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• W2023543531 abstract "A number of clinical situations tax our clinical skills and decision‐making to the extreme. One of these conundrums is whether or not to institute full‐dose anticoagulation therapy in a patient with an acute deep vein thrombosis (DVT) or pulmonary embolism (PE) who has had a recent (< 30 days) major bleeding event. Inserting an inferior vena cava (IVC) filter is an easy option, but unsettling because it does not arrest the thrombotic diathesis, it increases the risk of recurrent DVT, it and does not prevent PE (although it may prevent a ‘big’, potentially lethal PE). What happens if we boldly proceed to anticoagulate the patient? What is the incidence of recurrent bleeding? This problem is addressed by Nieto et al. [1Nieto J.A. Bruscas M.J. Ruiz‐Ribo D. Trujillo‐Santos J. Valle R. Ruiz‐Gimenez N. Monreal M. Acute venous thromboembolism in patients with recent major bleeding. The influence of the site of bleeding and the time elapsed on outcome.J Thromb Haemost. 2006; 4: 2367-72Abstract Full Text Full Text PDF PubMed Scopus (39) Google Scholar] in this issue, who used the Registro Informatizado de la Enfermedad Thrombo Embolico (RIETE) prospective venous thromboembolism (VTE) registry to analyze outcomes in 306 patients who had a major bleeding event less than 30 days before acute VTE was diagnosed. Overall, 97% of these patients received anticoagulation treatment a median of 0 day after VTE diagnosis, but the exact timing and intensity of anticoagulation treatment for each case was not specified. These findings extend an earlier analysis of this registry [2Nieto J.A. De Tuesta A.D. Marchena P.J. Tiberio G. Todoli J.A. Samperiz A.L. Monreal M. Clinical outcome of patients with venous thromboembolism and recent major bleeding: findings from a prospective registry (RIETE).J Thromb Haemost. 2005; 3: 703-9Abstract Full Text Full Text PDF PubMed Scopus (46) Google Scholar]. Importantly, the number of patients who rebled within 3 months was quite low – only 19 (6.2%). However, 13 (69%) of these patients who rebled died within 2 weeks. It is not easy to estimate the overall risks vs. benefits of starting full‐dose anticoagulation treatment of VTE in patients who have had a recent major hemorrhagic event when the exact timing and intensity of anticoagulation therapy is not specified. However, regardless of what was done, eight patients (2.6%) died of major bleeding and 10 (3.2%) died of acute PE, suggesting there is indeed a precarious balance between too much and too little anticoagulation treatment in these high‐risk patients. It would have been nice if the authors had described the specifics of how the patients who died of PE were treated, specifically if there was an absence or delay in the initiation of anticoagulation, and if the dosing of heparin or low‐molecular‐weight heparin (LMWH) was suboptimal. A shorter time period (< 2 weeks vs. > 2 weeks) between the initial bleed and the VTE event was associated with just over 2‐fold higher odds of rebleeding, and approximately 3‐fold higher odds of dying, suggesting that the closer the time between the bleeding event and the VTE, the more challenging the anticoagulation management becomes, which may be self‐evident. Missing in this report was a mention of any specific treatment for the underlying cause of the bleeding. Perhaps the lower incidence of rebleeding (and death) in the patients who were diagnosed with VTE over 2 weeks after the bleeding was a result of them being adequately treated for the cause of the bleeding, such as the use of antibotics to treat Helicobacter pylori infection, proton pump inhibition for patients with upper gastrointestinal ulceration, and dilatation and curettage for women with uterine bleeding. Perhaps the most surprising finding was the absence of any major rebleeding among the 94 patients who had suffered an intracranial bleed. Two‐thirds of the patients with intracranial bleeding had the VTE diagnosed over 2 weeks after the bleed, 30% were treated with an IVC filter, and the initial treatment dose of LMWH was significantly lower, all of which may partially explain the absence of any rebleeding in this cohort. Nevertheless, the absence of any rebleeding after an intracranial bleed was striking and unexpected, particularly as 89 of the 94 cases were anticoagulated almost immediately after diagnosis of VTE. Some of these patients must have had amyloid angiopathy or a condition associated with a high risk of rebleeding during the 3‐month follow‐up period [3Fang M.C. Chang Y. Hylek E.M. Rosand J. Greenberg S.M. Go A.S. Singer D.E. Advanced age, anticoagulation intensity, and risk for intracranial hemorrhage among patients taking warfarin for atrial fibrillation.Ann Intern Med. 2004; 141: 745-52Crossref PubMed Scopus (451) Google Scholar, 4Towfighi A. Greenberg S.M. Rosand J. Treatment and prevention of primary intracerebral hemorrhage.Semin Neurol. 2005; 25: 445-52Crossref PubMed Scopus (24) Google Scholar]. Although the authors state that consecutive patients with VTE were enrolled, the absence of any recurrent intracranial bleeding findings suggests that selection bias may have been present. Perhaps the authors are correct when they suggest that patients with more severe intracranial bleeding may have died before developing a VTE or that the intracranial hemorrhage patients who were enrolled in this registry had a lower incidence of significant comorbid medical illness, particularly cancer and renal insufficiency. How will the findings of this study change how I treat my patients? I will continue to aggressively work up the cause of all major bleeding events and aggressively treat the underlying cause, if possible. As soon as the bleeding is controlled, I will continue to consider restarting VTE prophylaxis. If one of my patients then develops symptomatic VTE, I will painstakingly go through the usual process of weighing the risks vs. the benefits of starting full‐dose anticoagulation therapy. This will continue to be particularly difficult for the patient with recent major bleeding in the presence of metastatic cancer. I will still start treatment with i.v. unfractionated heparin for at least several days, because I can reverse the effect of the heparin quickly if rebleeding occurs. Irrespective of the findings of this study, I will still have major concerns about starting anticoagulation in a patient who has had a recent intracranial hemorrhage, and I will continue to actively consult with my neurology and neurosurgical colleagues. Perhaps I will now feel a little less worried about starting heparin if the VTE developed over 2 weeks after the intracranial bleeding event, but I will continue to go over magnetic resonance imaging findings with neuroradiologists to make sure that there is no evidence of amyloid angiopathy. I will remain extremely anxious if my patient has angiodysplasia throughout the colon. I will not even comment about what I will do if a patient has severe bleeding that requires factor VIIa treatment and then immediately develops an acute VTE. Management of VTE in the patient who remains at high risk for bleeding remains one of the most challenging and vexing problems in clinical medicine. The author states that he has no conflict of interest." @default.
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• W2023543531 title "Anticoagulation therapy after recent bleeding: is it ever safe?" @default.
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