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Aptt

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Subject: Anticoagulant, Heparin, Antiphospholipid syndrome, Von Willebrand disease, Low molecular weight heparin, Knee replacement, Prekallikrein
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Aptt

"KccT" redirects here. For the radio station, see KCCT.

The partial thromboplastin time (PTT) or activated partial thromboplastin time (aPTT or APTT) is a performance indicator measuring the efficacy of both the "intrinsic" (now referred to as the contact activation pathway) and the common coagulation pathways. Apart from detecting abnormalities in blood clotting,[1] it is also used to monitor the treatment effects with heparin, a major anticoagulant. It is used in conjunction with the prothrombin time (PT) which measures the extrinsic pathway. Kaolin cephalin clotting time (KccT) is a historic name for the activated partial thromboplastin time.[2]

Method

Blood samples are collected in tubes with oxalate or citrate to arrest coagulation by binding calcium. The specimen is then delivered to the laboratory. In order to activate the intrinsic pathway, phospholipid, an activator (such as silica, celite, kaolin, ellagic acid), and calcium (to reverse the anticoagulant effect of the oxalate) are mixed into the plasma sample. The time is measured until a thrombus (clot) forms. This testing is performed by a medical technologist.

The test is termed "partial" due to the absence of tissue factor from the reaction mixture.

Interpretation

The typical reference range is between 30 seconds and 50 s (depending on laboratory). Shortening of the PTT is considered to have little clinical relevance, but some research indicates that it might increase risk of thromboembolism.[3] Normal PTT times require the presence of the following coagulation factors: I, II, V, VIII, IX, X, XI, & XII. Notably, deficiencies in factors VII or XIII will not be detected with the PTT test. Prolonged APTT may indicate:

To distinguish the above causes, mixing tests are performed, in which the patient's plasma is mixed (initially at a 50:50 dilution) with normal plasma. If the abnormality does not disappear, the sample is said to contain an "inhibitor" (either heparin, antiphospholipid antibodies or coagulation factor specific inhibitors), while if it does correct a factor deficiency is more likely. Deficiencies of factors VIII, IX, XI and XII and rarely von Willebrand factor (if causing a low factor VIII level) may lead to a prolonged aPTT correcting on mixing studies.

Laboratory findings in various platelet and coagulation disorders (V - T)
Condition Prothrombin time Partial thromboplastin time Bleeding time Platelet count
Vitamin K deficiency or warfarin Prolonged Normal or mildly prolonged Unaffected Unaffected
Disseminated intravascular coagulation Prolonged Prolonged Prolonged Decreased
Von Willebrand disease Unaffected Prolonged or unaffected Prolonged Unaffected
Hemophilia Unaffected Prolonged Unaffected Unaffected
Aspirin Unaffected Unaffected Prolonged Unaffected
Thrombocytopenia Unaffected Unaffected Prolonged Decreased
Liver failure, early Prolonged Unaffected Unaffected Unaffected
Liver failure, end-stage Prolonged Prolonged Prolonged Decreased
Uremia Unaffected Unaffected Prolonged Unaffected
Congenital afibrinogenemia Prolonged Prolonged Prolonged Unaffected
Factor V deficiency Prolonged Prolonged Unaffected Unaffected
Factor X deficiency as seen in amyloid purpura Prolonged Prolonged Unaffected Unaffected
Glanzmann's thrombasthenia Unaffected Unaffected Prolonged Unaffected
Bernard-Soulier syndrome Unaffected Unaffected Prolonged Decreased or unaffected
Factor XII deficiency Unaffected Prolonged Unaffected Unaffected
C1INH deficiency Unaffected Shortened Unaffected Unaffected

History

The aPTT was first described in 1953 by researchers at the University of North Carolina at Chapel Hill.[4]

References

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