Questions
- 1.
Which patients require preoperative coagulation evaluation?
- 2.
What laboratory tests are performed to diagnose preoperative coagulopathies?
- 3.
What are the most common perioperative coagulopathies?
- 4.
How are perioperative coagulopathies diagnosed?
- 5.
A 56-year-old man with hepatitis C cirrhosis and hepatocellular carcinoma involving segments II and III presents for left hepatectomy. Preoperative laboratory tests show hemoglobin concentration, 9.8 g/dL; platelet count, 102 × 10 9 /L; prothrombin time (PT), 16 seconds (normal PT range, 11–15 seconds); international normalized ratio (INR), 1.3; and partial thromboplastin time (PTT), 49 seconds (normal PTT range, 25–39 seconds).
1
Which patients require preoperative coagulation evaluation?
The goal of preoperative coagulation evaluation is to optimize patient safety by identifying prothrombotic and antithrombotic tendencies that may influence the perioperative course. The more recent paradigm shift toward evidence-based approaches to preoperative evaluation and testing includes coagulation. Increased evidence has exposed the shortcomings of routine laboratory testing and point-of-care (POC) devices for monitoring coagulation in goal-directed management of intraoperative coagulopathies is becoming more common.
“Routine” preoperative coagulation studies are not useful. Platelet count, PT, and PTT are rarely abnormal in patients without a clinical indication for such tests (e.g., excessive bleeding after dental procedures). Abnormalities in these screening tests rarely affect intraoperative blood loss but may lead to further unnecessary testing and increased exposure to blood products. Instead of routine laboratory testing, all preoperative coagulation evaluations should begin with a personal and family standardized bleeding history, medication history, and physical examination, with the goal of identifying patients in need of further investigation ( Table 47-1 ). When asked about medications, some patients neglect to mention homeopathic and natural remedies that may affect coagulation.
| Personal and Family History |
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| Physical Examination |
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| Medications |
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| Laboratory Tests |
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When adverse factors are identified, further investigation should be performed to define the specific coagulopathy. A perioperative management strategy can then be designed. An argument can be made for obtaining preoperative coagulation studies in the absence of a bleeding history if the scheduled procedure is associated with a catastrophic (e.g., intracranial surgery) or high (e.g., hepatic resection) risk of bleeding. Preoperative coagulation studies also may be indicated in situations where the patient cannot provide a history (e.g., unconscious patient) and is undergoing a high-risk procedure. However, preoperative coagulation abnormalities may not reflect the etiology of intraoperative coagulopathies.
2
What laboratory tests are performed to diagnose preoperative coagulopathies?
PTT was originally developed to monitor heparin effects on the intrinsic coagulation cascade ( Figure 47-1 ). PTT is sensitive to changes in factors I, II, V, VIII, IX, X, XI, and XII; heparin; fibrinogen degradation products; acquired or congenital factor inhibitors; hypothermia; and hypofibrinogenemia. PT was developed to monitor vitamin K antagonist medications (specifically warfarin) and their effects on the extrinsic coagulation cascade. PT is sensitive to changes in factors I, II, V, VII, and X. To overcome interlaboratory variation in PT caused by different reagents, INR was introduced. Different pretest variables can affect PT and PTT results. Automated PT/PTT instruments can be affected by elevated hematocrit (>55%), which prolongs clotting time; plasma turbidity owing to lipemia (in nonfasting patients), hemolysis, or elevated bilirubin. The time between specimen collection and PTT testing (i.e., >4 hours) can lead to a falsely prolonged clotting time because of factor VIII lability.
Platelets are critical for hemostasis. Tissue injury exposes extracellular matrix proteins to which platelets adhere using von Willebrand factor (vWF) as a bridge. Platelets are then “activated,” releasing fibrinogen, factor V, factor VIII, vWF, adenosine diphosphate, adenosine triphosphate, calcium, serotonin, histamine, an d epinephrine, all of which recruit and activate additional platelets as well as activate plasma-mediated coagulation. Exposed platelet glycoprotein (GP) IIb/IIIa receptors provide binding sites for fibrin cross-linking.
Platelet abnormalities can be either quantitative or qualitative. Quantitative platelet abnormalities are detected by platelet counts most commonly performed by automated machines but may require manual counts when platelet values are abnormally low. Hemodilution and ethylenediamine tetraacetic acid (EDTA)–induced platelet clumping are common causes of falsely low platelet counts. Generally, platelet counts >100 × 10 3 /μL are associated with adequate hemostasis. Although there are no absolute guidelines, platelet transfusion should be considered if the platelet count is <10 × 10 3 /μL or <50 × 10 3 /μL in a patient with bleeding or a perioperative patient. The decision to transfuse platelets must be weighed against the risk of viral or bacterial infection, transfusion-related acute lung injury (TRALI), stroke, and death.
Despite a normal platelet count, qualitative platelet abnormalities may exist (e.g., uremia, von Willebrand disease [vWD], antiplatelet therapy). Platelet function analyzers can detect qualitative platelet abnormalities (see Question 4 for further details). The treatment of qualitative platelet abnormalities depends on its etiology. For example, uremic patients may need dialysis, and patients with vWD may need desmopressin (DDAVP). For patients who are on antiplatelet therapy that can be discontinued safely, elective surgery should be delayed to allow for the effects of the antiplatelet therapy to resolve.
Fibrinogen is a major factor in both the intrinsic and the extrinsic coagulation cascades. Thrombin acts on fibrinogen to form fibrin strands, which are then cross-linked into an insoluble fibrin clot. This mechanism of action is used by the Clauss method to measure fibrinogen concentration. Thrombin is added to the patient’s plasma, and the time to coagulation is a reflection of the fibrinogen concentration. In the presence of colloid volume expanders, the fibrinogen concentration measured by the Clauss method may be artifactually high.
If preoperative coagulation studies are abnormal and sample error, medications, and systemic disease are ruled out as a cause, further testing is necessary to identify the underlying etiology. Mixing studies (i.e., mixing the patient’s plasma with normal plasma) are performed to differentiate between the presence of a factor deficiency or inhibitor, either congenital or acquired. Correction of the PT/PTT by mixing would indicate a factor deficiency, whereas noncorrection would imply the presence of a factor inhibitor. Further investigation would be necessary to identify either the factor deficiency (through specific factor assays) or the specific inhibitor present (e.g., lupus anticoagulant). Consultation with a hematologist may be prudent in the setting of complex preoperative coagulopathies.
3
What are the most common perioperative coagulopathies?
Common perioperative coagulopathies ( Table 47-2 ) include dilutional coagulopathy secondary to massive transfusion, platelet dysfunction, acquired or congenital factor deficiency or factor inhibitor, hyperfibrinolysis, disseminated intravascular coagulation (DIC), heparin excess, and thrombosis.
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