Avaliação da tromboflebite jugular experimental em equinos tratados com heparina

Borghesan, Alexandre Corrêa

doi:10.5016/dt000607665

Cited by 1 publication

(7 citation statements)

References 36 publications

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“…This finding was already described in works by Borghesan (2010) and Hussni et al (2009) and, in agreement with them, we do not believe that the reductions in the total platelet count and globular volume would be significant and is related to an augmentation of platelet aggregation caused by treatment with heparin. The "thrombocytopenia induced by the use of heparin" is a clinicopathological syndrome that occurs when IgG antibodies dependent on heparin bind to factor 4 of the platelet activation complex to produce a state of hypercoagulability (Maffei et al 2008, Borghesan 2010, Pavanelli & Spitzner 2011. The clinical signs commonly appear 5 days after the initiation of therapy with non-fractionated heparin, heparin presenting a low molecular weight (Linkins 2015).…”

Section: Thromboelastometrysupporting

confidence: 77%

“…In relation to the use of heparin as an anticoagulant in allopathic therapy or as a postoperative co-adjuvant after vascular surgeries, there is consensus on the importance of its laboratory monitoring with reagents of aPTT (more sensitive to the inhibitory effects of heparin on thrombin, the factors Xa and IXa) and the platelet count, being that the absence of thrombocytopenia at D16 and an increase not greater than 1.5 to 2.5 times (in seconds) of aPTT, in both groups, demonstrated that the lowest heparin dose utilized (150 UI/Kg, SC) is safe (Moore & Hinchcliff 1994, Dornbusch, 2005, Borghesan 2010). …”

Section: Discussionmentioning

confidence: 99%

“…The clinical signs commonly appear 5 days after the initiation of therapy with non-fractionated heparin, heparin presenting a low molecular weight (Linkins 2015). Its more severe form is associated with a high risk of thrombotic events that are potentially life threatening in human patients, especially those that present a diminution of 30 to 50% in the platelet count during heparin treatment, even when not presenting thrombocytopenia (Maffei et al 2008, Borghesan 2010, Linkins 2015. Different lowercase letters indicate significant differences between moments (p<0,05).…”

Section: Thromboelastometrymentioning

confidence: 99%

“…These alterations are identified when we speak of equine jugular thrombophlebitis, since we can observe, in non-criteria interventionism, situations that involve these risk factors, favoring their formation (Byars et al 2003, Barbosa et al 2009, Borghesan 2010.…”

Section: Introductionmentioning

confidence: 99%

“…In the occurrence of failures in controlling the hemostatic activity of blood, there is inadequate formation of the aggregation of figured elements of blood (thrombi) within the vascular bed, enabling total or partial obstruction of the lumen and, in sequence, a limitation in the regional blood drainage or perfusion (Bonagura et al 2010, Borghesan 2010, Rafael 2012.…”

Section: Introductionmentioning

confidence: 99%

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Thromboelastometric evaluation of horses submitted to experimental thrombosis and jugular thrombectomy

et al. 2016

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Jugular thrombosis in horses occurs commonly in iatrogenic situations, secondary to endotoxemic clinical condition and disseminated vascular coagulation, potentially leading to death. Thus, hemostatic evaluation becomes necessary and extremely important for monitoring the risks of systemic hypercoagulability and for the efficiency of allopathic and surgical treatment. This paper describes the hemostatic behavior in experimental jugular thrombosis of ten healthy equines, subsequently submitted to two thrombectomy techniques and receiving heparin sodium as anti-rethrombosis therapy. These animals were evaluated for 20 days by thromboelastometry (TEM), platelet count, hematocrit and fibrinogen, at four moments: pre-induction to phlebitis (D0-MPF); three days after thrombophlebitis induction (D3-MFM); 6 days after, -moment of thrombophlebitis -(D9-MT); and 54 (D16) and 126 (D19) hours after thrombectomies (PTM). Thrombectomy was performed via a Vollmar Ring (group 1, n=5) and Fogarty catheter (group 2, n=5). All the animals received heparin (150 UI/kg, SC) every 12 hours, for ten days after the respective thrombectomies. Through the blood samples were evaluated TEM, activated partial thromboplastin time (aPTT) and prothrombin time (PT), dosing of fibrinogen, hematocrit and platelet count at the abovementioned moments. For comparison between groups and moments the t test was applied at 5% significance level. No significant difference was verified between treatment groups at any of the moments. There were reductions in clotting time (CT) and clot formation time (CFT), with increase in maximum lysis (ML) until the moment D9-MT. Evaluation through INTEM ® reagent presented prolongations of CT and CFT with reduction of α angle and ML starting from D16 and D19. Similarly, aPTT presented significant differences between moments pre-(D0, 3 and 9) and post-(D16 and 19) anticoagulant and surgical treatment. The platelet numbers were diminished at moments D16 and D19. In evaluation with EXTEM ® reagent, prolongation of CT and CFT occurred only between the moments D0 vs. D3 and vs. D9. O PT did not present significant differences. The results obtained demonstrate that experimental jugular thrombophlebitis leads to local clinical alterations, with impairment of tissue and of the extrinsic coagulation pathway (EXTEM ® ), but without evidence of systemic hypercoagulability status, since there was no increase of the alpha angle or maximum clot firmness (MCF). Furthermore, TEM was shown useful and more sensitive than conventional coagulation tests (PT, aPTT and fibrinogen) for the monitoring of anticoagulant therapy, as demonstrated in other works. Houve diminuição do número de plaquetas nos momentos D16 e D19. Na avaliação com reagente extem ocorreu apenas o prolongamento do CT e CFT entre os momentos D0 e o D3 e D9. O TP não apresentou diferenças significativas. Os resultados obtidos demonstram que a tromboflebite jugular experimental leva a alterações clínicas locais, com comprometimento tecidual e da via extrínseca da coagulação ...

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