摘要
Hemorrhage following cardiac surgery with cardiopulmonary bypass (CBP) is a major adverse event. Before the COVID-19 pandemic, an average of 288 000 cardiac surgeries were performed yearly in the United States.1 Despite medical advances and improved surgical techniques, CPB still poses risks to the patient. Cardiopulmonary bypass affects the clotting cascade through the loss of receptors for fibrinogen and von Willebrand factor, resulting in dilutional thrombocytopenia and decreased platelet activation.2 Consequently, the altered clotting cascade can lead to acute postoperative bleeding in cardiac surgery patients. For the acute care nurse practitioner (ACNP), it is essential to respond quickly and appropriately to coagulation deficits. The ACNP can use thromboelastography (TEG) to guide blood product administration in the clinical setting.3 Although much of the existing literature has established the benefits of using TEG in the treatment of trauma patients,4 very little clinical research is available that applies to the role of the ACNP in the cardiovascular intensive care unit (CVICU). This article describes how TEG can be used to guide the ACNP in the acute postoperative management and resuscitation of the hemorrhagic cardiac surgery patient who has undergone CPB.The application of TEG has been proven to reduce blood product transfusions, transfusion-related adverse outcomes, and cost.3 Point-of-care testing means TEG results are available within minutes, allowing them to guide immediate clinical decisions during resuscitation when hemostatic abnormalities are suspected.5 There are known risks to blood transfusions, including acute kidney injury, transfusion-related circulatory overload, transfusion-related acute lung injury, and allergic reaction.5 Furthermore, approximately 10% to 15% of all blood products administered in the United States are used during cardiothoracic procedures.5 The literature suggests TEG is effective in patients undergoing complex aortic and cardiac procedures with notable abnormal bleeding.6 When TEG has been used following cardiac surgery, particularly with CPB, there is less need for mediastinal re-exploration and massive blood transfusion.7 As such, this column will review hemostasis, discuss TEG as a novel and innovative approach to evaluating hemostasis within the ACNP’s role, and describe the clinical application of TEG using a case example.Hemostasis is achieved when bleeding is terminated through the formation of a blood clot. The physiological process of hemostasis consists of primary and secondary mechanisms of clot formation followed by clot dissolution. Primary hemostasis occurs with vasoconstriction in response to endothelial injury and the development of a platelet plug through platelet activation, aggregation, and adhesion. Secondary hemostasis follows with the formation of a fibrin clot via coagulation. This formation of the fibrin clot is described as the coagulation cascade, a process that has an extrinsic pathway (tissue factor) and an intrinsic pathway (contact activation) where multiple clotting factors converge at a common pathway, at which point the conversion of fibrinogen to fibrin occurs by the enzyme thrombin. The fibrin strands bind to the platelet plug to create a blood clot. The blood clot will ultimately be broken down through fibrinolysis.This conventional understanding of hemostasis as a cascade does not reflect the dynamic processes occurring on cell surfaces when bleeding occurs. A cell-based model of hemostasis has been proposed to better reflect what is happening in vivo on cell surfaces.8,9 In this model, coagulation is described as overlapping phases that occur after endothelial tissue injury: initiation (factor VIIa and tissue factor), amplification (thrombin activates platelets), and propagation (thrombin/IIa burst).Clinicians’ ability to monitor hemostasis (either through the lens of the coagulation cascade or via the cell-based model) in a hemorrhagic post-CPB patient with traditional laboratory testing remains challenging. Traditional coagulation laboratory tests such as prothrombin time/international normalized ratio (PT/INR) indicate the functioning of the extrinsic pathway of the coagulation cascade. In contrast, partial prothrombin time (PTT) reflects the intrinsic way through fibrinogen and platelet levels. However, current coagulation testing does not predict bleeding. It has limited utility in guiding coagulation management due to a lack of real-time monitoring, inability to identify factor deficiencies, and lack of rapid assessment of fibrinolysis, platelet dysfunction, or hemostatic response to injury or surgery.10,11 Despite limited testing and monitoring, it is estimated that 16% of ICU patients have bleeding caused by a coagulation defect and another 66% have abnormal coagulation test results.12Approved by the US Food and Drug Administration in 2011 for adult patients for whom the evaluation of blood coagulation properties is desired, TEG is a method of viscoelastic testing to evaluate the efficacy of blood coagulation.13 Thromboelastography is based on the principle that the result of the hemostatic process is a clot, and the clot’s physical properties determine the patient’s hemostatic status,14 reflective of cell-based hemostasis. This point-of-care instrument places blood in a cup with a pin. The cup will rotate to imitate sluggish venous flow to activate coagulation. The pin senses the formation of the clot, and the clot formation is displayed in a graph with numerical measurements. The viscoelastic properties of a clot are measured to determine the rate, strength, and stability of a blood clot to determine normal hemostasis, hemorrhagic, or thrombotic characteristics by assessing the underlying cause of altered coagulation. Thromboelastography can show early alterations in coagulopathy so that the ACNP can provide treatment and guide treatment modalities in real-time.Instituting TEG for the CVICU ACNP requires no formal training. A review of the relevant literature can provide the ACNP with the principles of TEG and how to apply it to practice. One of the best ways to understand TEG is through case scenarios and clinical application, as this ensures the ACNP not only is able to conceptualize TEG but can also apply that knowledge in a real clinical scenario. Additionally, if TEG is offered at your hospital, an inservice for ACNPs can be provided by the laboratory developer to enhance understanding of TEG technology.There are 5 components to a TEG test, which measure coagulation and fibrinolysis: reaction time (R-time), kinetic time (K-time), α angle, maximum amplitude (MA), and lysis after 30 minutes (LY-30) (Figure, reflecting normal TEG results that include numerical and graphical data).Reaction time is the time, measured in minutes, from the start of the test to the initial fibrin formation. Like PT/PTT, reaction time measures the length of time for the initial clot to form, which may be prolonged in the setting of anticoagulant use or coagulation factor deficiencies. The reference range for an R-time is 4 to 8 minutes.Kinetic time is the speed to achieve a set level of clot strength (an amplitude of 20 mm), reflecting the interaction between platelets and thrombin. It may be prolonged in the setting of anticoagulation use, thrombocytopenia, or fibrinogen deficiency. The standard K-time is 80 to 130 seconds.The α angle measures the speed at which fibrin builds up and crosslinks. It reflects the kinetics of clot formation and may be increased in hypercoagulable conditions and decreased with anticoagulation. The reference range for the α angle is 53° to 72°.Maximum amplitude measures the maximum clot strength, reflecting platelet activity. The standard MA is 50 to 70 mm.Finally, fibrinolysis can be measured with LY-30, which measures the decrease in clot amplitude 30 minutes after maximum amplitude. This demonstrates how quickly the clot falls apart. Clots that fall apart quickly can be treated with antifibrinolytics, such as aminocaproic acid or tranexamic acid. The reference range for the LY-30 is 0% to 8%.Additionally, reagents, such as kaolin and heparinase, may be used to perform additional testing. Citrated kaolin (CK) and citrated kaolin with heparinase (CKH) will activate the intrinsic clotting cascade. The effect of inhibition by heparin can be seen with heparinase.15A 46-year-old male presented with a significant past medical history of heart failure with reduced ejection fraction of 10% to 15%, first diagnosed in 2021 secondary to ischemic cardiomyopathy with New York Heart Association class IV. He recently received an implantable cardioverter defibrillator and coronary artery bypass grafting and had hypertension and hyperlipidemia. He was admitted to the CVICU for cardiogenic shock, which was discovered following a routine right-sided heart catheterization, and he was evaluated for a heart transplant.The patient was promptly listed as status 1A for a heart transplant. Shortly after he was admitted, a suitable donor became available, and the patient underwent orthotopic heart transplantation with CPB. During the procedure, excessive scar tissue was notable, which caused significant bleeding. As a result, the patient received multiple blood products and remained coagulopathic during his initial presentation to the CVICU. After his procedure, TEG were conducted to manage his coagulopathy.The initial TEG analysis was completed immediately upon admission to the CVICU. The CK reflects the overall status of the coagulation cascade. In addition, since the use of heparin is standard protocol during cardiac surgery, the CKH gives the clinician an indication of the influence of the remnants of circulating heparin on the coagulation cascade from surgery. In this case, the patient’s TEG results indicated that the coagulation cascade was abnormal. Even before the CVICU team received the TEG results, there was concern for surgical bleeding because of a higher-than-expected amount of sanguineous drainage from the chest tube, in excess of 150 milliliters per hour. However, the TEG results obtained upon admission to the CVICU suggest that an abnormal coagulation cascade was the primary cause for any excess ouput from the chest tubes.After the procedure, the CVICU team primarily focused on the results of the CK and the CKH. The TEG results indicate that the coagulation cascade was suboptimal. Both the CK reaction time (14.7 minutes) and the CKH reaction time (13.9 minutes) were elevated, indicating that the patient was taking longer than usual to develop a clot in active bleeding. Considering that the patient in this case report is a postoperative cardiac surgery patient, the development of a clot is most likely due to the influence of circulating heparin. The K-time (1.7 minutes) and α angle (67.5°) indicated that once the clot is initiated, it develops at normal speed and has sufficient strength and consistency to be maintained. On the basis of this data, the indicated treatment was the administration of fresh frozen plasma (FFP), of which the patient was given 1 unit.After the FFP was administered, the patient’s chest output slightly decreased, but the amount of drainage continued to be higher than an ideal similar cardiac surgery patient. After the initial unit of FFP was administered, a follow-up TEG was completed. The graphical results showed an improved reaction time in both the CK and CKH, indicating that the administration of FFP had positively improved the coagulation cascade, and the clot was forming in a shorter period of time. This interpretation was supported by the numerical data, which shows a slight improvement in the CK reaction time (13.2 minutes) and the CKH reaction time (9.4 minutes). In addition, both the K-time and the α angle remained within normal limits, which reassures the clinician that the development of a clot remains normal. At this point, the clinical judgment was to administer an additional 2 units of FFP.After administering the 2 additional units of FFP, it was noted that the chest tube output had significantly decreased to acceptable limits, less than 50 milliliters per hour. The final TEG results showed a normalization of the coagulation cascade. Considering that the clinical picture and the diagnostic data were in accordance, no additional intervention was required.There are limitations to the implementation of TEG in clinical practice. A systematic review found the overall research on the use of TEG had a low quality of evidence with a high risk of bias, but with benefits in favor of TEG.10 Thromboelastography reduced overall mortality (7.4% vs 3.9%; risk ratio, 0.52; 95% CI 0.28-0.95) and affected the proportion of red blood cells, FFP, platelets administered, and overall transfusions.10 However, our clinical experience supports the clinical application of TEG at the point-of-care, where ACNPs can leverage the test for early detection and treatment of post-CPB hemorrhage. More research is needed, including multicenter studies that employ interdisciplinary approaches, to have long-term data on patient outcomes, improve the quality of evidence for using TEG, and establish sound evidence-based transfusion algorithms.16Additionally, TEG is a point-of-care test requiring trained technicians to run the test and maintain the equipment. Point-of-care testing often requires frequent quality control and demonstrated operator competency. Operator variability can affect TEG tracings and results.In the CVICU, ACNPs provide direct care following complex cardiac surgery. The ACNP must rapidly treat postoperative bleeding in cardiac surgery patients through knowledge, diagnostics, and clinical judgment. Swift decisions and actions are critical to avoid complications and further patient deterioration during the acute recovery phase. Fluid resuscitation using crystalloid, colloid, and blood products must be judiciously administered with the highest level of critical decision-making to avoid cardiac compromise.Clinicians understand that the indiscriminate administration of blood products can cause unnecessary postoperative complications because of inappropriate or inadequate treatment of the underlying condition. In addition, nationwide blood shortages require that diagnostic testing increase accuracy in administering this scarce resource.17 Institutions that do not have the appropriate blood products readily available may need alternatives to blood product administration (Table). Protamine, desmopressin, aminocaproic acid, and tranexamic acid can also be used with the appropriate TEG based on clinical judgment.With the use of TEG, the ACNP can interpret a TEG result and guide transfusions accordingly and best manage these complex cardiac patients (Table). Thromboelastography has been proven to be cost-effective, enable a rapid response, and improve clinical outcomes, thereby providing a crucial adjunct in managing the hemorrhagic cardiac surgery patient.3, 18 As the case study demonstrates, TEG can guide resuscitation by allowing the ACNP to determine the correct type of blood products needed to correct coagulopathy, thus reducing the need to return to the operating room for exploration of bleeding.The use of TEG by ACNPs in the clinical area has successfully treated hemorrhagic cardiac surgery patients. Thromboelastography is cost-effective and improves decision-making and clinical outcomes. Thromboelastography is a coagulation test that looks at the entire coagulation process and can be used to guide blood product administration through algorithms, thus improving management of blood products. This knowledge can effectively be used in the direction of blood products in the immediate postoperative period of the bleeding cardiac surgery patient. Thromboelastography provides a quantifiable approach to rapidly identifying and addressing deficiencies in the coagulation cascade through targeted administration of blood products. In addition, TEG can give the cardiac surgery ACNP additional resources to provide rapid and effective treatment of postsurgical bleeding with no major training required.