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Coordinating PT and PTT Results

Here is some follow-up to the question posted last week by Julie Schartiger MLT (ASCP) from Holzer Medical Center, Gallipolis, OH. Julie wrote: “I was wondering if there was a list of the specific disease states and the correction factors involved.  For example, if a specimen was corrected by the addition of normal pooled plasma, but the Russell viper venom test was abnormal, what disease state would this indicate?  It would be nice to have a chart for quick reference.”

It occurred to me that we need a summary of presumed acquired and congenital coagulation deficiencies related to prothrombin time (PT) and partial thromboplastin time (PTT) results in bleeding patients. Here is a table that may be useful…

  Use this table when bleeding suggests a coagulopathy and the patient is not receiving an anticoagulant.
PT and PTT  Acquired Disorder  Congenital Disorder 
PT prolonged
PTT normal Liver disease
Vitamin K deficiency1 Factor VII deficiency2
PT normal
PTT prolonged Factor VIII inhibitor3
Lupus anticoagulant4 Factor VIII, IX, or XI deficiency5
PT prolonged
PTT prolonged DIC
Liver disease
Lupus anticoagulant
Fibrinogen6, prothrombin, factor V or X deficiency7
PT normal
PTT normal Thrombocytopenia
Qualitative platelet disorder
Acquired von Willebrand disease Mild factor deficiency
Mild von Willebrand disease
Factor XIII deficiency8
1. To distinguish liver disease from vitamin K deficiency, assay factors V and VII. If only VII is deficient, suspect vitamin K deficiency, if both are deficient suspect liver disease. In liver disease, vitamin K therapy may be unsuccessful.

2. Congenital factor VII deficiency is rare and causes mild to moderate bleeding in childhood. The intensity of bleeding correlates poorly with factor VII activity.

3. Factor VIII inhibitor in a non-hemophilic is a rare but life-threatening autoimmune disease called “acquire hemophilia.” The inhibitor is detected using PTT mixing studies and the factor VIII assay. It is measured using the Bethesda titer.

4. Lupus anticoagulant is seldom associated with bleeding but often associated with thrombophilia. Lupus anticoagulant is detected and confirmed with a series of assays and mixing studies described in “Thrombophilia.”

5. Factor VIII and IX deficiencies, hemophilia A and B, are X-linked and are diagnosed in childhood unless mild. Factor XI deficiency, hemophilia C, is autosomal recessive and is most common in Ashkenazi Jews, though it may be found in any ethnic group. The intensity of hemophilia C bleeding correlates poorly with factor XI activity.

6. Fibrinogen deficiency prolongs both PT and PTT, but only when the concentration is < 100 mg/dL. When hypofibrinogenemia is suspected, perform the fibrinogen assay, available from acute and primary care laboratories.

7. Congenital deficiencies of prothrombin, factor V, or factor X are rare.

8. Factor XIII deficiency is established using the urea solubility test or a specific factor XIII assay. This assay may not be available in the acute care facility.

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