Platelet Aggregation in Microsurgical Anastomotic Failure, Term Paper Example

During some surgeries, many patients experience complications in the form of platelet aggregation and promote the formation of thrombosis (Nesbitt et.al, 2009). Microvascular surgery also leads to complications with anastomotic failure due to the poor vessel sizing matches (Rickard et.al, 2009). During microsurgery, there is always a risk of platelet aggregation even under circumstances where inhibition factors are present (Jokuszies et.al, 2012). Microsurgery often utilizes heparin to reduce platelet aggregation and subsequent thrombosis; however, there is an increased risk of bleeding that must also be considered (Mo et.al, 2009). Therefore, it is imperative to determine how to perform microsurgery in order to minimize possible complications and the risks associated with platelet aggregation and thrombosis.

The prevention of microsurgical anastomotic failure and platelet aggregation is essential for patient recovery; however, there is no single method that has been proven effective for all patients who face these risks (Dumont et.al, 2011). Therefore, the decision is left to the surgeon to determine which method or approach might be most appropriate (Dumont et.al, 2011). Microsurgical-based techniques and medication administration are essential to success in many types of surgeries and the ability to monitor any events that may lead to platelet aggregation and possible thrombosis (Djohan et.al, 2010). In this context, it is important to recognize that microsurgery remains a relatively new practice and requires additional effort to achieve the desired results with minimal complications for most patients (Djohan et.al, 2010). With this perspective in mind, platelet aggregation remains a common phenomenon with many types of microsurgery and is difficult to avoid, particularly since medication-based alternatives have mixed results (Djohan et.al, 2010). These developments demonstrate that there is a significant opportunity for surgeons to better examine platelet aggregation and to determine the best possible alternatives on a case-by-case basis so that this event is reduced as much as possible (Djohan et.al, 2010).

Antiplatelet Therapy and its Impact on Graft Survival

Administering antiplatelet therapy is an effective resource in promoting successful grafting, particularly for bypass surgery (Jackson et.al, 2010). It is known that “The current recommendation is that all patients are on an antiplatelet agent following bypass grafting, the only intervention with significant evidence supporting use” (Jackson et.al, 2010, p. 612). Another perspective indicates that the use of dual forms of anticoagulant therapy do not provide any real benefits to patients and therefore, should not be pursued after grafting is complete (Banerjee et.al, 2011). In any case, a single method of antiplatelet therapy is of critical importance as a means of preventing further complications and the possible rejection of grafts (Banerjee et.al, 2011). In the process of coronary artery bypass graft (CABG) surgery, it is evident that antiplatelet therapies continue to be questioned by some experts for their safety and efficacy during these surgeries (Kulik et.al, 2009). It is known that “Despite > 30 years of experience with antiplatelet agents during CABG, questions remain regarding their perioperative safety and efficacy” (Kulik et.al, 2009, p. 169). Therefore, additional research-based evaluation is recommended in order to reduce the risk of graft rejection and the potential complications of this type of therapeutic intervention (Kulik et.al, 2009).

It is recommended that patients who are administered antiplatelet therapy for CABG must continue this treatment because if it is discontinued, there is a much greater risk of serious complications and death for many patients (Montalescot et.al, 2010). Therefore, it is important to recognize these limitations and to take them seriously in an effort to produce effective outcomes for this patient population and to promote graft survival as best as possible (Montalescot et.al, 2010). It is also necessary to consider the early administration of antiplatelet therapies prior to CABG to minimize the risks associated with this type of surgery and the promotion of graft survival, in spite of the potential bleeding risks related to this treatment (Trachoitis, 2010). One therapy to consider terminating prior to surgery is aspirin due to the high risks associated with bleeding while using this therapy (Oscarsson et.al, 2010). It is important to consider the different options that are available the risks that are involved in sustaining antiplatelet therapy for CABG to reduce graft rejection.

Antiplatelet therapy should also be considered for its potential counterindications, as some patients become resistant to this type of therapy and find it difficult to obtain benefits from it (Gurbel and Tantry, 2013). Therefore, it is important to consider the different options available when considering the administration of antiplatelet therapy to surgical patients, such as phenotyping or genotyping events to determine if there is a potential resistance associated with this pharmacological therapy (Gurbel and Tantry, 2013). Furthermore, antiplatelet function is critical in achieving optimal recovery from CABG, but heavy and routine monitoring must be conducted on these patients in order to achieve the desired outcomes (Patni et.al, 2012). Platelet function must be continuously monitored and evaluated in an effort to prevent coronary bypass graft rejection in as many cases as possible (Patni et.al, 2012).

The development of successful methods to address antiplatelet therapy in patients who require coronary artery bypass graft surgery must be based upon existing knowledge as demonstrated by surgeons and researchers in this area in order to achieve effective results with this patient population. This determination is made by exploring the different elements of antiplatelet therapies, including their benefits and risks, as a means of influencing outcomes effectively.

References

Banerjee, S., Ahmad, I.., Master, R., Wiedeman, R., Little, B., Rao, S.V., and Brilakis, E.S. (2011). Dual antiplatelet therapy following coronary artery bypass surgery: predictors and outcomes. JACC, 57(14), 1.

Djohan, R.S., Gage, E., and Bernard, S.L. (2010). Microsurgical techniques. Plastic and Reconstructive Surgery, 89-100.

Dumont, L.A., Gangloff, G., Grolleau-Raoux, J.L., Chavoin, J.P., and Garrido-Stowhas, I. (2011). Evidence-based medicine and prevention of thrombosis in microsurgery. Critical review. Annales de chirugie plastique et estitique, 56(3), 219-231.

Gurbel, P.A., and Tantry, U.S. (2013). Antiplatelet drug resistance and variability in response: the role of antiplatelet therapy monitoring. Antiplatelet and Anticoagulation Therapy, 45-112.

Jackson, A.J., Coats, P., Orr, D.J., Teenan, R.P., and Wadsworth, R.M. (2010). Pharmacotherapy to improve outcomes in infrainguinal bypass graft surgery: a review of current treatment strategies. Annales de chirugie plastique et estitique, 24(4), 612-624.

Jokuszies, A., Herold, C., Niederbichler, A.D., and Vogt, P.M. (2012). Anticoagulative strategies in reconstructive surgery – clinical significance and applicability. German Medical Science, 10, retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/pmc3263521/

Kulik, A., Chan, V., and Ruel, M. (2009). Antiplatelet therapy and coronary artery bypass graft surgery: perioperative safety and efficacy. Informa Plc, 8(2), 169-182.

Land, A.F., Montalescot, G., Hulot, J.S., and Collet, J.P. (2010). Antiplatelet therapy and coronary artery bypass graft surgery. Journal of the American College of Cardiology, 56(24), 2003-2005.

Mo, W., Zhang, Y.L., Chen, H.S., Wang, L.S., and Song, H.Y. (2009). A novel hirudin derivative characterized with anti-platelet aggregations and thrombin inhibition. Journal of Thrombosis and Thrombolysis, 28(2), 230-237.

Montalescot, G., Hulot, J.S., and Collet, J.P. (2010). Antiplatelet therapy and coronary artery bypass graft surgery. Journal of the American College of Cardiology, 56(24), 2003-2005.

Nesbitt, W.S., Westein, E., Tovar-Lopez, F.J., Tolouei, E., Mitchell, A., Fu, J., Carberry, J., Fouras, A., and Jackson, S.P. (2009). A shear gradient-dependent platelet aggregation mechanism drives thrombus formation. Nature Medicine, 15(6), 665-675.

Oscarsson, A., Gupta, A., Fredrikson, M., Jarhult, J., Nystrom, M., Pettersson, E., Darvish, B., Krook, H., Swahn, E., and Entrei, C. (2010). To continue or discontinue aspirin in the perioperative period: a randomized, controlled clinical trial. British Journal of Anaesthesia, 104(3), 305-312.

Patni, R., Nawaz, A., Macys, A., Chan, J., and Punjabi, P. (2012). Assessment of platelet function in patients on antiplatelet therapy undergoing cardiac surgery: a review. Heart, Lung and Circulation, 21(8), 455-462.

Rickard, R.F., Meyer, C., and Hudson, D.A. (2009). Computational modeling of microterial anastomoses with size discrepancy (small-to-large). Journal of Surgical Research, 153(1), 1-11.

Trachiotis, G.D. (2010). Early antiplatelet therapy in coronary artery bypass grafting: a calculated benefit. Innovations: Technology & Techniques in Cardiothoracic & Vascular Surgery, 5(5), 317-325.