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Evaluation of a Prolonged Prothrombin Time

Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO.

^aAddress correspondence to this author at: Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110. E-mail eby@wustl.edu.

The first 300 words of the full text of this article appear below.

CASE DESCRIPTION

A 47-year-old African American woman was evaluated for a prolonged prothrombin time (PT) result obtained before she underwent right total hip arthroplasty. The patient had no history of gastrointestinal or intracranial bleeding, epistaxis, or hemarthrosis. However, she reported a tendency toward easy limb bruising and menorrhagia, which required iron supplementation. She had a negative family history of abnormal bleeding. Initial laboratory studies included findings within reference intervals for complete blood cell count and activated partial thromboplastin time (aPTT) (30.8 s, reference interval 23–36 s), prolonged PT (20.3 s, reference interval 11.0–15.0 s), and International Normalized Ratio (INR) (1.78, reference interval 0.9–1.2). No preanalytical artifacts were identified, and the result of a repeat PT was also prolonged.

DISCUSSION

laboratory evaluation of prolonged results for screening coagulation tests
PT and aPTT are commonly requested screening tests. In vivo, the initiation of coagulation depends on tissue factor–mediated factor VII (FVII) activation, and sustained thrombin generation requires activation of factors XI, IX, VIII, X, and V. For the interpretation of PT and aPTT results, however, coagulation factor activation culminating in a fibrin clot can be organized into intrinsic, extrinsic, and common pathways (Fig. 1 ). An isolated result showing aPTT prolongation suggests a deficiency or inhibitor of one or more of the intrinsic pathway clotting factors (prekallikrein, high molecular weight kininogen, factors XII, XI, IX, and VIII). An isolated PT prolongation suggests a deficiency or inhibition of the extrinsic pathway (FVII), but mild factor X, V, and II deficiencies are also possible causes. Prolongation of both aPTT and PT suggests a deficiency or inhibition of the common pathway coagulation factors (factor X, V, and II), or a qualitative or quantitative fibrinogen defect.

View larger version (13K):   Figure 1. Coagulation factor activation culminating in the generation of a fibrin clot. HMWK, high molecular weight kininogen; PK, prekallikrein; TF, tissue factor.

When evaluating an unexpected prolonged aPTT and/or PT result, the first . . . [Full Text of this Article]

additional patient data
diagnosis
overview of fvii deficiency
patient management
POINTS TO REMEMBER
summary and recommendations