If a coagulation study shows that a mixing test fails to correct a prolonged aPTT, which explanation is most likely?

If a coagulation study shows that a mixing test fails to correct a prolonged aPTT, which explanation is most likely?

• A. Mixing study corrects with normal plasma
• B. Mixing study fails to correct
• C. Platelet count high
• D. Fibrinogen low

Answer: (B)

The test is about distinguishing whether a prolonged intrinsic-pathway coagulation test (aPTT) is due to a true factor deficiency or the presence of an inhibitor in the patient's plasma using a mixing study. When normal plasma is added, if the aPTT shortens and remains corrected, it points to a factor deficiency because the missing factor from normal plasma fixes the problem. If the aPTT does not correct with mixing, it suggests an inhibitor that neutralizes coagulation factors in both the patient and the added normal plasma. This is the scenario described, where the mixing study fails to correct. So, a persistent prolongation after mixing is most consistent with an inhibitor such as lupus anticoagulant or a specific factor inhibitor (for example, factor VIII inhibitors). The other options don’t fit because a high platelet count doesn’t explain a prolonged aPTT in this context, and a true fibrinogen deficiency would typically be corrected by the addition of normal plasma supplying fibrinogen.

The test is about distinguishing whether a prolonged intrinsic-pathway coagulation test (aPTT) is due to a true factor deficiency or the presence of an inhibitor in the patient's plasma using a mixing study. When normal plasma is added, if the aPTT shortens and remains corrected, it points to a factor deficiency because the missing factor from normal plasma fixes the problem. If the aPTT does not correct with mixing, it suggests an inhibitor that neutralizes coagulation factors in both the patient and the added normal plasma. This is the scenario described, where the mixing study fails to correct.

So, a persistent prolongation after mixing is most consistent with an inhibitor such as lupus anticoagulant or a specific factor inhibitor (for example, factor VIII inhibitors). The other options don’t fit because a high platelet count doesn’t explain a prolonged aPTT in this context, and a true fibrinogen deficiency would typically be corrected by the addition of normal plasma supplying fibrinogen.