Coagulation
 

Activated Partial Thromboplastin Time (APTT)

 
 
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Overview

      • Normal Range

      • 25 - 40 sec
    • Important Lab Points

    • Collected in a sodium citrate tube to prevent coagulation prior to testing.
    • Performed by contact activation - methods vary between labs.
    • Tests the intrinsic and common pathways - kininogen, prekallikrein, XII, XI, IX, VIII, X, V, II, fibrinogen
    • Practical Points

    • APTT can be used to monitor patients on heparin infusions.
    • APTT does not correspond to the coagulative status of patients on novel anticoagulants such as dabigatran, rivaroxaban and apixaban.
    • APTT does not correspond to the coagulative status of patients with liver disease, and most often these patients are also coagulopathic.

Prolonged APTT

    • Causes of Prolonged APTT

    • Isolated Prolonged APTT

    • Unfractionated heparin - therapeutic or contamination
    • Overcoagulation with low molecular weight heparin
    • Factor deficiency - VIII, IX, VI, XII
    • Factor inhibitors
    • Von Willebrand disease
    • Lupus anticoagulant (antiphospholipid antibody)
    • Prolonged APTT and PT/INR

    • Artefactual - high haematocrit
    • Liver disease
    • Disseminated intravascular coagulation (DIC)
    • Common pathway deficiency - X, V, II, fibrinogen
    • Severe vitamin K deficiency
    • Excess heparin (e.g. from heparin in the line)
    • Warfarin
    • Factor IIa inhibitors (dabigatran)
    • Factor Xa inhibitors (rivaroxaban, apixaban)
    • Approach

    • Determine whether the patient is on heparin or any other anticoagulants.
    • Check the patient’s haematocrit, which if elevated will falsely elevate PT/INR and APTT.
    • Look for evidence of chronic liver disease, either in the patient’s past medical history or current clinical state.
    • Assess the patient’s risk of DIC given their clinical state.
    • If unsure about the cause of prolonged APTT, mixing studies can be performed.

    APTT Mixing Studies

    • The patient's plasma is mixed 50:50 with control plasma, and then the APTT is measured.
      • Significance

      • APTT mixing studies to determine the cause of prolonged APTT.
      • Interpretation

      • APTT corrects - factor deficiencyCongenital factor deficiency, Von Willebrand disease, DIC, liver failure, supratherapeutic warfarin
      • APTT does not correct - inhibitor presentHeparin, factor IIa inhibitors, lupus anticoagulant, specific factor inhibitors

    APTT in Heparin Monitoring

    • The APTT is used to monitor the coagulative state of patients on heparin infusions, to ensure that they are receiving a therapeutic dose.
      • Practical Points

      • Consult local guidelines for heparin bolusing, rates and titration.
      • Do not take a sample for APTT testing from the same limb through which the patient is recieving heparin. If there is no other option, then stop the heparin infusion, flush the line and wait several minutes before taking the APTT sample.
      • Excess heparin in the line, e.g. in lines that were heparin locked, will prolong both the PT/INR and APTT.
     
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     Barras M. Anti-Xa assays. Australian Prescriber. 2013 Jun 1;36(3). Besser MW, MacDonald SG. Acquired hypofibrinogenemia: current perspectives. Journal of blood medicine. 2016;7:217. Chitolie A, Mackie IJ, Grant D, Hamilton JL, Machin SM. Inaccuracy of the'derived'fibrinogen measurement. Blood coagulation & fibrinolysis. 1994 Dec 1;5(6):955-7.
    Chng WJ, Sum C, Kuperan P. Causes of isolated prolonged activated partial thromboplastin time in an acute care general hospital. Singapore medical journal. 2005 Sep;46(9):450.
     Chopra N, Doddamreddy P, Grewal H, Kumar PC. An elevated D-dimer value: a burden on our patients and hospitals. International journal of general medicine. 2012;5:87. Eisenberg JM, Clarke JR, Sussman SA. Prothrombin and Partial Thromboplastin Times as Preoperative Screening Tests. Arch Surg. 1982; 117(1): 48-51.  Eisenberg JM, Clarke JR, Sussman SA. Prothrombin and Partial Thromboplastin Times as Preoperative Screening Tests. Arch Surg. 1982; 117(1): 48-51. Giannitsis E, Mair J, Christersson C, Siegbahn A, Huber K, Jaffe AS, Peacock WF, Plebani M, Thygesen K, Möckel M, Mueller C. How to use D-dimer in acute cardiovascular care. European Heart Journal: Acute Cardiovascular Care. 2017 Feb;6(1):69-80. Kamal AH, Tefferi A, Pruthi RK. How to interpret and pursue an abnormal prothrombin time, activated partial thromboplastin time, and bleeding time in adults. InMayo Clinic Proceedings 2007 Jul 31 (Vol. 82, No. 7, pp. 864-873). Elsevier. Katayev A, Balciza C, Seccombe DW. Establishing Reference Intervals for Clinical Laboratory Test Results: Is There a Better Way?. Am J Clin Pathol. 2010; 133(2): 179. Levi M, Opal SM. Coagulation abnormalities in critically ill patients. Critical care. 2006 Jul 19;10(4):222. Lowe GD, Rumley A, Mackie IJ. Plasma fibrinogen. Ann Clin Biochem. 2004; 41: 430. Mani H. Interpretation of coagulation test results under direct oral anticoagulants. International journal of laboratory hematology. 2014 Jun 1;36(3):261-8. Oliver Speer O, Schmugge M, Metzger C, Albisetti M. Reference Ranges of Coagulation Tests. Methods in molecular biology. 2013; 992: 85. Palta S, Saroa R, Palta A. Overview of the coagulation system. Indian journal of anaesthesia. 2014 Sep;58(5):515. Peyvandi F, Garagiola I, Baronciani L. Role of von Willebrand factor in the haemostasis. Blood Transfusion. 2011 May;9(Suppl 2):s3. Wakai A, Gleeson A, Winter D. Role of fibrin D-dimer testing in emergency medicine. Emergency Medicine Journal. 2003 Jul 1;20(4):319-25.
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