PT and aPTT patterns
Screening patterns, specimen checks, and mixing studies
Prothrombin time (PT) and activated partial thromboplastin time (aPTT) measure clotting after different reagents activate citrated plasma. The factors shared by the two tests explain why either one or both times can be prolonged.1
Patterns and possible explanations2
| Screening pattern | Possibilities to investigate | Interpretive limit |
|---|---|---|
| PT prolonged aPTT in range | VII deficiency/inhibitor; early vitamin K deficiency or warfarin. | Also possible with liver disease or direct factor Xa inhibitors. |
| aPTT prolonged PT in range | VIII, IX, XI, or contact-factor deficiency/inhibitor; heparin; lupus anticoagulant. | Contact-factor deficiency usually causes no bleeding. Lupus anticoagulant can accompany thrombosis. |
| Both prolonged | Common/multiple-factor deficiency: vitamin K deficiency, liver disease, or disseminated intravascular coagulation; anticoagulants. | Compare with platelets, fibrinogen, medications, and targeted tests. |
Specimen and method checks
An underfilled tube leaves excess citrate for the plasma volume and may prolong times. Hematocrit above 55% also reduces plasma volume; adjust citrate under the procedure. Check for clots, heparin from a line draw, delays, and optical interference.3
Anticoagulant effects depend on drug, concentration, and method. Normal times cannot exclude a direct oral anticoagulant.2
What a mixing study shows
Equal volumes of patient and normal plasma supply missing factors. If the time corrects by the method's criteria, deficiency is more likely. Failure to correct suggests an inhibitor or drug. Some inhibitors become apparent only after incubation.1
Mixing also dilutes inhibitors, so a weak inhibitor may be missed. Anticoagulant drugs can mimic an inhibitor pattern.1
Normal screening times do not exclude every bleeding disorder. They can occur in von Willebrand disease, platelet dysfunction, mild factor deficiencies, and factor XIII deficiency.2