INR for Hemophilia A patient.

Nurses General Nursing

Published

Ok.... so I understand why aPTT would skyrocket for patient with Hemophilia A and Factor VIII level of ....!!!

How does this same patient have a normal PT/INR?

I know some patients with mild-to-moderate Hemophilia can have normal PT/INR levels... but this guy has practically no Factor VIII...

how is he clotting?

:confused:

Specializes in ER, L&D, RR, Rural nursing.

Have you asked the lab? I have found all sorts of interesting facts from the lab. Also is this an anomaly? Maybe the test was false normal. I would want to have access to his other INR results as well as lytes, ect. Also INR tests the tendency to clot via the extrinsic pathway, that doesn't mean that he will in fact clot. I would suggest checking out the following site:

http://www.med.unibs.it/~marchesi/blood.html#clinical

Also try looking in your unit lab manual. There are many variables that could explain the weirdness. Good Luck I really hate it when the labs don't appear to make sense.

Specializes in Med-Surg, Geriatrics, Wound Care.

APTT is a test for hemophilia (lacking FVII or FIX). That test checks the intrinsic pathway (The clotting factor that doesn't occur with the release of tissue factor). The PT - would test for things like anti-coagulants. The PT is a prothrombin time, and is part of the extrinsic system. It is one of the final parts of the coagulation cascade, bypassing the activities of VIII (and IX).

The PT doesn't take into account the lack of FVIII. It takes into account inhibitors agains the final clots (thrombin/fibrin formation). A person with heparin in their system will inhibit the PT clotting time.

The coagulation tests are done using blood collected with sodium citrate. Sodium citrate binds divalent cations (calcium). Calcium is reuqired for blood to clot. An APTT will combine the patient's sample with an equal part of factor deficient plasma (so, another hemophilic plasma). APTT reagent is added (it is like adding platelets, for the chemical reactions to occur on). Then, a lot of calcium is added, and coagulation can occur (if there is enough FVIII/FIX in the patient sample, or via the extrinsic pathway).

I forget how the PT works, but I'd assume it will add complete plasma or thrombin, and then use the calcium to get the coagulation to occur. If there is heparin in the plasma, the patient will not clot. This is also why you can't use heparin tubes to collect blood for coagulation assays. The heparin inhibits coagulation.

I hope that makes some sense.

If you recall, blood clotting can occur by two pathways. One is referred to as the extrinsic pathway, and occurs when factor VII is released from vascular endothelium. The other (the 'instrinsic' pathway) begins with the activation of factor XII, proceeds through a variety of steps, and as pointed out above uses calcium as a cofactor.

Both these pathways converge when they reduce factor X to Xa, which converts prothrombin to thrombin.

The reason we test both PT and aPTT is that each measure the activity of a specific pathway. The PT tests the functionality of the extrinsic pathway, while the aPTT tests the intrinsic pathway.

Factor VIII is only involved in the intrinsic pathway, and is not necessary for the extrinsic pathway. Therefore, a person with Factor VIII deficiency, no matter how severe, should have a normal PT.

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