1 How can you identify a patient at risk for bleeding?

Preoperative evaluation includes history, physical examination, and performance of appropriate laboratory tests. Questions about bleeding disorders and problems (e.g., tendency to form large hematomas after minor trauma, severe bleeding while brushing teeth) and bleeding after previous surgical procedures (e.g., dental extractions, tonsillectomy) are important. Prior surgery without transfusion suggests the absence of an inherited coagulation disorder. Review of medications is necessary to identify medications with anticoagulant potential (e.g., nonsteroidal antiinflammatory drugs [NSAIDs], antiplatelet drugs, and anticoagulants). Coagulation studies may confirm a clinical suspicion that the patient has a bleeding disorder. No evidence supports the value of preoperative coagulation studies in asymptomatic patients.

2 What processes form the normal hemostatic mechanism?

Three intertwined processes ensure that blood remains in a liquid state until vascular injury occurs: primary hemostasis, secondary hemostasis, and fibrinolysis.

3 Describe primary hemostasis

Within seconds of vascular injury, platelets become activated and adhere to the subendothelial collagen layer of the denuded vessel via glycoprotein receptors; this interaction is stabilized by von Willebrand’s factor (vWF). Collagen and epinephrine activate phospholipases A and C in the platelet plasma membrane, resulting in formation of thromboxane A2 (TXA2) and degranulation, respectively. TXA2 is a potent vasoconstrictor that promotes platelet aggregation. Platelet granules contain adenosine diphosphate (ADP), TXA2, vWF, factor V, fibrinogen, and fibronectin. ADP alters the membrane glycoprotein IIb/IIIa, facilitating the binding of fibrinogen to activated platelets. Thus a platelet plug is constructed and reinforced.

4 Review secondary hemostasis

Secondary hemostasis involves the formation of a fibrin clot. The fibrin network binds and strengthens the platelet plug. Fibrin can be formed via two pathways (intrinsic and extrinsic) and involves activation of circulating coagulation precursors. Regardless of which pathway is triggered, the coagulation cascade results in the conversion of fibrinogen to fibrin.

5 What are the intrinsic and extrinsic coagulation pathways?

Traditionally these two pathways have been viewed as separate mechanisms that merge after the formation of activated factor X (Figure 7-1). This rigid division has lost absolute validity because of the crossover of many factors. For instance, factor VIIa can activate factor IX; but factors IXa, Xa, thrombin, and XIIa can activate factor VII. However the classic two-pathway model is still useful for the interpretation of in vitro coagulation studies.

Figure 7-1 The clotting cascade, including intrinsic and extrinsic pathways. The roman numerals indicate the different clotting factors. The letter “a” indicates the activated form. HMWK, high-molecular-weight heparin; TF, tissue factor; wVF, von Willebrand’s factor.

(From Griffin J, Arif S, Mufti A: Crash course: immunology and hematology, ed 2, St. Louis, 2004, Mosby.)

The intrinsic pathway occurs within the blood vessel and is triggered by the interaction between subendothelial collagen with circulating factor XII, high-molecular-weight kininogen, and prekallikrein. Platelet phospholipid (PF3) serves as a catalyst to this pathway. The extrinsic pathway begins with the release of tissue thromboplastin (factor III) from the membranes of injured cells.

6 Explain fibrinolysis

The fibrinolytic system is activated simultaneously with the coagulation cascade and functions to maintain the fluidity of blood during coagulation. It also serves in clot lysis once tissue repair begins. When a clot is formed, plasminogen is incorporated and then converted to plasmin by tissue plasminogen activator (tPA) and fragments of factor XII. Endothelial cells release tPA in response to thrombin. Plasmin degrades fibrin and fibrinogen into small fragments. These fibrin degradation products possess anticoagulant properties because they compete with fibrinogen for thrombin; they are normally cleared by the monocyte-macrophage system.

7 Why doesn’t blood coagulate in normal tissues?

Coagulation is limited to injured tissue by localization of platelets to the site of injury and maintenance of normal blood flow in noninjured areas. The monocyte-macrophage system scavenges activated coagulation factors in regions of normal blood flow. Normal vascular endothelium produces prostacyclin (prostaglandin I₂); it is a potent vasodilator that inhibits platelet activation and helps confine primary hemostasis to the injured area. In addition, antithrombin III, proteins C and S, and tissue factor pathway inhibitor are coagulation inhibitors that are normally present in plasma. Antithrombin III complexes with and deactivates circulating coagulation factors (except factor VIIa). Protein C inactivates factors Va and VIIIa; protein S augments the activity of protein C. Finally tissue factor pathway inhibitor antagonizes factor VIIa.

8 What is an acceptable preoperative platelet count?

A normal platelet count is 150,000 to 440,000/mm³. Thrombocytopenia is defined as a count of <150,000/mm³. Intraoperative bleeding can be severe with counts of 40,000– to 70,000/mm³, and spontaneous bleeding usually occurs at counts <20,000/mm³. The minimal recommended platelet count before surgery is 75,000/mm³. However, qualitative differences in platelet function make it unwise to rely solely on platelet count. Thrombocytopenic patients with accelerated destruction but active production of platelets have relatively less bleeding than patients with hypoplastic disorders at a given platelet count.

Assessment of preoperative platelet function is further complicated by lack of correlation between bleeding time or any other test of platelet function and a tendency for increased intraoperative bleeding. However, normal bleeding times range from 4 to 9 minutes, and a bleeding time >1.5 times normal (>15 minutes) is considered significantly abnormal.

9 List the causes of platelet abnormalities

Thrombocytopenia

Dilution after massive blood transfusion

Decreased platelet production caused by malignant infiltration (e.g., aplastic anemia, multiple myeloma), drugs (e.g., chemotherapy, cytotoxic drugs, ethanol, hydrochlorothiazide), radiation exposure, or bone-marrow depression after viral infection

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