DOCSLIB.ORG

Management of Anti-Platelet Agents in Patients Undergoing an Oral Surgery

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Management of Anti-Platelet Agents in Patients Undergoing an Oral Surgery 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
Load more

Recommended publications
  • AHFS Pharmacologic-Therapeutic Classification System
    AHFS Pharmacologic-Therapeutic Classification System Abacavir 48:24 - Mucolytic Agents - 382638 8:18.08.20 - HIV Nucleoside and Nucleotide Reverse Acitretin 84:92 - Skin and Mucous Membrane Agents, Abaloparatide 68:24.08 - Parathyroid Agents - 317036 Aclidinium Abatacept 12:08.08 - Antimuscarinics/Antispasmodics - 313022 92:36 - Disease-modifying Antirheumatic Drugs - Acrivastine 92:20 - Immunomodulatory Agents - 306003 4:08 - Second Generation Antihistamines - 394040 Abciximab 48:04.08 - Second Generation Antihistamines - 394040 20:12.18 - Platelet-aggregation Inhibitors - 395014 Acyclovir Abemaciclib 8:18.32 - Nucleosides and Nucleotides - 381045 10:00 - Antineoplastic Agents - 317058 84:04.06 - Antivirals - 381036 Abiraterone Adalimumab; -adaz 10:00 - Antineoplastic Agents - 311027 92:36 - Disease-modifying Antirheumatic Drugs - AbobotulinumtoxinA 56:92 - GI Drugs, Miscellaneous - 302046 92:20 - Immunomodulatory Agents - 302046 92:92 - Other Miscellaneous Therapeutic Agents - 12:20.92 - Skeletal Muscle Relaxants, Miscellaneous - Adapalene 84:92 - Skin and Mucous Membrane Agents, Acalabrutinib 10:00 - Antineoplastic Agents - 317059 Adefovir Acamprosate 8:18.32 - Nucleosides and Nucleotides - 302036 28:92 - Central Nervous System Agents, Adenosine 24:04.04.24 - Class IV Antiarrhythmics - 304010 Acarbose Adenovirus Vaccine Live Oral 68:20.02 - alpha-Glucosidase Inhibitors - 396015 80:12 - Vaccines - 315016 Acebutolol Ado-Trastuzumab 24:24 - beta-Adrenergic Blocking Agents - 387003 10:00 - Antineoplastic Agents - 313041 12:16.08.08 - Selective
    [Show full text]
  • Systematic Review of Tranexamic Acid Adverse Reactions
    arm Ph ac f ov l o i a g n il r a n u c o e J Journal of Pharmacovigilance Calapai et al., J Pharmacovigilance 2015, 3:4 ISSN: 2329-6887 DOI: 10.4172/2329-6887.1000171 Review Open Access Systematic Review of Tranexamic Acid Adverse Reactions Gioacchino Calapai2*, Sebastiano Gangemi1, Carmen Mannucci2, Paola Lucia Minciullo1, Marco Casciaro1, Fabrizio Calapai3, Maria Righi4 and Michele Navarra5 1Operative Unit of Allergy and Clinical Immunology, Department of Clinical and Experimental Medicine, University of Messina, Italy 2Department of Clinical and Experimental Medicine, University of Messina, Italy 3Centro Studi Pharma.Ca, Messina, Italy 4Department of Biomedical Sciences and Morphological and Functional Images, University of Messina, Italy 5Department of Drug Sciences and Health Products, University of Messina, Italy *Corresponding author: Gioacchino Calapai, Department of Clinical and Experimental Medicine, University of Messina, Via Consolare Valeria 5, 98125 Messina, Italy, Tel: +39 090 2213646; Fax: +39 090 221; E-mail: [email protected] Received date: July 06, 2015; Accepted date: July 14, 2015; Published date: July 20, 2015 Copyright: © 2015 Calapai G, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Abstract Background Tranexamic acid is a synthetic lysine derivate that exerts its antifibrinolytic effect by reversible blocking lysine binding sites on plasminogen preventing fibrin degradation. It is widely used for haemorrhage or risk of haemorrhage in increased fibrinolysis or fibrinogenolysis. Aim The aim of our work was to review the literature regarding the best evidence on tranexamic adverse reactions and to describe them according to the apparatus involved.
    [Show full text]
  • Basic Science of ITP
    CHAPTER 1 Basic sc*ience of ITP Editor: John W. Semple 1.1 Megakaryocyte differentiation and platelet produc*tion A.S. Weyrich 1.2 Autoimmune mechanisms and T regula*tory cell disturbances in ITP K. Yazdanbakhsh 1.3 Mouse models o*f ITP J.W. Semple 1.4 Peptide therapy for patients with* ITP S.J. Urbaniak * Basic science of ITP 1.1 Megakaryocyte differen*tiation and platelet production Andrew S. Weyrich CHAPTER 1.1 • Megakaryocyte differentiation and platelet production 1. Introduction Platelets are anucleate cells that circulate in the bloodstream for approximately 10 days. The average adult must produce roughly 1 x 10 11 platelets per day to maintain normal platelet counts, a level of production that increases dramatically in a variety of clinical scenarios (1). In 1906, Wright provided the first evidence that megakaryocytes give rise to blood platelets. Since then, our understanding of the molecular basis of thrombopoiesis has progressed substantially and is arguably in a logarithmic growth phase. This chapter will review our current understanding of thrombopoiesis and highlight how the field is evolving. The history of megakaryocytes and platelets is fairly young. In 1841, Addison first described platelets and in 1882, Bizzozero named and identified platelets in the circulation and determined that they could induce clotting. In 1890, Howell named megakaryocytes, and 16 years later, Wright discovered that these were actually the precursors of platelets. Thus, the late 1880’s and early 1900’s were a period of prolific activity in the elucidation of megakaryocytes. Several discoveries were made about platelets and also about erythropoietin, which implied that a humoral substance also regulated platelet production though its exact nature was not yet known.
    [Show full text]
  • The Phytochemistry of Cherokee Aromatic Medicinal Plants
    medicines Review The Phytochemistry of Cherokee Aromatic Medicinal Plants William N. Setzer 1,2 1 Department of Chemistry, University of Alabama in Huntsville, Huntsville, AL 35899, USA; [email protected]; Tel.: +1-256-824-6519 2 Aromatic Plant Research Center, 230 N 1200 E, Suite 102, Lehi, UT 84043, USA Received: 25 October 2018; Accepted: 8 November 2018; Published: 12 November 2018 Abstract: Background: Native Americans have had a rich ethnobotanical heritage for treating diseases, ailments, and injuries. Cherokee traditional medicine has provided numerous aromatic and medicinal plants that not only were used by the Cherokee people, but were also adopted for use by European settlers in North America. Methods: The aim of this review was to examine the Cherokee ethnobotanical literature and the published phytochemical investigations on Cherokee medicinal plants and to correlate phytochemical constituents with traditional uses and biological activities. Results: Several Cherokee medicinal plants are still in use today as herbal medicines, including, for example, yarrow (Achillea millefolium), black cohosh (Cimicifuga racemosa), American ginseng (Panax quinquefolius), and blue skullcap (Scutellaria lateriflora). This review presents a summary of the traditional uses, phytochemical constituents, and biological activities of Cherokee aromatic and medicinal plants. Conclusions: The list is not complete, however, as there is still much work needed in phytochemical investigation and pharmacological evaluation of many traditional herbal medicines. Keywords: Cherokee; Native American; traditional herbal medicine; chemical constituents; pharmacology 1. Introduction Natural products have been an important source of medicinal agents throughout history and modern medicine continues to rely on traditional knowledge for treatment of human maladies [1]. Traditional medicines such as Traditional Chinese Medicine [2], Ayurvedic [3], and medicinal plants from Latin America [4] have proven to be rich resources of biologically active compounds and potential new drugs.
    [Show full text]
  • Aon Exchange Formulary
    GEISINGER HEALTH PLAN 2021 member formulary List of covered drugs AON Exchange medication benefit General Formulary Information This formulary is applicable to the AON Exchange Prescription Medication Benefit plans offered by Geisinger Health Plan, Geisinger Choice PPO and Geisinger Health Options. We encourage you to contact our Pharmacy Customer Service Team if you have any questions about this information or the type of benefit in which you are enrolled. Also, please refer to your benefit documents, as formulary exclusions may differ based on the specific benefit. This formulary represents the Aon Exchange Prescription Medication benefit. This formulary was designed to be a useful tool if you have prescription medication coverage. It lists the medications covered by your plan. Medications are listed in this formulary by medication category; individual medications can be looked up by using the index at the back. Please note that you can also view the formulary online at www.geisinger.org/health-plan. Pharmacy Customer Service Team Contact Information Telephone: (800) 988-4861 or (570)-271-5673; TDD/TTY 711 Fax: 570-300-2122 Mailing address: Geisinger Health Plan Pharmacy Department Internal Mail Code 24-10 100 North Academy Avenue Danville, PA 17822 AON Exchange Benefit The Aon Exchange benefit assigns each prescription medication to one of three different tiers, each representing a set copay amount. The copay amount will depend on your prescription medication rider. Additional medications, other than those included in this formulary, may be covered under the Triple Choice benefit. The definitions of the copay levels are listed below: • Tier 1 - Includes most generic medications and has the lowest copayment.
    [Show full text]
  • Doptelet (Avatrombopag) Policy Number: C16445-A
    Prior Authorization Criteria Doptelet (avatrombopag) Policy Number: C16445-A CRITERIA EFFECTIVE DATES: ORIGINAL EFFECTIVE DATE LAST REVIEWED DATE NEXT REVIEW DATE 05/2019 07/31/2019 07/31/2020 J CODE TYPE OF CRITERIA LAST P&T APPROVAL/VERSION J8499 (NOC): Prescription Q3 2019 drug, oral, non RxPA 20190828C16445-A chemotherapeutic, nos PRODUCTS AFFECTED: Doptelet (avatrombopag) DRUG CLASS: Thrombopoietic agent -Small molecule thrombopoietin (TPO) receptor agonist ROUTE OF ADMINISTRATION: Oral PLACE OF SERVICE: Specialty Pharmacy The recommendation is that medications in this policy will be for pharmacy benefit coverage and patient self-administered AVAILABLE DOSAGE FORMS: Tablet, oral: 20 mg FDA-APPROVED USES: Treatment of thrombocytopenia in adult patients with chronic liver disease who are scheduled to undergo a procedure. Thrombocytopenia in adult patients with chronic immune thrombocytopenia who have had an insufficient response to a previous treatment COMPENDIAL APPROVED OFF-LABELED USES: None COVERAGE CRITERIA: INITIAL AUTHORIZATION DIAGNOSIS: Chronic liver disease-associated thrombocytopenia REQUIRED MEDICAL INFORMATION: A. THROMBOCYTOPENIA IN CHRONIC LIVER DISEASE (TICL): 1. The patient has a diagnosis of chronic liver disease-associated thrombocytopenia AND 2. The patient is scheduled to undergo a procedure (excluding patients undergoing neurosurgical interventions, thoracotomy, laparotomy, or organ resection) AND 3. The medication is being initiated 10 to 13 days prior to the scheduled procedure AND 4. The patient is undergoing the procedure 5 to 8 days after the last dose AND Page 1 of 5 Molina Healthcare, Inc. confidential and proprietary © 2018 This document contains confidential and proprietary information of Molina Healthcare and cannot be reproduced, distributed or printed without written permission from Molina Healthcare.
    [Show full text]
  • AHFS Pharmacologic-Therapeutic Classification (2012).Pdf
    AHFS Pharmacologic-Therapeutic Classification 4:00 Antihistamine Drugs 4:04 First Generation Antihistamines 4:04.04 Ethanolamine Derivatives 4:04.08 Ethylenediamine Derivatives 4:04.12 Phenothiazine Derivatives 4:04.16 Piperazine Derivatives 4:04.20 Propylamine Derivatives 4:04.92 Miscellaneous Derivatives 4:08 Second Generation Antihistamines 4:92 Other Antihistamines* 8:00 Anti-infective Agents 8:08 Anthelmintics 8:12 Antibacterials 8:12.02 Aminoglycosides 8:12.06 Cephalosporins 8:12.06.04 First Generation Cephalosporins 8:12.06.08 Second Generation Cephalosporins 8:12.06.12 Third Generation Cephalosporins 8:12.06.16 Fourth Generation Cephalosporins 8:12.07 Miscellaneous -Lactams 8:12.07.04 Carbacephems 8:12.07.08 Carbapenems 8:12.07.12 Cephamycins 8:12.07.16 Monobactams 8:12.08 Chloramphenicol 8:12.12 Macrolides 8:12.12.04 Erythromycins 8:12.12.12 Ketolides 8:12.12.92 Other Macrolides 8:12.16 Penicillins 8:12.16.04 Natural Penicillins 8:12.16.08 Aminopenicillins 8:12.16.12 Penicillinase-resistant Penicillins 8:12.16.16 Extended-spectrum Penicillins 8:12.18 Quinolones 8:12.20 Sulfonamides 8:12.24 Tetracyclines 8:12.24.12 Glycylcyclines 8:12.28 Antibacterials, Miscellaneous 8:12.28.04 Aminocyclitols 8:12.28.08 Bacitracins 8:12.28.12 Cyclic Lipopeptides 8:12.28.16 Glycopeptides 8:12.28.20 Lincomycins 8:12.28.24 Oxazolidinones 8:12.28.28 Polymyxins 8:12.28.30 Rifamycins 8:12.28.32 Streptogramins 8:12.28.92 Other Miscellaneous Antibacterials* 8:14 Antifungals 8:14.04 Allylamines 8:14.08 Azoles 8:14.16 Echinocandins 8:14.28 Polyenes 8:14.32
    [Show full text]
  • Long Term in Vivo Study of Rapidly Degradable Synthetic Arterial Grafts R
    Society for Biomaterials Annual Meeting and Exposition 2013 Biomaterials Revolution Transactions of the 37th Annual Meeting Volume XXXV Boston, Massachusetts, USA 10-13 April 2013 Volume 1 of 2 ISBN: 978-1-62748-128-1 ISSN: 1526-7547 Copyright and Disclaimer Society For Biomaterials Transactions of the 37th Annual Meeting Volume XXXV Published by: Society For Biomaterials 15000 Commerce Parkway, Suite C Mount Laurel, NJ 08054 (856)439-0826 Copyright © 2013 Society For Biomaterials, USA ISSN# 1526-7547 All rights reserved. No part of this publication may be reproduced in any form by Photostat, microfilm, retrieval system, or any other means, without written permission from the publisher. The materials published in this volume are not intended to be considered by the reader as statements of standards of care or definitions of the state of the art in patient care or applications of the scientific principles described in the contents. The statements of fact and opinions expressed are those of the respective authors who are identified in the abstracts. Publications of these materials by the Society For Biomaterials does not express or imply approval or agreement of the officers, staff, or agents of the Society with the items presented herein and should not be viewed by the reader as an endorsement thereof. Neither the Society For Biomaterials nor its agents are responsible for inaccuracies or omissions in this Publication. Every effort has been made to faithfully reproduce these Transactions as submitted. No responsibility is assumed by the Organizers for any injury and/or damage to persons or property as a matter of product liability, negligence or otherwise, or from any use or operation of any methods, products, instructions or ideas contained in the material herein.
    [Show full text]
  • Ankaferd Blood Stopper Is More Effective Than Adrenaline Plus Lidocaine and Gelatin Foam in the Treatment of Epistaxis in Rabbits Mehmet Kelles, MD1; M
    Current Therapeutic Research VOLUME ,NUMBER ,OCTOBER Ankaferd Blood Stopper Is More Effective Than Adrenaline Plus Lidocaine and Gelatin Foam in the Treatment of Epistaxis in Rabbits Mehmet Kelles, MD1; M. Tayyar Kalcioglu, MD1; Emine Samdanci, MD2; Erol Selimoglu, MD1; Mustafa Iraz, MD3; Murat Cem Miman, MD4; and Ibrahim C. Haznedaroglu, MD5 1Department of Otorhinolaryngology, Inonu University, Malatya, Turkey; 2Department of Pathology, Inonu University, Malatya, Turkey; 3Department of Pharmacology, Bezmialem Vakif University, Istanbul, Turkey; 4Department of Otorhinolaryngology, Kocatepe University, Afyon, Turkey; and 5Department of Hematology, Hacettepe University, Ankara, Turkey ABSTRACT Background: Epistaxis is an important emergency that can sometimes be life threatening without effective intervention. Persistent and recurrent bleeding can lead to aspiration, hypotension, hypoxia, or even severe and mortal cardiovascular com- plications. Providing prompt hemostasis is important, and the hemostatic method used must be easily and locally applicable, efficient, and inexpensive. Objective: The aim of this study was to assess the hemostatic efficacy of Ankaferd Blood Stopper (ABS) in an experimental epistaxis model and to determine the histopathologic alterations with topical ABS application. Methods: Twenty-eight New Zealand rabbits were evaluated in 4 study groups. Topical ABS, gelatin foam (GF), adrenalin ϩ lidocaine (AL), and serum physiologic as negative control (C) were applied to the animals for controlling epistaxis. The bleeding was generated with a standard mucosal incision in all groups. Cotton pieces soaked with ABS, AL, C, and GF were applied to the nasal bleeding area. Time of hemostasis was recorded. Tissue samples were obtained after hemostasis for histopathologic examination. The samples were stained with hematoxylin and eosin (HE) and phosphotungstic acid hematoxylin (PTAH) and were examined under a light microscope.
    [Show full text]
  • Comparison Between the Clot-Protecting Activity of a Mutant Plasminogen Activator Inhibitor-1 with a Very Long Half-Life and 6-Aminocaproic Acid
    EXPERIMENTAL AND THERAPEUTIC MEDICINE 9: 2339-2343, 2015 Comparison between the clot-protecting activity of a mutant plasminogen activator inhibitor-1 with a very long half-life and 6-aminocaproic acid DANIEL GLENN KINDELL1, RICK WAYNE KECK1 and JERZY JANKUN1-3 1Urology Research Center, Department of Urology, University of Toledo, Health Science Campus, Toledo, OH 43614, USA; 2Protein Research Chair, Department of Biochemistry, College of Sciences, King Saud University, Riyadh 11451, Kingdom of Saudi Arabia; 3Department of Clinical Nutrition, Medical University of Gdańsk, Gdańsk, Pomerania 80‑211, Poland Received August 20, 2014; Accepted November 17, 2014 DOI: 10.3892/etm.2015.2399 Abstract. Plasminogen activator inhibitor (PAI)-1 is a serpin Introduction glycoprotein that can stabilize blood clots by inhibiting fibrino- lysis. However, wild-type PAI-1 has the disadvantage of a short Coagulation, the formation of a clot, is an essential process half-life of ~2 h. A very long half-life (VLHL) PAI-1 mutant in the maintenance of homeostasis under normal condi- was developed previously with an active-form half-life of tions and during traumatic events. Numerous agents are >700 h, making it a possible candidate for use in hemorrhagic used to initiate clotting and prevent uncontrolled bleeding. therapy. Current treatments for mitigating hemorrhage, other However, only a few agents, with limited efficacy, are used than inducers of blood clotting, are limited to lysine analog anti- in clinical practice to protect formed clots against premature fibrinolytics, including 6‑aminocaproic acid and tranexamic lysis (1,2). The crosslinked polymer, fibrin, is dissolved into acid. VLHL PAI-1 has been previously demonstrated to limit fibrin degradation products by plasmin.
    [Show full text]
  • Core Curriculum for Iv Therapy
    DIRECT ENTRY MIDWIFERY LEGEND DRUGS AND DEVICES INITIAL EDUCATION Oregon Health Licensing Agency Board of Direct Entry Midwifery 700 Summer Street N.E., Suite #320 Salem, Oregon 97301-1287 (503) 378 - 8667 Fax: (503) 370-9004 E-mail: [email protected] LEGEND DRUGS AND DEVICES INITIAL EDUCATION 40 hours The Initial Legend Drugs and Devices Education Program shall consist of 40 total hours of instruction in the following: 8 hours - Pharmacology; 4 hours - Administration of medications through injection; 4 hours - Treatment of shock; 10 hours – I.V. Therapy; 4 hours - Neonatal resuscitation specific to out of hospital birth and 10 hours - Suturing. See core curriculum for learning objectives and other details. Course / Description Hours Required PHARMACOLOGY: 8 hours ADMINISTRATION OF MEDICATIONS THROUGH INJECTION: 4 hours TREATMENT OF SHOCK: 4 hours I.V. THERAPY: 10 hours NEONATAL RESUSCITATION: 4 hours SUTURING: 10 hours TOTAL HOURS: 40 HOURS In the course of study the candidate shall receive theory instruction, classroom instructor demonstrations and/or guided practical experience under the supervision of the authorized provider. The amounts of time a candidate devotes to theory and practice are flexible provided the minimum hour requirements listed above are met. In addition to the forty hours of instruction, the course must include assessment of theory and skills. 2 CORE CURRICULUM FOR PHARMACOLOGY – 1 of 2 Objectives Dosage Guidelines Standards for Resources Instructors Define a drug Synthetic Oxytocin (Pitocin, Licensed Current Define"legend drugs and Syntocin & Generic) IM: 10U Pharmacist Edition of the devices" Explain OAR’s (1ml), may repeat at 2 hour (not limited following: concerning legend drugs and intervals as necessary to to Oregon Pharmacology devices Define and explain maintain uterine tone.
    [Show full text]
  • Antithrombotic Prophylaxis for Surgery
    ARTICLE Platelet Biology & its Disorders Antithrombotic prophylaxis for Ferrata Storti Foundation surgery-associated venous thromboembolism risk in patients with inherited platelet disorders. The SPATA-DVT Study Francesco Paciullo,1 Loredana Bury,1 Patrizia Noris,2 Emanuela Falcinelli,1 Federica Melazzini,2 Sara Orsini,1 Carlo Zaninetti,2,3 Rezan Abdul-Kadir,4 Deborah Obeng-Tuudah,4 Paula G. Heller,5,6 Ana C. Glembotsky,5,6 Fabrizio Fabris,7 Jose Haematologica 2020 Rivera,8 Maria Luisa Lozano,8 Nora Butta,9 Remi Favier,10 Ana Rosa Cid,11 Volume 105(7):1948-1956 Marc Fouassier,12 Gian Marco Podda,13 Cristina Santoro,14 Elvira Grandone,15,16 Yvonne Henskens,17 Paquita Nurden,8 Barbara Zieger,19 Adam Cuker,20 Katrien Devreese,21 Alberto Tosetto,22 Erica De Candia,23,24 Arnaud Dupuis,25 Koji Miyazaki,26 Maha Othman27 and Paolo Gresele1 1Department of Medicine, Section of Internal and Cardiovascular Medicine, University of Perugia, Italy; 2Department of Internal Medicine, IRCCS Policlinico S. Matteo Foundation, University of Pavia, Pavia, Italy; 3PhD program in Experimental Medicine, University of Pavia, Pavia, Italy; 4Haemophilia Centre and Haemostasis Unit, The Royal Free Foundation Hospital and University College London, London, UK; 5Hematología Investigación, Instituto de Investigaciones Médicas Alfredo Lanari, Universidad de Buenos Aires, Buenos Aires, Argentina; 6CONICET, Universidad de Buenos Aires, Instituto de Investigaciones Médicas - IDIM-, Buenos Aires, Argentina; 7Clinica Medica 1 - Medicina Interna CLOPD, Dipartimento Assistenziale
    [Show full text]