Evaluation of a Bleeding Patinet

From the point of evaluation of a bleeding patients haemostasis can be divided into the following parts.

  1. Platelets,
  2. Vessel wall
  3. Coagulation system: The coagulation system has the three parts intrinsic pathway, extrinsic pathway and common pathway.  The framework of intrinsic pathway, extrinsic pathway and common pathway are useful to understand how to interpret coagulation tests but does not reflect how coagulation proceeds in vivo.
    1. Intrinsic pathway: Coagulation by the intrinsic pathway starts by contact activation of factor XII, this in turn sequentially activates factors XI and IX. Activated factor XI with its cofactor activated factor VIII lyse and activate factor Xa. Factor XII has no role in coagulation in vivo.
    2. Extrinsic pathway: Coagulation by the extrinsic pathway involves activation of factor VII by tissue factor.  Activated factor VII then activates factor X.
    3. Common Pathway: Common pathway includes factor X, its cofactor factor V, prothrombin and thrombin
  4. Thrombolytic system.

The first step in the evaluation of a patients with a bleeding tendency is to perform screening tests to determine which part of the clotting system  is involved. This can be done with the use of the following tests.

  1. Prothrombin time: Prothrombin time asses the efficiency of extrinsic coagulation pathway.
  2. Activated Partial Thromboplastin Time: Activate partial Thromboplastin time assess the efficiency of intrinsic coagulation pathway
  3. Thrombin Time: Thrombin time asses the amount and quality of fibrin.
  4. Platelet Counts

The results of first-line tests are interpreted as follows.

    1. All tests deranged (Prolonged PT, APTT and TT and Low platelets): Derangement of all screening tests for coagulation is seen in patients with disseminated intravascular coagulation, coagulopathy of chronic liver disease, and acute live cell failure. Patients who have received a massive transfusion may also show this pattern of first line tests. In addition to there being a history of massive transfusion, these patients do not show increase in fibrin degradation products (D-dimer).
    2. Global coagulation defect with normal platelet counts (prolonged PT, prolonged APTT, prolonged PT normal platelets): All three first-line tests are abnormal in patients with primary fibrinogenolysis, fibrinogen deficiency, dysfibrinogenaemia, liver disease or treatment with conventional heparin.
    3. Global coagulation defect with normal fibrinogen and platelets (Prolonged PT and APTT normal TT and Platelets):
      1. Fibrinogen synthesis is not vitamin K dependent. Lack of vitamin K coenzyme activity, as is seen in vitamin K deficiency or use of warfarin like anticoagulants, affects the factors of the intrinsic system (factor II and IX ) and extrinsic system (factor VII). The PT and APTT prolong but TT which depends only on fibrinogen remains normal.
      2. The components of the common pathway include factor V, X and factor II. Deficiency of these factors or the presence of inhibitors against any of these factors causes prolongation of PT and APTT but a normal TT.  A rare autosomal recessive disorder, combined factor V and VIII deficiency can cause prolongation of PT and APTT with a normal TT.
      3. Some patients with liver disease may have a prolonged PT and TT.
    4. Isolated prolongation of APTT (Normal PT, Prolonged APTT, Normal TT, Normal Platelets counts): The commonest cause of isolated prolongation of APTT is deficiency or inhibitors of factor VIII or factor IX. Deficiency of other components of the intrinsic pathway including factors XI and XII and prekallikrein can cause isolated prolongation of APTT. Of these only deficiency of factor IX deficiency causes bleeding. Deficiency on factor XII and prekallikrein are not associated with bleeding.
    5. Isolated Prolongation of PT (Prolonged PT, Normal APTT, Prolonged TT and normal platelet count):
      1. The commonest cause of isolated prolongation of PT is a deficiency of factor VII. This may be seen in
        1. Vitamin K deficiency/Use of Warfarin type oral anticoagulants: Factors II, VII, IX and X are vitamin K dependent and have half-lives of 65hrs, 5hrs, 25hrs and 40hrs respectively. When vitamin K co-factor activity is not available either as a result of vitamin K deficiency or the use of warfarin type of oral anticoagulants, the synthesis of vitamin K dependent factors decreases.  The half-life of factor VII is considerably shorter than that of other factors and the levels of factor VII fall the earliest. This results in a prolonged PT but a normal APTT. With time other factor levels fall and the APTT also prolongs.
        2. Early Liver disease
      2. The other causes of isolated prolongation of PT include inherited factor VII deficiency, dysfibrinogenaemia or mild factor VIII, IX or IX deficiency
    6. Isolated prolongation of TT: Isolated prolongation of TT is seen in fibrinogen deficiency or dysfibrinogenaemia
    7. Coagulopathy with normal first-line coagulation tests: May be seen in platelet function defects, vascular coagulation defects, mild von Willebrand’s disease, factor XIII deficiency, disorders of fibrinolysis, dysfibrinogenaemia and α2-Plasmin inhibitor deficiency.
    8. Isolated thrombocytopenia: Isolated thrombocytopenia may be seen in bone marrow failure syndromes, immunethrombocytopenia, following viral infection and in patients with hypersplensim or inherited thrombocytopenia.

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