Acquired Causes of Prolonged Prothrombin Time (PT) and Activated Partial Thromboplastin Time (APTT)
PT | APTT | Cause |
---|---|---|
Prolonged | Normal | Warfarin or other vitamin K antagonist therapy |
Vitamin K deficiency | ||
Liver disease | ||
Acquired factor VII deficiency | ||
Inhibitor of factor VII | ||
Normal | Prolonged | Heparin therapy |
Inhibitors of factors VIII, IX, XI or XII | ||
Acquired von Willebrand disease (usually associated with autoimmune or clonal proliferative disorders) | ||
Lupus anticoagulant (associated with thrombosis) | ||
Prolonged | Prolonged | Liver disease |
Disseminated intravascular coagulation | ||
Excess heparin | ||
Excess warfarin or other vitamin K antagonist therapy (ingestion of rat poison) | ||
Heparin+warfarin therapy | ||
Primary amyloidosis-associated factor X deficiency | ||
Inhibitors of prothrombin, fibrinogen or factors V or X | ||
Variable | Variable | The direct-acting oral anticoagulants (dabigatran, rivaroxaban and apixaban) have variable effects on the PT and APTT, depending on the drug, its concentration (the dose-response is not always linear) and the particular laboratory assay. If you have a patient taking one of these drugs who is bleeding, always consult a haematologist. A reversal agent for dabigatran is now available (idarucizumab). See Chapter 103. |