTT include very high hemoglobin or hematocrit levels, contamination with heparin.
Children have a longer of PTT than adults.