SCIENTIFIC ARCHIVES OF DENTAL SCIENCES (ISSN: 2642-1623) Volume 3 Issue 12 December 2020 Research Article Management of Anti-Platelet Agents in Patients Undergoing an Oral Surgery Maria Luisa Martinez-Garcia* and Samuele Curci Oral Surgery Department, Dentistry School, Universidad Europea de Madrid, Spain *Corresponding Author: Maria Luisa Martinez-Garcia, Oral Surgery Department, Dentistry School, Universidad Europea de Madrid, Spain. Received: October 20, 2020; Published: November 21, 2020 Abstract In oral surgery, bleeding associated with antiplatelet agents is a frightening situation to deal with, from a simple extraction to more complicated surgeries such as implant, periodontal or orthognathic surgeries. For this reason, each dentist needs to balance the risk of interrupting or not the antiplatelet agent. Systemic complications associated with the interruption of the drug outweigh the haemorrhagic complication associated with continuation of the same. Moreover, oral surgeries are considered at low risk of haemorrhage and hemostatic measure are in most of the cases enough to prevent excessive bleeding or platelet transfusion. In these situations, clinicians are in front of a question: Is bleeding worse than dying? Meaning that on one side, bleeding associated with should be obvious: stopping antiplatelet agent monotherapy or dual antiplatelet therapy is not anymore acceptable. Furthermore, continuation of antiplatelet agent, on the other side the remote but significant chance of lethal cardiovascular event. The decision special attention should be given to all those patients on dual antiplatelet therapy or combined anticoagulant/antiplatelet therapy because the risk of bleeding will be always higher compared to antiplatelet monotherapy and the anti-haemorrhagic measures such as gauze compression, collagen sponge, topical thrombin and sutures, are even more indispensable. From this point for a correct management of these drugs and in order to provide the best treatment to the patient, clinical history knowing the risk of thromboembolic event, additional antiplatelet tests, consultation with the cardiologist would be necessary and a teaching session and recommendations for the patient to explain how to manage at home post-operative bleeding is essential. Keywords: Anti-Platelets Agents; Oral Surgery; Hemostatic Measures; Thrombosis; Oral Hemorrhages Abbreviations Introduction Hemostasis and thrombosis Excessive bleeding can become one of the most frightening situ- CV: Cardiovascular; TXA2: Thromboxane A2; ADP: Adenosine - ations a dental health care provider can face; for this reason, it is Diphosphate; NSAID: Non-Steroidal Anti-inflammatory Drugs; cyclin; GI: Gastrointestinal; MI: Myocardial Infarction; ESC: Euro- important to know the physiologic mechanisms of bleeding, those COX-1: Cyclooxygenase 1; COX-2: Cyclooxygenase 2; PGI2: Prosta induced by drugs and the anti-hemorrhagic measures that prevent - pean Society of Cardiology; DAPT: Dual Antiplatelet Therapy; INR: response to an injury with the aim of arrest bleeding, is called he- International Normalized Ratio; aPTT: Activated Partial Throm major complications. The series of physiologic events that occur in mostasis [1]. According to this we distinguish between primary he- boplastin Time; PT: Prothrombin Time; CHADS: Congestive Heart Failure, Hypertension, Age, Diabetes, Stroke Citation: Maria Luisa Martinez-Garcia and Samuele Curci. “Management of Anti-Platelet Agents in Patients Undergoing an Oral Surgery". Scientific Archives Of Dental Sciences 3.12 (2020): 06-21. Management of Anti-Platelet Agents in Patients Undergoing an Oral Surgery 07 mostasis and secondary hemostasis. In primary hemostasis plate- Anticoagulants and antiplatelet agents All these processes are the underlying causes of acute or chronic due to the capacity of releasing vasoactive mediators that provoke lets, are essential and have a first-line role in atherothrombosis artery or venous diseases that are treated acutely and chronically platelets adhesion and aggregation and subsequent plug formation with antithrombotic and/or anticoagulants agents to reduce car- diovascular (CV) risks but exposing the patient to a higher risk of the fragmentation of megakaryocytes coming from bone marrow [1,2]. The development of these blood components derived from bleeding. and regulated by thrombopoietin, which is an hormone produced in the kidneys and the liver [3]. While in secondary hemostasis is a Different situations can individuate risk factors: age that is series of processes called coagulation cascade that takes place and proven to be a relevant factor that increases the risk of thrombosis, - the formation of fibrin is essential to stabilize the clot. tion, diabetes, hypercholesterolemia, obesity, diet, lack of exercise, different major surgeries, and tumors, hypertension, atrial fibrilla smoking, intravascular devices (mechanical cardiac valves, artery the blood vessels due to the accumulation of atherosclerotic plaque Atherosclerosis is defined as the degeneration of the walls of stents) [5]. - [2]. Thrombosis, instead, is the formation of a clot in a blood ves It is essential to distinguish and explain these drugs. Firstly, an- ischemic cardiovascular diseases are sustained by the progression sel that hinder or impede normal blood circulation. The related ticoagulant acts in secondary hemostasis and the coagulation cas- of atherosclerotic plaque or the disruption of the atherosclerotic cade. Among the different anticoagulant agents there are: heparins plaque by an exposition of thrombogenic substrates that lead to a that binds to the enzyme inhibitor antithrombins III inactivating thrombosis that can occlude partially or completely the blood ves- thrombin, vitamin K antagonists preventing the action of factor sels or the rupture of the plaque that can release atherosclerotic have been developed: apixaban, rivaroxaban, and edoxaban which II,VII, IX, X and new oral anticoagulants that in the last few years debris into the blood flow producing an embolism. - tran instead, is a direct inhibitor of thrombin [6]. are direct inhibitor of factor Xa in a dose-dependent way. Dabiga Anticoagulants Inhibitor of antithrombin III Warfarin/Acenocoumarin Vitamin K antagonist Heparin Oral anticoagulants: • Apixaban • Rivaroxaban Inhibitor of factor Xa • Edoxaban Direct inhibitor of thrombin Figure 1: Possible way of progression of atherosclerotic plaque. • Dabigatran Source: Gale AJ. Continuing Education Course #2: Current Under- Table 1: Different anticoagulant agents and their action. standing of Hemostasis. Toxicol Pathol. 2011;39(1):273-80. Source: Harter K, Levine M, Henderson SO. Anticoagulation drug On the other hand, regarding the venous system, thrombosis is therapy: A review. West J Emerg Med. 2015;16(1):11–7. secondary to conditions that compromise the venous return, pro- duce damage to the vessel and endothelial dysfunction or provoke a state of hypercoagulability [4]. Citation: Maria Luisa Martinez-Garcia and Samuele Curci. “Management of Anti-Platelet Agents in Patients Undergoing an Oral Surgery". Scientific Archives Of Dental Sciences 3.12 (2020): 06-21. Management of Anti-Platelet Agents in Patients Undergoing an Oral Surgery On the other side, antiplatelet agents act modifying or inhibit- 08 ing adhesion and aggregation processes, acting on thromboxane as effective as aspirin in secondary prevention of cerebrovascular dogrel and prasugrel and ticagrelor. Ticlopidine, first-generation, is events but it has been replaced by clopidogrel due to bone marrow receptors or on adenosine diphosphate (ADP). and hematologic toxicity [4]. Clopidogrel which have rapid absorp- A2 (TXA2) from arachidonic acid or/and glycoprotein GPIIb/IIIa tion, is an irreversible inhibitor of P2Y12 adenosine diphosphate - and it is recommended for patients at high risk of coronary artery There are different antiplatelet drugs: aspirin, clopidogrel, pra receptor. It is administered orally and it has a half-life of 8 hours sugrel, ticlopidine, ticagrelor, abciximab and tirofiban. disease and in most of the cases in combination with aspirin [4,11]. Prasugrel works as the previous ones but it is more potent, rapid Aspirin is the most studied one, it is classified in the group of absorption and well metabolized by the organism. Compared with that blocks the synthesis of prostanoids, lipid mediators that regu- NSAIDs (non-steroidal anti-inflammatory drugs), a class of drugs clopidogrel it produces an increased risk of bleeding and for this late numerous physiological and pathological processes in the reason, is contraindicated in patients with active bleeding or a his- body. Aspirin itself inhibits irreversibly the Cyclooxygenase 1 and - 2 dines acts inhibiting reversibly ADP-induced receptor and prevents tory of stroke [4,11]. Ticagrelor in contrast to the other thienopyri (COX-1 and COX-2) of the enzyme prostaglandin H-synthase-1/2 which are precursors of TXA2 and prostacyclin (PGI2) in a dose- a better risk reduction over clopidogrel in a patient with myocar- the binding of ‘G’ protein to the ADP binding site [8]. It is shown dependent way [7]. The inhibition of COX-1 occurs with a low dose dial infarction (MI) and relative CV death. Among the side effects - ranging from 75 - 150 mg while inhibition of COX-2 occurs with a of ticagrelor, there has been an increased frequency of dyspnoea higher dosage [4]. The inhibition of TXA2 prevents vasoconstric (an effect related to the metabolism of adenosine) and ventricular 30 min to