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A patient with calf pain
Published in Tim French, Terry Wardle, The Problem-Based Learning Workbook, 2022
DVT results from a complex series of events involving coagulation factors, platelets, red blood cells and the vessel wall. The components of Virchow’s triad can be used to predict the risk factors for developing thrombosis and its pathogenesis: venous stasishypercoagulabilityvessel wall disease.
Lower Limb
Published in Bobby Krishnachetty, Abdul Syed, Harriet Scott, Applied Anatomy for the FRCA, 2020
Bobby Krishnachetty, Abdul Syed, Harriet Scott
Emboli rank first for being the culprit for acute limb ischaemia and most commonly arise from the heart, a proximal arterial aneurysm or atherosclerosis. Thrombosis may be induced by any of the three factors of Virchow’s triad: static or turbulent blood flow, hypercoagulability and endothelial injury.
Venous Thromboembolic Disease
Published in James M. Rippe, Lifestyle Medicine, 2019
It is likely that truly idiopathic VTE or PE is rare and that the majority of VTE occurs in the context of at least one, and often multiple, risk factors.21 The risk factors that predispose the patient to clot can be divided generally into two groups: inherited (including anatomical variations and genetic clotting disorders) or acquired (e.g., undergoing surgery or presence of comorbid disease such as cancer).22 Though these risk factors might appear varied and unrelated, the final common pathway of clotting is the perturbation of the local vascular microenvironment such that some or all of Virchow’s triad is satisfied.23 There are several published datasets that enhance our understanding of both the relative individual strength of risk factors and the interplay of acquired and innate risks when present concurrently.24
Enoxaparin adherence for venous thromboembolism prophylaxis in hospitalized patients with sickle cell disease
Published in Expert Review of Hematology, 2023
Colleen Sakon, Miley Nikirk, Andrew Ross Wickman O’Brien
Venous thromboembolism (VTE) is a common cause of morbidity and mortality in patients with sickle cell disease (SCD) [1]. Due to the nature of the disease, every part of Virchow’s triad is affected in this patient population: increased coagulability, endothelial dysfunction, and impaired blood flow [2]. It has been shown that rates of pulmonary embolism (PE) in hospitalized patients with SCD less than 40 years of age was 3.5 times higher than controls [3]. The mean age of PE in this group was 28 years as opposed to 65 years in the general population. Despite this evidence, there are no clear guidelines for VTE prophylaxis in this patient population. Due to the lack of direct evidence, providers must make clinical decisions by extrapolating other data. Based on general VTE prevention guidelines, pharmacological prophylaxis is generally recommended in the SCD patient population while hospitalized [4,5]. A study assessing the safety of pharmacologic VTE prophylaxis noted that enoxaparin 40 mg was the most commonly prescribed agent in patients hospitalized with SCD [6].
New prophylaxis strategies to reduce the risk of thromboembolism in cancer
Published in Expert Review of Anticancer Therapy, 2021
Vasileios Papadopoulos, Konstantinos Tsapakidis, Alexandra Markou, Alexandros Kokkalis, Chrissovalantis Aidarinis, Athanasios Kotsakis
In December 2019, Wuhan became the center of an outbreak of pneumonia of unknown cause [64]. Chinese scientists isolated a new virus which was named novel coronavirus. Later, it was designated as coronavirus disease 2019 (COVID-19) [64]. By March 2020, World Health Organization (WHO) declares COVID-19 a global pandemic [64]. There are many references that patients with COVID-19 are in a hypercoagulable state and have an increased risk of venous thromboembolism [65]. This state has been termed thrombo-inflammation or COVID-19-associated coagulopathy (CAC) by some experts [65]. Virchow’s triad contributes to clot formation and applies to severe COVID-19 infection [64]. Immobilization can cause stasis of blood flow in all hospitalized and critically ill patients. A number of changes in circulating prothrombotic factors have been reported or proposed in patients with severe COVID-19 infection, like elevated factor VIII, elevated fibrinogen, circulating prothrombotic microparticles, neutrophil extracellular traps (NETs). Finally, there is evidence of direct invasion of endothelial cells by the SARS-CoV-2 virus, potentially leading to cell injury [64]. The incidence of venous thromboembolism in hospitalized patients with COVID‐19, even with thromboprophylaxis, is higher [66].
Bilateral superior ophthalmic vein thrombosis associated with high altitude
Published in Orbit, 2021
Abtin Shahlaee, Lauren M. Hennein, Bryan J. Winn, William P. Dillon, Nailyn Rasool
Virchow’s triad provides an understanding of the three components which contribute to venous thrombosis: hypercoagulability, hemodynamic alterations and endothelial dysfunction. These same mechanisms remain responsible for superior ophthalmic vein thrombosis which can occur from both septic and aseptic etiologies. Septic causes most commonly involve infections of the paranasal sinuses; however, orbital, dental and facial infections have also been implicated.,3,4 Aseptic causes of SOVT include vascular, hypercoagulable, lymphoproliferative, and inflammatory etiologies. Vascular malformations such as dural arteriovenous fistulae, venous malformations, and facial trauma disrupting normal flow have all been implicated in SOVT.5,6 Hypercoagulable disorders such as antiphospholipid syndrome,7,8 sickle cell,9 and drug-induced hypercoagulability due to hormonal therapy (oral contraceptives and tamoxifen) have been reported.10–13 Lymphoproliferative disorders14 as well as diffuse and localized inflammatory conditions such as systemic lupus erythematosus,1,5 ulcerative colitis3, Graves’ orbitopathy,15,16 and idiopathic orbital inflammatory disease17 have all been seen in association with SOVT. Altitude, however, has not been recognized as a risk factor for SOVT.