Bleeding Tendency Dr Mervat Khorshied Ass Prof of

Bleeding Tendency Dr. Mervat Khorshied Ass. Prof. of Clinical and Chemical Pathology

A bleeding disorder is an acquired or inherited tendency to bleed excessively. Normally, the body stops the blood loss through a complex clotting process called hemostasis.

During hemostasis, the injured blood vessel constricts to reduce blood flow, the platelets adhere to the injury site and aggregate together to form a loose platelet plug, and a process of clot formation is initiated through activation of coagulation cascade.

Platelet Function Adherence Only Direction of Blood Flow Aggregation & Release

Once the coagulation cascade has been initiated, coagulation factors are activated one after the other in a sequential process. Initiation of the coagulation cascade (either intrinsic or extrinsic pathways), fibrinogen changes into insoluble fibrin threads.

These threads crosslink together to form a fibrin net that then stabilizes the clot at the injury site. The fibrin net adheres to the site of injury along with aggregated platelets to form a stable blood clot. This barrier prevents additional blood loss and remains in place until the injured area has healed.

Hemostasis is a dynamic process, though, so once a clot is formed, certain factors are activated to slow the clotting process (natural anticoagulants). They eventually begin to dissolve the clot in a process called fibrinolysis so that the clot is removed when the injury site is healed.

Bleeding disorders occur when something goes wrong with the clotting process. If a component is missing, deficient, or dysfunctional, excessive bleeding may occur. Abnormalities may involve: 1 -Platelet defect. 2 - Vascular defect. 3 -Coagulation coagulation factor defect.

• Vasular defect: defective structure of the blood vessels. • Platelet defects: decreased platelet count (Thrombocytopenia) or defective platelets function (Thromaesthenia). • Coagulation factor defects: as defective production or function of one or more of the coagulation factors.

Approach to a bleeding patient: For accurate diagnosis of the cause of bleeding, we should follow certain scheme to reach our goal: - Proper history taking. - Screening tests for various components of the normal haemostatic mechanism. - Further tests as directed by the screening tests.

The following questions should be considered as part of the patient's history: • What is the duration of the bleeding disorder (is inherited or acquired)? • Is there a family history of bleeding (for inherited disorders)? • Is it spontaneous bleeding or following surgery or trauma (for defibrination disorders as DIC)? • What is the location and type of bleeding? • History of liver diseases (for Factor K dependent factors defiency).

Bleeding disorder testing is a step-by-step investigative procedure. A-Screening tests for platelets and vascular defects: 1 -Complete blood cell count (CBC): to evaluate the number and morphology of platelets. • For thrombocytopenia, BM aspiration is recommended to check platelet production. Platelet lifespan and isotypic recovery. • If the platelet count is normal or slightly decreased, go for platelet function tests which are platelet aggregation, platelet adhesiveness and clot retraction test.

2 -Bleeding time (BT): It is a screening test for platelet number, platelet function. 3 -For vascular purpura, Capillary Hess test is recommended

B- Screening tests for coagulation defects: • Prothrombin Time (PT): PT evaluates the extrinsic and common coagulation pathways (Factors V, X, Prothrombin and fibrinogen). It is also used to monitor the effect of oral anticoagulant therapy.

Prolonger PT can be encountered in cases with defective or decreased synthesis of vitamin K dependent factors (F II, VII and X), intake of oral anticoagulants, F V deficiency, end stage liver disease, obstructive jaundice, DIC, hypofidrinogenemia, circulating anticoagulants or excess fibrin degradation products (FDPs).

PT is not a sensitive test o factor IX activity. To overcometh is problem, we do the Thrombotest of Owren which measurest he PT together ith F IX. If the PT is prolonged, proceed to correction tests. If the PT is corrected, it is factor deficiency and proceeds to individual factor assay.

Activated Partial Thromboplastin time (a. PTT): • a. PTT evaluates the intrinsic and common coagulation pathways (measures all factors except VII and XIII). It is also used to screen for lupus anticoagulant and to monitor Heparin therapy. a. PTT is not a sensitive test o detect mild factor deficiency as mild defiency of F VIII. Many a. PTT reagents vary in detecting the lupus anticoagulant.

• If the a. PTT is prolonged, proceed to corrections studies. If the a. PTT is corrected, it is factor deficiency and proceeds to individual factor assay. If not, this may be due to: -Heparin therapy: Measure thrombin time (TT) and reptilase clotting time. Prolonged TT with normal reptilase time indicates that Heparin is present. -Presence of lupus anticoagulant: Test for lupus anticoagulant. -Presence of factor inhibitors.

• Thrombin time (TT): TT tests the last stage of the coagulation process which is the conversion of fibrinogen to fibrin. It is commonly performed when there is prolonged PT and PTT as in fibrinogen deficiency (quantitative or qualitative), heparin or presence of fibrin degradation products (FDPs). If TT is prolonger, proceed to reptilase clotting time, if normal it indicated the presence of Heparin. If not, test for FDPs and assays for fibrinogen (functional and immunologic).

Testsf or fibrinolysis: • • • Fibrinogen titre. Whole blood clot lysis test: screening test for acute fibrinolysis. Euglobin clot lysis test: assay for plasminogen activators. Fibrinogen estimation. Detection of FDPs (fibrinogen and fibrin degradation products): by immunological methods as Latex aggregation. • D-Dimers (fibrin degradation products): by immunological methods as Latex aggregation.

Laboratory evaluation of a prolonged prothrombin time (PT) and activated partial thromboplastin time (a. PTT). Bombeli T , Spahn D R Br. J. Anaesth. 2004; 93: 275 -287 © The Board of Management and Trustees of the British Journal of Anaesthesia 2004