Coronary Artery Bypass Graft (CABG)

Patients undergoing CABG are initially in a state of imbalance toward hypercoagulable state. The exposure of the patient's blood to the cardiopulmonary bypass (CPB) circuitry diminishes the hypercoagulable state and proceeds into an imbalanced hypocoagulable phase. Exposure to negatively-charged CPB surfaces invariably leads to the activation of platelets and the intrinsic pathway, while the tissue traumatized by surgery exposes TF to the blood stream, leading to activation of the extrinsic pathway. In addition, exposing the blood to artificial surfaces, the accompanying flow turbulence, the effect of the oxidation by the CPB pump further leads to platelet activation and damage. All this leads to consumption of coagulation proteins and platelets, and together with the dilutional coagulopathy results in approximately 50% reduction in platelet number and coagulation factors, shifting the balance from a hypercoagulable to hypocoagulable state. Also, in 5-7% of patients undergoing CPB cardiac procedures the endothelium reacts to the trauma of surgery by releasing high levels of TPA, which in the presence of a hypocoagulable state, leads to primary fibrinolysis. Accordingly, as we treat the patient to achieve a restoration of normal hemostasis and recovery of vascular integrity with blood products and/or pharmaceutical agents, we shift the hypocoagulable state to normal or beyond to a hypercoagulable state. The CPB circuit activates the hemostasis process, introduces emboli, and even microscopic debris that further activates these elements once circulating in the patient's vasculature. Once the patient reaches the post-protamine stage, a restoration of his initial "normal" hemostasis - an imbalance towards hypercoagulability -- is reinstated.

Case Study


 
57yo female with Marfan syndrome and history of aneurysm presents now with a second aneurysm. Platelet count is approximately 16K.
Progress/Findings TEG® tracings
(normal shown for comparison)
(Normal tracing)
Platelet count 16K, MA and CI are low.
On pump. Lower MA indicates minimal platelet function; clot is mostly fibrin. CI is very low and R slightly elongated, attributable to low levels of phospholipid surfaces to support the enzymatic reaction.
Rewarming. Platelet function is still deteriorating. 12 U platelets given.
Post protamine. All parameters are approaching normal. The patient was oozing, and typically would not be treated, to allow time for the heparin/protamine to be metabolized. New platelets are forming, platelets are rewarming, coming back into circulation, etc. However, in this case, the Marfan syndrome was a concern, and another 6 units of platelets were administered.
Post-op. After treatment, everything looks normal. The patient's first hour chest tube drainage was less than 100 cc.
 
References

Spiess BD, "Transfusion and Outcome in Heart Surgery". Ann Thorac Surg 2002; 74:986-7.

Editorial that calls for a reduction of transfusions in cardiac, especially CABG, surgery to lower complications, mortality, and morbidity rates associated with transfusions.

Von Kier S, Wade C, Cheung V, Royston D. "Benefit of Intraoperative TEG® algorithm to reduce platelet transfusion associated adverse outcome in higher risk cardiac surgery patients." Abstract presented at the American Society of Anesthesiologists, 2001.

Details a prospective study of 37 patients that shows platelet transfusions are associate with adverse outcomes in higher risk patients, and how use of the TEG®-guided hemostasis and blood management algorithm is associated with an 8-fold reduction in platelet administration.



Coronary Artery Bypass Graft (CABG)
Liver transplantation
Exposure to artificial surface devices (ASD)
Percutaneous Coronary Angioplasty (PTCA)
Disseminated Intravascular Coagulation (DIC)



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