Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Through an innovative electron microscopy technique, thrombi and fibrotic tissue taken from 14 explanted vena cava filters were observed. Twelve cases showed the presence of micro-and nano-sized inorganic, non biodegradable nor biocompatible particles which did not belong to the metal the device was made of and which could be the sole cause or, more likely, a pre-existing cause for thrombosis. In two cases, those debris activated immunological reactions typical of a foreign body. The presence of inorganic particles in the blood was never detected before and their effects on human health are hardly known. Their thrombogenicity should be added to the Virchow's Triad as a fourth factor and could be the explanation to many of the cases of pulmonary embolism where no thrombotic focus could be demonstrated.
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PMID:In-vivo short- and long-term evaluation of the interaction material-blood. 1636 24

Autopsy is an important source of data for education and quality control. The aim of this study was comparison of ante- to post-mortem findings to detect weak points of intensive care unit (ICU) care. Patients who died in our 14-bed university medical ICU care and underwent an autopsy examination over 20 months (September 2007 to May 2009) were included. Modified Goldman's criteria were used to categorise discrepancies between diagnoses and post-mortem findings. A triad algorithm was constructed to analyse individual ante- to post-mortem findings. One hundred and seventy post-mortem examinations were conducted (45.6% autopsy rate). Major diagnostic discrepancies were detected in 20 patients (11.8%); four class I (2.4%) and 16 class II (9.4%). Massive pulmonary embolism with cardiac arrest was the most common class I discrepancy (75%). Triad analysis of major class I discrepancies showed that all patients had a history of chronic disease; the majority (75%) had a short ICU length of stay. In 75% adequate tests were used to detect disorders. There were interpretation problems of bedside data in complex emergency clinical conditions, especially with less experienced ICU physicians. Inappropriate or incorrectly interpreted diagnostic procedures were performed in more than half of cases with class II discrepancies (9/16, 56%). Abdominal ultrasonography was misleading in 31% (5/16) cases with class II discrepancies. In conclusion, triad algorithm analysis revealed problematic interpretation of bedside diagnostics in emergency cases by inexperienced physicians in class I major discrepancies detected at autopsy. No correct test and wrong interpretation of abdominal ultrasonography were major causes of class II discrepancies.
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PMID:A triad algorithm for analysing individual ante- and post-mortem findings to improve the quality of intensive care. 2216 63

Venous thrombosis (VT) is the third most common cause of cardiovascular death worldwide. Complications from VT and pulmonary embolism are the leading cause of lost disability-adjusted life years. Risks include genetic (e.g., non-O blood group, activated protein C resistance, hyperprothrombinemia) and acquired (e.g., age, surgery, cancer, pregnancy, immobilisation, female hormone use) factors. Pathophysiologic mechanisms that promote VT are incompletely understood, but involve abnormalities in blood coagulability, vessel function, and flow (so-called Virchow's Triad). Epidemiologic studies of humans, animal models, and biochemical and biophysical investigations have revealed contributions from extrinsic, intrinsic, and common pathways of coagulation, endothelial cells, leukocytes, red blood cells, platelets, cell-derived microvesicles, stasis-induced changes in vascular cells, and blood rheology. Knowledge of these mechanisms may yield new therapeutic targets. Characterisation of mechanisms that mediate VT formation and stability, particularly in aging, are needed to advance understanding of VT.
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PMID:New findings on venous thrombogenesis. 2787 6

Deep vein thrombosis (DVT) is a major preventable cause of morbidity and mortality worldwide. Venous thromboembolism (VTE), which includes DVT and pulmonary embolism (PE), affects an estimated 1 per 1,000 people and contributes to 60,000-100,000 deaths annually. Normal blood physiology hinges on a delicate balance between pro- and anti-coagulant factors. Virchow's Triad distills the multitude of risk factors for DVT into three basic elements favoring thrombus formation: venous stasis, vascular injury, and hypercoagulability. Clinical, biochemical, and radiological tests are used to increase the sensitivity and specificity for diagnosing DVT. Anticoagulation therapy is essential for the treatment of DVT. With few exceptions, the standard therapy for DVT has been vitamin K-antagonists (VKAs) such as warfarin with heparin or fractionated heparin bridging. More recently, a number of large-scale clinical trials have validated the use of direct oral anticoagulants (DOACs) in place of warfarin in select cases. In this review, we summarize the pathogenesis, diagnosis, and medical management of DVT, with particular emphasis on anticoagulation therapy and the role of DOACs in the current treatment algorithm.
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PMID:Deep vein thrombosis: pathogenesis, diagnosis, and medical management. 2939 31