Bleeding After Cardiac Surgery




Abstract


Excessive bleeding after cardiac surgery is a serious complication that affects the patient’s outcome significantly. Therefore, detection of ongoing bleeding, knowledge of risk factors for bleeding, rapid therapeutic decision, and adequate treatment are of utmost importance for appropriate patient management. Here we present a typical case of postoperative bleeding and then discuss all options for diagnosis and hemostatic treatment.




Keywords

blood products, cardiac surgery, hemostasis, postoperative bleeding, risk factors

 




Case Synopsis


A 73-year-old man presents with a history of aortic stenosis, coronary artery disease, peripheral vascular disease, dyspnea at rest, and chronic renal failure (creatinine level 1.6 mg/dL). Myocardial function is moderately reduced (left ventricular ejection fraction is 35%). Combined aortic valve replacement and coronary artery bypass graft surgery is performed. Total cardiopulmonary bypass (CPB) time is 142 minutes. Postoperative bleeding as measured by chest tube output was 2200 mL in the first 24 hours, which is significantly elevated.




Problem Analysis


Definition


Excessive bleeding after cardiac surgery is basically divided into two categories: surgical and nonsurgical. Surgical bleeding can originate from multiple locations—most frequently, vascular anastomoses, cannulation sites, mammary harvesting sites, sternal wires, or atrial and ventricular access sites. Therefore minimizing surgical bleeding requires adequate surgical technique. Nonsurgical bleeding refers to coagulopathy, which recently was categorized as hemodilution, activation, and consumption. For appropriate therapy, all these conditions require specific knowledge about pathophysiologic circumstances that might appear during cardiac surgery.


Recognition


Before reversal of heparinization by an adequate amount of protamine is started, a critical inspection of the surgical field for major vascular bleeding should be performed. To distinguish between surgical and nonsurgical bleeding, it is of utmost importance that surgical suture lines are tight and macroscopic bleeding is avoided by sophisticated surgical hemostasis. If there is ongoing bleeding after protamine administration without a visible vascular leakage, it is up to the anesthesiologist to look for and correct any hemostatic disturbances. Postoperatively, mediastinal chest tube drainage is monitored hourly. As a rough rule of thumb, drainage should not exceed 100 to 125 mL/h for the first 4 postoperative hours, 250 mL for any hour during this period, or 50 to 75 mL/h for the subsequent 24 hours.


Life-threatening hypotension from postoperative bleeding can result from cardiac tamponade or hypovolemia. Nonsurgical hemostatic bleeding should be determined, and appropriate laboratory analysis should be initiated early to obtain results in the operating room (OR) before the patient is transferred to the intensive care unit. Timely detection of particular hemostatic deficiencies ensures specific therapy instead of nonspecific transfusion (“shotgun therapy”) of multiple types of blood products and coagulation therapies.


Risk Assessment


Risk factors for postoperative bleeding include the following:




  • Patient related:




    • Advanced age



    • Chronic steroid use



    • Female gender



    • Chronic liver insufficiency



    • Hematologic/hemostatic disease



    • Preoperative treatment with anticoagulant drugs




  • Procedure related:




    • Prolonged duration of CPB



    • Repeat cardiac procedures



    • Combined procedures (e.g., bypass grafting and valve surgery)



    • Low body temperature after surgery



    • Increased cell salvage usage



    • Unexpected surgical difficulties



    • Intraaortic balloon counterpulsation



    • Internal mammary artery harvesting




Individual screening of patient-related risk factors in the preoperative period is essential to identify patients at increased risk for postoperative bleeding. In addition to medical history, a standardized questionnaire with regard to clinical hemostatic irregularities must be completed and carefully evaluated.


Drugs that affect the coagulation system or platelet function are commonly used in patients scheduled for cardiac surgery. Glycoprotein IIb/IIIa inhibitors, such as abciximab, eptifibatide, and tirofiban, are increasingly used as adjuncts to heparin or aspirin therapy in patients with acute coronary syndromes or in those having preoperative percutaneous coronary interventions. They may even be used for secondary long-term antithrombotic prophylaxis. It is also likely that patients requiring emergent cardiac surgery will have received anticoagulation therapy, specifically antiplatelet therapy, in the catheterization laboratory before transferal to the OR. When in doubt, additional laboratory analysis for specific coagulation disorders may be indicated.


In contrast, procedure-related risk factors are only partially predictable in the preoperative period. Some of the most affecting issues such as duration of CPB, intraaortic balloon counterpulsation, and increased cell salvage can arise during surgery. The same also applies for unexpected surgical difficulties. Whatever the risk factor, the anesthesiologist must determine the hematologic cause of the disorder for a specific treatment.


Implications


The major difference of cardiac surgery compared with other surgical disciplines is the use of the heart-lung machine. This extracorporeal circulation offers the surgeon the opportunity to separate the heart from the blood circuit and maintain the perfusion of the body. However, this procedure requires a temporary iatrogenic inhibition of the coagulation system to avoid clotting in the extracorporeal circuit. This inhibition is almost always performed with a large intravenous dose of heparin. Additionally, use of CPB has multiple implications on the pathogenesis of coagulopathy such as transient activation of platelets, hemodilution, hypothermia, and heparin and protamine.


Mechanical Stress and Contact Activation


When connected to the CPB circuit, the patient’s blood becomes exposed to the artificial surface of the CPB tubes. This contact leads to an activation of the coagulation, fibrinolytic, and inflammatory cascades. Additionally, blood is pumped through the system by a roller pump. This mechanical squeezing means stress to all corpuscular cells in the bloodstream and leads to potentially detrimental damage. Consequently, platelet function is affected, which is considered to be a major contributor to postoperative bleeding. Additionally, the use of pericardial suction devices during surgery damages blood cells and returns activators of coagulation to the CPB system via the venous reservoir. Some of these effects on the hemostatic system have been proposed to be reduced by the use of closed reservoirs, coated CPB circuits, and retransfusion of the suctioned blood after processing in a cell saver.


Hemodilution


Crystalloid CPB priming and cardioplegic solutions lead to a more or less significant dilution of the patient’s blood. The concentration of erythrocytes, platelets, and coagulation factors is reduced depending on the patient’s intravascular volume and the volume of the CPB and cardioplegia. Improvements in the miniaturization of the CPB components for adult patients led to a reduction of the priming volume from well above 2 L in the 1990s to almost 1 L in the 2010s. With that downsizing, the amount of clinical hemodilution and its effect on hemostasis could be reduced significantly. Therefore hemodilution is rarely the sole cause of postoperative bleeding because coagulation factor concentrations of 25% to 30% and platelet counts of 50,000 to 100,000/μL can be tolerated without excessive bleeding if platelet function is normal. Because miniaturization of the CPB circuit is limited by technical issues, the smallest patients, children and newborns, are affected by the largest amount of hemodilution, as much as 200% or more, depending on the individual volume ratio. Nonetheless, progressive evolution led to first clinical reports demonstrating transfusion-free cardiac surgical procedures.


Hypothermia


Hypothermia may result in impaired platelet function and reduced function of temperature-dependent coagulation factors. Also, laboratory coagulation system assessment is uniformly done at 37° C. Therefore misleading results may appear when analyzing cold blood samples obtained during hypothermic CPB. Cooling to more tepid temperatures (mild hypothermia) has been proposed to reduce the activation of inflammatory cascades and lessen coagulation disturbances.


Cell Salvage Systems


Because coagulation factors and platelets are removed during routine red blood cell salvage, retransfused products from cell salvage devices are almost free of these plasmatic components. Additionally, it should be mentioned that direct reinfusion of shed mediastinal blood from postoperative chest tube drainage is not a suitable alternative because it is not recommended as a means of blood conservation and may cause harm (Society of Thoracic Surgeons/Society of Cardiovascular Anesthesiologists [STS/SCA] guidelines, 2008).


Heparin and Protamine


Heparin is the most commonly used anticoagulant that is administered before the patient is connected to the CPB system and extracorporeal circulation is started. After discontinuation from bypass, the anticoagulatory effect is reversed by administration of protamine. Knowing that not only heparin but also protamine has an anticoagulatory effect, the importance of an appropriate dosage is clear. The heparin-protamine complex itself partially suppresses platelet function, which is measureable with a platelet function analyzer. Despite initial adequate neutralization with protamine, heparin rebound can occur 2 to 6 hours afterward, leading to inhibition of platelet function.

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Feb 18, 2019 | Posted by in ANESTHESIA | Comments Off on Bleeding After Cardiac Surgery

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