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排序方式: 共有328条查询结果,搜索用时 31 毫秒
1.
Luiz A Benvenuti Francisco O S Fran?a Kátia C Barbaro José R Nunes Jo?o L C Cardoso 《Toxicon》2003,42(3):331-334
A 36-year old woman was bitten on the left ankle by a Bothrops jararacussu, and died 45 min after the bite. At necropsy, there were local signs of envenoming with haemorrhage, thrombosis and necrosis of the subcutaneous and muscular tissue. Multiple fibrin and platelet thrombi were found in the microcirculation of the heart and lungs, suggesting the occurrence of disseminated intravascular coagulation. Pulmonary haemorrhage probably secondary to the action of haemorrhagins, consumption coagulopathy and disseminated intravascular coagulation was the immediate cause of death. Intravenous inoculation of the venom could have occurred in the present case, which would explain the rapid onset of coagulation disorders, haemorrhage and death. 相似文献
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Blood coagulation activation is frequently found in patients with malaria. Clinically apparent bleeding or disseminated intravascular coagulation (DIC) is associated with very severe disease and a high mortality. Protein C, protein S, and antithrombin levels were found to be low in P. falciparum, but were normal in P. vivax infection. Plasma levels of plasminogen activator inhibitor-1 were high in cases of P. falciparum infection whereas tissue plasminogen activator levels were low. Elevated plasma levels of von Willebrand factor (vWF) and vWF propeptide, thrombomodulin, endothelial microparticles have been reported in P. falciparum-infected patients. It has been demonstrated that severe P. falciparum infection is associated with acute endothelial cell (EC) activation, abnormal circulating ultralarge vWF multimers, and a significant reduction in plasma ADAMTS13 function. These changes may result in intravascular platelet aggregation, thrombocytopenia, and microvascular disease. It has also been shown that P. falciparum-parasitized red blood cells (pRBCs) induce tissue factor (TF) expression in microvascular ECs in vitro. Recently, loss of endothelial protein C receptor (EPCR) localized to sites of cytoadherent pRBCs in cerebral malaria has been demonstrated. Severe malaria is associated with parasite binding to EPCR. The cornerstone of the treatment of coagulopathy in malaria is the use of effective anti-malarial agents. DIC with spontaneous systemic bleeding should be treated with screened blood products. Study in Thailand has shown that for patients who presented with parasitemia > 30% and severe systemic complications such as acute renal failure and ARDS, survival was superior in the group who received exchange transfusion. The use of heparin is generally restricted to patients with DIC and extensive deposition of fibrin, as occurs with purpura fulminans or acral ischemia. Antiplatelet agents interfere with the protective effect of platelets against malaria and should be avoided. 相似文献
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Dental extractions are a common part of general dental practice. While dentists routinely screen for medical contraindications during the preoperative assessment, undiagnosed coagulopathies have the potential to severely complicate a seemingly routine extraction. We report a case of surgical removal of a mandibular third molar in a patient with undiagnosed Von Willebrand Disease. 相似文献
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Sven Van Poucke Kris Stevens Cécile Kicken Antoine Simons Abraham Marcus Marcus Lancé 《Artificial organs》2016,40(3):288-293
Alterations in platelet function are a common finding in surgical procedures involving cardiopulmonary bypass and hypothermia. Although the combined impact of hypothermia and artificial circulation on platelets has been studied before, the ultimate strategy to safely minimize the risk for bleeding and thrombosis is yet unknown. The aim of this study was to evaluate the use of a mock circulation loop to study the impact of hypothermia for platelet‐related hemostatic changes. Venous blood was collected from healthy adult humans (n = 3). Closed mock circulation loops were assembled, each consisting of a centrifugal pump, an oxygenator with integrated heat exchanger, and a hardshell venous reservoir. The experiment started with the mock circulation temperature set at 37°C (T0 [0 h]). Cooling was then initiated at T1 (+2 h), where temperature was adjusted from 37°C to 32°C. Hypothermia was maintained from T2 (+4 h) to T3 (+28 h). From that point in time, rewarming from 32°C to 37°C was initiated with similar speed as cooling. From time point T4 (+30 h), normothermia (37°C) was maintained until the experiment ended at T5 (+32 h). Blood samples were analyzed in standard hematological tests: light transmission aggregometry (LTA) (arachidonic acid [AA], adenosine diphosphate [ADP], collagen [COL], thrombin‐receptor‐activating‐peptide‐14 [TRAP]), multiple electrode aggregometry (MEA) (AA, ADP, COL, TRAP), and rotational thromboelastometry (ROTEM) (EXTEM, FIBTEM, PLTEM). Hemoglobin, hematocrit, and platelet count decrease more substantially during temperature drop (37–32°C) than during hypothermia maintenance. Hb and Hct continue to follow this trend during active rewarming (32–37°C). PC increase from the moment active rewarming was initiated. None of the values return to the initial values. LTA values demonstrate a similar decrease in aggregation after stimulation with the platelet agonists between the start of the mock circulation and the start of cooling. Except for platelet stimulation using COL, this trend continues during temperature drop from 37°C to 32°C. LTA values using AA and TRAP demonstrate a considerable decline in platelet function throughout the experiment that was most pronounced after 24 h of circulation at 32°C. LTA values using ADP and COL further decline after rewarming. MEA ADP, ASPI, and COL identify platelet dysfunction patterns analogous with LTA, between the start of the mock circulation and the start of cooling. Except for MEA TRAP, this trend continues during temperature drop from 37°C to 32°C. MEA ASPI and ADP demonstrate a considerable decline in platelet function throughout the experiment, which was most pronounced after 24 h of circulation at 32°C. For MEA COL and TRAP, further decline in platelet function is observed after rewarming. This study quantitatively assessed the effect of temperature changes on platelet function during experimental mock circulation demonstrating a considerable decline in platelet function during hypothermia without uniform recovery of platelet function observed after rewarming. 相似文献
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