RESUMO
The purpose of the present work was to observe local hemostatic function during dental surgery in patients under oral anticoagulant therapy with an INR between 1.7 and 2.5. Thirty seven dental treatments were performed in 15 patients. Group A: nineteen dental treatments (13 scalings, 1 root canal therapy and 5 dental extractions), treated with oral rinse with tranexamic acid (250 mg dissolved in 10 ml of water). Group B: eighteen dental procedures (13 scaling, 1 root canal therapy and 14 dental extractions), in which oral rinse was utilized. Antibiotics were indicated for those patients with root canal therapy or with signs of infection. A cool soft diet was recommended to all patients during the three days following the surgical procedure. Only in five (13.5%) dental extractions (1 from group A and 4 from B) bleeding prolonged was observed, however periodontal disease was also present in those patients hone of them required blood products or withdrawal of the anticoagulant. The results suggest that mouth washing with tranexamic acid prevents excessive oral bleeding in patients treated with oral anticoagulants with an INR between 1.7 and 2.5.
Assuntos
Anticoagulantes/efeitos adversos , Antifibrinolíticos/uso terapêutico , Perda Sanguínea Cirúrgica/prevenção & controle , Raspagem Dentária , Hemorragia Gengival/prevenção & controle , Hemostasia Cirúrgica/métodos , Antissépticos Bucais , Hemorragia Pós-Operatória/prevenção & controle , Tratamento do Canal Radicular , Extração Dentária , Ácido Tranexâmico/uso terapêutico , Varfarina/efeitos adversos , Antifibrinolíticos/administração & dosagem , Transtornos da Coagulação Sanguínea/complicações , Transtornos da Coagulação Sanguínea/tratamento farmacológico , Avaliação de Medicamentos , Hemorragia Gengival/induzido quimicamente , Hemorragia Gengival/etiologia , Gengivite/complicações , Humanos , Abscesso Periapical/complicações , Periodontite/complicações , Hemorragia Pós-Operatória/induzido quimicamente , Hemorragia Pós-Operatória/etiologia , Ácido Tranexâmico/administração & dosagemRESUMO
The study was designed to know the effect of oral vitamin K (VK) treatment, on clotting factors II-VII-IX-X and the protein induced by VK absence from factor II (PIVCA II) on full term infants. Seventy healthy newborns were studied and each was randomly placed in one of two groups: Group A, newborns that received human milk and milk formula (mixed feeding)and group B, newborns that were exclusively breast fed. These groups were also divided in two subgroups: I received 2mg of VK1 orally and II (control) did not receive VK. Clotting activity of the coagulation factors and PIVCA II was determined from blood plasma obtained immediately after birth and 48 hours after VK administration. Basal activity of the factors analyzed was similar in all groups with values ranging from 25% to 40%. After 48 hours a significant increase in all factors studied and a decrease of PIVKA II was observed in those children who received oral VK. The results suggest that oral VK effectively increases VK dependent factors and prevents the risk of hemorrhagic disease in the newborn, with the advantage of being less traumatic and less risky to the infant than intramuscular VK.
Assuntos
Fator VII/análise , Fator X/análise , Protrombina/análise , Vitamina K/farmacologia , Humanos , Recém-NascidoRESUMO
Platelets are blood cells that participate in the human primary hemostatic mechanism. Platelets need to be activated to perform all their functions and this activation can be initially produced after an endothelial injury that exposes subendothelial structures to the blood flow. Platelet adhesiveness can also occur by the intervention of high shear forces of the blood stream leading to the attachment of platelets to the subendothelium, forming a monolayer with platelet shape changes and pseudopod emission, that covers all the exposed subendothelial surface. Adhesiveness results from the participation of three components: Glycoprotein Ib, von Willebrand factor and collagen. Fibronectin and vitronectin can also participate in this process. Aggregation (platelet-platelet interaction) has as the final purpose to produce a platelet thrombi that constitutes the primary hemostatic plug. Aggregation involves a sequence of biochemical reactions that are initiated by the contact of an agonist agent (ADP, collagen, thrombin) with receptors on the platelet membrane, this is followed by the fibrinogen binding to Glycoprotein IIb/IIIa complex serving as a link with other surrounding platelets, the aggregation process is then amplified and becomes irreversible with the secretion of the platelet intragranular substances through the release reaction. These series of reactions have their own mechanisms of control that regulate or modulate platelet activation as the Ca2+/cAMP relationship, the balance between PGI2 and TxA2 and the enzymatic system of kinases and phosphatases. The relationship between platelets and other blood cells such as erythrocytes and leukocytes probably modulate the platelet aggregatory response during a vascular injury promoting mechanisms of thrombogenesis and wound healing. On the other hand, the multiple compounds released by the endothelial cell that inhibit platelet function, specially prostacyclin (PGI2) and recently the endothelial derived relaxing factor (EDRF) or nitric oxide have focused new understanding on the physiologic role of platelets in the control of hemostatic and thrombotic processes.