scholarly journals Effect of Antithrombotic Therapy on Secondary Bleeding After Proctological Surgery

Cureus ◽  
2021 ◽  
Author(s):  
Ryo Maemoto ◽  
Shingo Tsujinaka ◽  
Yasuyuki Miyakura ◽  
Erika Machida ◽  
Taro Fukui ◽  
...  
2020 ◽  
Author(s):  
Ryo Maemoto ◽  
Shingo Tsujinaka ◽  
Yasuyuki Miyakura ◽  
Erika Machida ◽  
Nao Kakizawa ◽  
...  

Abstract Background: The purpose of this study was to identify the incidence and severity of secondary bleeding after proctological surgery for patients with or without antithrombotic therapy.Methods: We retrospectively identified 113 patients who underwent proctological surgery in our hospital from March 2009 to February 2019. In general, antiplatelet drugs were continued and anticoagulant drugs were either substituted or withdrawn prior to the surgery. The severity of secondary bleeding was classified as mild, moderate, severe.Results: Eighteen patients underwent antiplatelet therapy (A group) and 95 patients did not undergo antithrombotic therapy (N group). Secondary bleeding was observed in nine patients (8.0%) and patients in the A group exhibited significantly higher rate of secondary bleeding rate than patients in the N group (39% vs. 2.4%, P < 0.01). The median interval from surgery to the onset of secondary bleeding was 5 (range: 0-11days). The severity of bleeding was the highest in patients administered direct oral anticoagulants (DOAC) and was the lowest in those administered aspirin. There was no mortality or cardiovascular event.Conclusions: Antithrombotic therapy is associated with high risk of secondary bleeding after proctological surgery, particularly in patients who undergo anticoagulant therapy. Delaying of postoperative resumption of anticoagulants may be considered in balancing the individual risk of postoperative thromboembolic complications against the risk of secondary bleeding. Future prospective studies with larger number of patients are needed to determine the appropriate timing of resuming antithrombotic therapy.


2001 ◽  
Vol 21 (03) ◽  
pp. 82-96 ◽  
Author(s):  
D. Hoppensteadt ◽  
O. Iqbal ◽  
R. L. Bick ◽  
J. Fareed

SummaryThrombotic disorders are the most common cause of death in the United States. About two million individuals die each year from an arterial or venous thrombosis or related disorders. About 80% to 90% of all cases of thrombosis can now be defined with respect to cause. Of these, over 50% occur in patients who harbor a congenital or acquired blood coagulation protein or platelet defect which caused the thrombotic event. It is obviously of major importance to define those individuals harboring such a defect as this allows: 1) appropriate antithrombotic therapy to decrease risks of recurrence; 2) determination of the length of time the patient must remain on therapy for secondary prevention; and 3) allow for testing of family members of those harboring a blood coagulation protein or platelet defect which is hereditary (about 50% of all coagulation and platelet defects mentioned above). Aside from mortality, significant additional morbidity occurs from both arterial or venous thrombotic events, including, but not limited to paralysis (non-fatal thrombotic stroke), cardiac disability (repeated coronary events), loss of vision (retinal vascular thrombosis), fetal waste syndrome (placental vascular thrombosis), stasis ulcers and other manifestations of post-phlebitic syndrome, etc.


1996 ◽  
Vol 76 (06) ◽  
pp. 1020-1029 ◽  
Author(s):  
Laurent Macchi ◽  
Gisèle Clofent-Sanchez ◽  
Gérald Marit ◽  
Claude Bihour ◽  
Catherine Durrieu-Jais ◽  
...  

SummaryIn idiopathic thrombocytopenic purpura (ITP), autoantibodies reacting with antigens on the platelet membrane bring about accelerated platelet destruction. We now report PAICA (“Platelet-Associated IgG Characterization Assay”), a method for detecting autoantibodies bound to specific membrane glycoproteins in total platelet lysates. This monoclonal antibody (MAb) capture assay takes into account the fact that antibodies on circulating platelets may be translocated to internal pools as well as being on the surface. A total of twenty ITP patients were examined by PAICA, and the results compared with those obtained by measuring (i) serum antibodies bound to paraformaldehyde-fixed control platelets by ELISA, (ii) IgG bound to the surface of the patient’s own platelets by flow cytometry (PSIgG), (iii) total platelet-associated IgG (PAIgG) by ELISA and (iv) serum antibodies reacting with control platelets by MAIPA (“Monoclonal Antibody-specific Immobilization of Platelet Antigens”). Of twelve patients with elevated PAIgG, nine had increased PSIgG yet eleven reacted positively in PAICA. Of these, eight possessed antibodies directed against GP Ilb-IIIa, two against GP Ib-IX and one patient possessed antibodies directed against GP Ilb-IIIa and GP Ia-IIa respectively. Only seven of the patients possessed serum antibodies detectable by MAIPA. PAICA was also able to detect platelet-associated c7E3 (the chimeric form of Fab fragments of the MAb 7E3) following its infusion during antithrombotic therapy, when it proved more sensitive over a seven-day period than a MAIPA assay adapted for assessing surface-bound antibody. We propose that PAICA provides added sensitivity to the detection of platelet-associated antibodies in immune thrombocytopenias or following therapy with humanized MAbs.


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