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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To understand the pathophysiology of high-altitude pulmonary edema (HAPE), we examined the pathway of adaptation to high altitude in lifelong of Tibet. The Tibetan natives had higher exercise performance, but lower maximal oxygen uptake and lower blood lactate concentrations than did acclimatized Han newcomers. Clinical and basic studies done to determine the pathophysiologic characteristics of 47 patients with HAPE and of subjects susceptible to HAPE. The altitude of onset was 2,680 m to 3,190 m above sea level. Results of hemodynamic studies and the presence of protein-rich edema fluid indicated that HAPE is noncardiogenic and is a type of increased permeability edema. The levels of IL-1 beta, IL-6, IL-8, and TNF-alpha in bronchoalveolar lavage fluid from subjects with HAPE were high on admission. The subjects susceptible to HAPE had much greater increases in an index of pulmonary vascular resistance than did the controls, which resulted in much higher levels of pulmonary arterial pressure during both acute hypoxia and hypobaria. The subjects susceptible to HAPE also has blunted hypoxic ventilatory drives. We studied whether human leukocyte antigen DR-6 functions as a genetic predisposition to HAPE. The frequency of DR-6 was increased in the subjects susceptible to HAPE, which suggests that they have a constitutional abnormality in the pulmonary circulatory, and ventilatory responses to hypoxia and hypobaria, and that genetic factors may be involved in the development of HAPE.
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PMID:[High-altitude pulmonary edema in Japan]. 875 74

Transfusion related acute lung injury (TRALI) is a relatively rare but potentially severe complication of blood transfusion. Acute respiratory distress syndrome in this case is due to noncardiogenic pulmonary oedema without hypervolaemia. The passive transfer of anti-human leukocyte antigen (HLA) or antineutrophil antibodies in the donated blood products are responsible for the pathophysiological process in TRALI. Less commonly, the recipient may have antibodies which interact with white cells in the donor products. Most commonly TRALI may appear during whole blood, packed cells and fresh frozen plasma transfusions. The increased risk of TRALI is observed when a donors are multiparous women and additionally when older, stored blood components are used for transfusion. The only therapy which can be recommended as standard treatment of TRALI is ventilatory assistance and saline infusion. The case of 70-year-old woman with the fracture of the right femoral bone, who developed TRALI after transfusion of packed red cells is presented in the paper. It is the first case of TRIALI reported in our department.
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PMID:[Transfusion related acute lung injury (TRIALI)--case report]. 1504 18

Transfusion-related acute lung injury (TRALI) is an underreported complication of transfusion therapy, and it is the third most common cause of transfusion-associated death. TRALI is defined as noncardiogenic pulmonary edema temporally related to transfusion therapy. The diagnosis of TRALI relies on excluding other diagnoses such as sepsis, volume overload, and cardiogenic pulmonary edema. Supportive diagnostic evidence includes identifying neutrophil or human leukocyte antigen (HLA) antibodies in the donor or recipient plasma. All plasma-containing blood products have been implicated in TRALI, with the majority of cases linked to whole blood, packed RBCs, platelets, and fresh-frozen plasma. The pathogenesis of TRALI may be explained by a "two-hit" hypothesis, with the first "hit" being a predisposing inflammatory condition commonly present in the operating room or ICU. The second hit may involve the passive transfer of neutrophil or HLA antibodies from the donor or the transfusion of biologically active lipids from older, cellular blood products. Treatment is supportive, with a prognosis substantially better than most causes of clinical acute lung injury.
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PMID:Transfusion-related acute lung injury: a review. 1600 80

Transfusion-related acute lung injury (TRALI) is a serious clinical syndrome associated with the transfusion of plasma-containing blood components. Recently, TRALI has come to be recognized as the leading cause of transfusion-related death in the United States and United Kingdom. This complication typically presents as shortness of breath, hypoxemia, hypotension, fever and noncardiogeneic pulmonary edema, all occurring during or within 6 h after transfusion. Although the mechanism of TRALI has not been fully elucidated, it has been associated with human leukocyte antigen antibodies (class I, class II or neutrophil alloantigens) and with biologically active mediators in stored cellular blood components. Most of the donors implicated in cases of TRALI are multiparous women. Rarely diagnosed, TRALI can be confused with other causes of acute respiratory failure. Greater knowledge regarding TRALI on the part of clinicians could be crucial in preventing and treating this severe complication of blood transfusion.
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PMID:Transfusion-related acute lung injury. 1772 41

The leading cause of transfusion-related morbidity and mortality in the United States is transfusion-related acute lung injury (TRALI). Diagnostic criteria for TRALI have recently been developed and primarily consist of hypoxia and bilateral pulmonary edema occurring during or within 6 h of a transfusion in the absence of cardiac failure or intravascular volume overload. The primary differential diagnosis is transfusion-associated circulatory overload and differentiation can be difficult. Treatment is supportive with oxygen and mechanical ventilation. Diuresis is not indicated and the role of steroids is unproven. Patients typically recover within a few days. All types of blood products have been associated with TRALI, however, the plasma-rich components, such as fresh frozen plasma and apheresis platelets, have been most frequently implicated. The pathogenesis of TRALI is not completely understood. Leukocyte antibodies in donor plasma have been implicated in most cases with antibodies directed at human leukocyte antigen (HLA) class I, HLA class II or neutrophil-specific antigens, particularly HNA-3a. Activation of pulmonary endothelium is important in the development of TRALI and may account for most cases being observed in surgical or intensive care unit patients. Transfused leukoagglutinating antibodies bind to recipients' neutrophils localized to pulmonary endothelium resulting in activation and release of oxidases and other damaging biologic response modifiers that cause capillary leak. In a minority of TRALI cases, no antibodies are identified and it is postulated that neutrophil priming factors in the transfused component can mediate TRALI in a patient with pulmonary endothelial activation, the so called "two hit" mechanism. Recognition of the role of anti-leukocyte antibodies has led to new strategies to reduce the risk of TRALI. Female blood donors with a previous pregnancy frequently have HLA antibodies with an overall prevalence of 24% and increasing prevalence related to the number of previous pregnancies. Since HLA antibodies have been implicated in TRALI, blood centers have adopted policies to produce plasma components primarily from male donors. Strategies to reduce the risk from apheresis platelets are problematic and are likely to involve testing female apheresis platelet donors for HLA antibodies. Much more research is needed to understand the blood component and patient risk factors for TRALI so that novel strategies for treatment and additional measures to reduce the risk of TRALI can be developed.
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PMID:Transfusion-related acute lung injury: current concepts for the clinician. 1922 81

Transfusion-related acute lung injury (TRALI) is the leading cause of transfusion-associated mortality in the United States and other countries. In most TRALI cases, human leukocyte antigen (HLA) class II antibodies are detected in implicated donors. However, the corresponding antigens are not present on the cellular key players in TRALI: neutrophils and endothelium. In this study, we identify monocytes as a primary target in HLA class II-induced TRALI. Monocytes become activated when incubated with matched HLA class II antibodies and are capable of activating neutrophils, which, in turn, can induce disturbance of an endothelial barrier. In an ex vivo rodent model, HLA class II antibody-dependent monocyte activation leads to severe pulmonary edema in a relevant period of time, whenever neutrophils are present and the endothelium is preactivated. Our data suggest that in most TRALI cases, monocytes are cellular key players, because HLA class II antibodies induce TRALI by a reaction cascade initiated by monocyte activation. Furthermore, our data support the previous assumption that TRALI pathogenesis follows a threshold model. Having identified the biologic mechanism of HLA class II antibody-induced TRALI, strategies to avoid plasma from immunized donors, such as women with a history of pregnancy, appear to be justified preventive measures.
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PMID:Mechanism of transfusion-related acute lung injury induced by HLA class II antibodies. 2123 22

Transfusion-related acute lung injury (TRALI) is characterized by acute hypoxemia and noncardiogenic pulmonary edema. At the very least, descriptions of cases consistent with TRALI date back to the early 1950s. Early articles from the 1950s and 1960s documented transfusion-associated pulmonary edema without evidence of volume overload. Explanations for this phenomenon included hypersensitivity and transfused leukoagglutinins. Descriptions from the 1970s also implicated transfused antileukocyte antibodies and noted that blood products containing such antibodies often came from multiparous female donors. Cases implicating recipient anti-human leukocyte antigen antibody reacting with transfused donor leukocytes and donor antibodies reacting with another donor's leukocytes were also described. The 1980s marked the emergence of the Mayo Clinic as a leading contributor to the understanding of TRALI. The descriptions of the syndrome that was named "TRALI" by Mayo Clinic investigators were the most extensive and complete to date and are presented in detail. The Mayo Clinic has remained in the forefront of TRALI investigation, particularly as it pertains to the critically ill, and recent studies from this center are also presented in detail. The common thread connecting the Mayo Clinic's descriptions in the 1980s to the more contemporary studies is Dr S. Breanndan Moore. Dr Moore passed away recently, but his crucial work in the area of TRALI lives on.
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PMID:Transfusion-related acute lung injury, an evolving syndrome: the road of discovery, with emphasis on the role of the Mayo Clinic. 2113 28

Transfusion-related acute lung injury (TRALI), a previously ill-defined transfusion reaction, has emerged as the leading cause of transfusion-related morbidity and mortality reported to the Food and Drug Administration (FDA). A 3-year-old male with a history of acute lymphoblastic leukemia (ALL) developed TRALI after receiving three units of platelets and a partial unit of packed red cells. He recovered after 24 hours in the pediatric intensive care unit. Laboratory investigation revealed that two of the four blood donors, from which the platelets and packed red cells had derived, had positive human leukocyte antigen (HLA) antibody screens. Further testing of these two donors revealed that one had a specific HLA antibody matching an antigen of the patient. This donor was implicated in the TRALI reaction. TRALI is often mistaken for other transfusion reactions, most notably pulmonary edema caused by circulatory overload or congestive heart failure. It is difficult to gauge which transfusion recipients are at risk for TRALI. Good judgment and transfusion practices when ordering blood products and recognition of the clinical manifestations, diagnosis and treatment of TRALI is critical.
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PMID:Transfusion-related acute lung injury (TRALI): a case report and literature review. 2147 18

Transfusion-related acute lung injury (TRALI) is a serious complication of blood transfusion, which is characterized by the acute onset of non-cardiogenic pulmonary edema and hypoxemia following the administration of blood products. We report a case of possible TRALI during thoracic endovascular aortic repair (TEVAR). The patient was a 61-year-old man (161 cm in height, 61 kg in weight) who underwent TEVAR for the traumatic injury at the isthmus of aorta. He had a light preexisting lung injury. About 1 hour following the blood transfusion (red cell concentrates, fresh-frozen plasma, and platelet concentrates), he suddenly fell into severe hypoxemia (PaO2 52 mmHg in FI(O2) of 1.0). The radiographic examination showed pulmonary edema, i. e., bilateral infiltrates and pleural effusion. No evidence of circulatory overload was observed. Anti-human leukocyte antigen antibodies in his serum and anti-granulocyte antibodies in the donor blood were detected. In spite of intensive care including artificial ventilation with positive end-expiratory pressure and the administration of methylprednisolone and a granulocyte elastase inhibitor, he died of exacerbated hypoxemia and hypotension 4 hours after the onset of acute lung injury. Of great importance is being aware of an unexpected occurrence of TRALI during and soon after blood transfusion.
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PMID:[Case of possible transfusion-related acute lung injury during thoracic endovascular aortic repair]. 2217 73

Transfusion-related acute lung injury (TRALI) is a noncardiogenic pulmonary edema that occurs during or within 6 hours after transfusion. Risk factors for TRALI, which is relatively common in critically ill patients, include recent surgery, hematologic malignancy, and sepsis. Here, we report a case of TRALI induced by anti-human leukocyte antigen (anti-HLA) class II antibodies (HLA-DR) occurring after transfusion of platelet concentrates in a patient with acute leukemia. Although most patients with TRALI show improvement within 48-96 hours, our patient's condition rapidly worsened, and he did not respond to supportive treatment. TRALI is a relatively common and serious adverse transfusion reaction that requires prompt diagnosis and management.
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PMID:A case of transfusion-related acute lung injury induced by anti-human leukocyte antigen antibodies in acute leukemia. 2332 11


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