43 research outputs found

    Approach to leg edema

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    Edema is defined as a palpable swelling caused by an increase in interstitial fluid volume. Leg edema is a common problem with a wide range of possible causes and is the result of an imbalance in the filtration system between the capillary and interstitial spaces. Major causes of edema include venous obstruction, increased capillary permeability and increased plasma volume secondary to sodium and water retention. In both hospital and general practice, the patient with a swollen leg presents a common dilemma in diagnosis and treatment. The cause may be trivial or life-threatening and it is often difficult to determine the clinical pathway. The diagnosis can be narrowed by categorizing the edema according to its duration, distribution (unilateral or bilateral) and accompanying symptoms. This work provides clinically oriented recommendations for the management of leg edema in adults

    A complicated case of pulmonary embolism in a patient with renal failure

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    We describe a case of pulmonary embolism with instable hemodynamics in a patient with renal failure; the case is complicated by heparin-induced thrombocytopenia (HIT). Renal failure has a high prevalence in hospitalized patients and is a restriction on administration of low molecular weight heparins (LMWH) and fondaparinux. HIT is a potentially life-threatening complication, therefore a precocious diagnosis is essential. Therapy consists in the immediate stop of heparin’s administration and in the administration of non-heparin antithrombotic drugs

    Rivaroxaban for the treatment of noncirrhotic splanchnic vein thrombosis: an interventional prospective cohort study.

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    Heparins and vitamin K antagonists are the mainstay of treatment of splanchnic vein thrombosis (SVT). Rivaroxaban is a potential alternative, but data to support its use are limited. We aimed to evaluate the safety and efficacy of rivaroxaban for the treatment of acute SVT. In an international, single-arm clinical trial, adult patients with a first episode of noncirrhotic, symptomatic, objectively diagnosed SVT received rivaroxaban 15 mg twice daily for 3 weeks, followed by 20 mg daily for an intended duration of 3 months. Patients with Budd-Chiari syndrome and those receiving full-dose anticoagulation for >7 days prior to enrollment were excluded. Primary outcome was major bleeding; secondary outcomes included death, recurrent SVT, and complete vein recanalization within 3 months. Patients were followed for a total of 6 months. A total of 103 patients were enrolled; 100 were eligible for the analysis. Mean age was 54.4 years; 64% were men. SVT risk factors included abdominal inflammation/infection (28%), solid cancer (9%), myeloproliferative neoplasms (9%), and hormonal therapy (9%); 43% of cases were unprovoked. JAK2 V617F mutation was detected in 26% of 50 tested patients. At 3 months, 2 patients (2.1%; 95% confidence interval, 0.6-7.2) had major bleeding events (both gastrointestinal). One (1.0%) patient died due to a non-SVT-related cause, 2 had recurrent SVT (2.1%). Complete recanalization was documented in 47.3% of patients. One additional major bleeding event and 1 recurrent SVT occurred at 6 months. Rivaroxaban appears as a potential alternative to standard anticoagulation for the treatment of SVT in non-cirrhotic patients. This trial was registered at www.clinicaltrials.gov as #NCT02627053 and at eudract.ema.europa.eu as #2014-005162-29-36

    Державне регулювання системи факторів оцінки та мінімізації ризиків легалізації коштів, одержаних злочинним шляхом в процесі фінансового моніторингу комерційних банків України

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    Основною ціллю данної статті є формулювання важливості впливу чітко визначених факторів, які впливають на процеси фінансового моніторингу в комерційних банків України. Виходячи з поставлених цілей, завданнями даної статті є розроблення моделі оцінки ризиків банківської установи щодо протидії легалізації коштів одержаних злочинним шляхом в системі внутрішньобанківського фінансового моніторингу, та використання в подальшому запропонованих стратегій управління наслідками даних ризиків

    Association Between Preexisting Versus Newly Identified Atrial Fibrillation and Outcomes of Patients With Acute Pulmonary Embolism

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    Background Atrial fibrillation (AF) may exist before or occur early in the course of pulmonary embolism (PE). We determined the PE outcomes based on the presence and timing of AF. Methods and Results Using the data from a multicenter PE registry, we identified 3 groups: (1) those with preexisting AF, (2) patients with new AF within 2 days from acute PE (incident AF), and (3) patients without AF. We assessed the 90-day and 1-year risk of mortality and stroke in patients with AF, compared with those without AF (reference group). Among 16 497 patients with PE, 792 had preexisting AF. These patients had increased odds of 90-day all-cause (odds ratio [OR], 2.81; 95% CI, 2.33-3.38) and PE-related mortality (OR, 2.38; 95% CI, 1.37-4.14) and increased 1-year hazard for ischemic stroke (hazard ratio, 5.48; 95% CI, 3.10-9.69) compared with those without AF. After multivariable adjustment, preexisting AF was associated with significantly increased odds of all-cause mortality (OR, 1.91; 95% CI, 1.57-2.32) but not PE-related mortality (OR, 1.50; 95% CI, 0.85-2.66). Among 16 497 patients with PE, 445 developed new incident AF within 2 days of acute PE. Incident AF was associated with increased odds of 90-day all-cause (OR, 2.28; 95% CI, 1.75-2.97) and PE-related (OR, 3.64; 95% CI, 2.01-6.59) mortality but not stroke. Findings were similar in multivariable analyses. Conclusions In patients with acute symptomatic PE, both preexisting AF and incident AF predict adverse clinical outcomes. The type of adverse outcomes may differ depending on the timing of AF onset.info:eu-repo/semantics/publishedVersio

    Venous Thromboembolism in Sepsis: From Bench to Bedside

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    Septic patients were commonly affected by coagulation disorders; thus, they are at high risk of thrombotic complications. In the last decades, novel knowledge has emerged about the interconnected and reciprocal influence of immune and coagulation systems. This phenomenon is called immunothrombosis, and it indicates an effective response whereby immune cells and the coagulation cascade cooperate to limit pathogen invasion and endothelial damage. When this network becomes dysregulated due to a systemic inflammatory activation, as occurs during sepsis, it can result in pathological thrombosis. Endothelium, platelets and neutrophils are the main characters involved in this process, together with the TF and coagulation cascade, playing a critical role in both the host defense and in thrombogenesis. A deeper understanding of this relationship may allow us to answer the growing need for clinical instruments to establish the thrombotic risk and treatments that consider more the connection between coagulation and inflammation. Heparin remains the principal therapeutical response to this phenomenon, although not sufficiently effective. To date, no other significant alternatives have been found yet. In this review, we discuss the role of sepsis-related inflammation in the development and resolution of venous thromboembolism and its clinical implications, from bench to bedside

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    Antiphospholipid Syndrome During Septic Shock: Hyper- or Hypocoagulability?: A Case Report

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    We report the clinical case of a septic patient with antiphospholipid syndrome who developed ischemia in all 4 limbs, despite a normal systemic blood pressure. Prolonged coagulation times suggested a hemorrhagic diathesis, requiring transfusion of fresh-frozen plasma and discontinuation of heparin infusion. In contrast, the study of the viscoelastic properties of the clot by thromboelastography suggested an uncontrolled activation of the coagulation cascade. This observation led to the reintroduction of heparin with improvement in the patient's laboratory findings. Anesthesiologists should consider thromboelastography to correct coagulopathies in patients with septic shock in the presence of antiphospholipid antibodies
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