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Interpretation of PT and PTT in coagulation disorders
1. Interpretation of PT and
PTT in coagulation disorders
Interpretation of PT and
PTT in coagulation disorders
Dr. Amal Mohamed Ibrahem
Clinical Pathology Specialist
Dr. Amal Mohamed Ibrahem
Clinical Pathology Specialist
2.
3.
4. Causes of prolonged PT include the following:
Warfarin use
Vitamin K deficiency from malnutrition, biliary obstruction,
malabsorption syndromes, or use of antibiotics
Liver disease, due to diminished synthesis of clotting factors
Deficiency or presence of an inhibitor to factors VII, X,
II/prothrombin, V, or fibrinogen
Disseminated intravascular coagulopathy (DIC)
Fibrinogen abnormality (e.g. hypofibrinogenemia,
afibrinogenemia, dysfibrinogenemia)
After bolus administration of heparin (PT may be transiently
elevated)
Massive blood transfusion due to dilution of plasma clotting
proteins
5. PT, large clot in tube • Falsely long redraw.
Consumed factors are gone.
PTT, tube 2/3 full • Falsely long redraw.
Sodium citrate works by binding calcium; in a
short draw tube, the 9:1 ratio of blood
to anticoagulant is not maintained.
There is more citrate than is required for the
smaller amount of plasma (where the calcium is).
Citrate binds all of the patient calcium and the
excess citrate will then bind the calcium provided
in the reagents for a PT or PTT.
Therefore, reagent calcium will not be
available, causing prolonged
clotting times
6. Moderate hemolysis in a PT specimen •No affect
report.
Tissue factor is released when RBCs are damaged.
Excess TF is present in the PT reagent, so its
presence due to hemolysis does not affect the PT.
Moderate hemolysis in a PTT specimen •Falsely short
redraw.
TF is not present in the PTT reagents but it is an
activator.
If it is introduced into the test system due to
hemolysis, the cascade will be partially activated
PRIOR TO adding PTT reagents.
Once PTT reagents are added, the cascade has a
shorter distance to go, so the PTT time will be falsely
short.