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

Transfusion-related acute lung injury (TRALI) is an infrequent but life-threatening complication of hemotherapy. The findings in 36 cases are described. The typical clinical presentation includes acute respiratory distress characterized by hypoxemia and fulminant pulmonary edema. The onset is usually within 4 hours of transfusion and is accompanied by hypotension. In most patients (81%), recovery is rapid and complete. In 89 percent of cases, granulocyte or lymphocytotoxic antibodies are found in the serum of the implicated blood product which contained plasma. HLA-specific antibodies were identified in donor serums in 65 percent of cases evaluated. The passive transfer of these antibodies may promote complement activation and subsequent pulmonary injury. TRALI is an important cause of transfusion-associated morbidity and is probably often misdiagnosed. Blood banks need to identify donors whose plasma causes these reactions in order to prevent their recurrence.
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PMID:Diagnostic and pathogenetic considerations in transfusion-related acute lung injury. 407 3

Febrile non-hemolytic transfusion reactions occur not infrequently following transfusion. Our understanding of the molecular biology of these reactions has increased dramatically over the past few years. A variety of biological response modifiers have been shown to play a role in these reactions. These chemical messengers include cytokines, complement fragments, antibodies and adhesion molecules. Many of the clinical symptoms associated with these reactions are attributable to activation and generation of these substances. This review article will cover the role of cytokines in generation of non-hemolytic febrile transfusion reactions and the role of activation of adhesion molecules in the generation of TRALI (non-cardiogenic pulmonary edema). Our ability to modulate the generation of these chemical messengers could help us control clinical symptoms associated with these transfusion reactions.
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PMID:The role of cytokines and adhesive molecules in febrile non-hemolytic transfusion reactions. 771 94

Transfusion-related acute lung injury (TRALI) is a serious complication of hemotherapy. During blood storage, lipids are generated and released into the plasma. In this study, the role of these lipids in TRALI was investigated using an isolated, perfused rat lung model. Rats were pretreated with endotoxin (LPS) or saline in vivo and the lungs were isolated, ventilated, and perfused with saline, or (a) 5% (vol/ vol) fresh human plasma, (b) plasma from stored blood from the day of isolation (D.0) or from the day of outdate (D.42), (c) lipid extracts from D.42 plasma, or (d) purified lysophosphatidylcholines. Lungs from saline or LPS-pretreated rats perfused with fresh (D.0) plasma showed no pulmonary damage as compared with saline perfused controls. LPS pretreatment/D.42 plasma perfusion caused acute lung injury (ALI) manifested by dramatic changes in both pulmonary artery pressure and edema. Incubation of LPS pre-tx rats with mibefradil, a Ca2+ channel blocker, or WEB 2170, a platelet-activating factor (PAF) receptor antagonist, inhibited ALI caused by D.42 plasma. Lung histology showed neutrophil sequestration without ALI with LPS pretreatment/saline or D.0 plasma perfusion, but ALI with LPS pretreatment/D.42 plasma perfusion, and inhibition of D.42 plasma induced ALI with WEB 2170 or mibefradil. A significant increase in leukotriene E4 was present in LPS-pretreated/D.42 plasma-perfused lungs that was inhibited by WEB 2170. Lastly, significant pulmonary edema was produced when lipid extracts of D.42 plasma or lysophosphatidylcholines were perfused into LPS-pretreated lungs. Lipids caused ALI without vasoconstriction, except at the highest dose employed. In conclusion, both plasma and lipids from stored blood produced pulmonary damage in a model of acute lung injury. TRALI, like the adult respiratory distress syndrome, may be the result of two insults: one derived from stored blood and the other from the clinical condition of the patient.
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PMID:Plasma and lipids from stored packed red blood cells cause acute lung injury in an animal model. 952 89

Transfusion-related acute lung injury is an uncommon condition characterized by the rapid onset of respiratory distress soon after transfusion. Our understanding of its pathophysiology is based on animal models of complement (C5a) and antibody-induced lung injury and a limited number of autopsies. These models suggest that transfusion-related acute lung injury is induced by granulocytes that aggregate in the pulmonary microvasculature after activation by transfusion-derived antibodies or biologically active lipids. The published autopsy reports provide little support for this model, as they are invariably confounded by underlying pulmonary infection, preexisting disease, and resuscitation injury. We report the case of a previously well 58-year-old man who died of transfusion-related acute lung injury within 2 hours of the onset of pulmonary distress; autopsy showed evidence of massive pulmonary edema with granulocyte aggregation within the pulmonary microvasculature and extravasation into alveoli. Electron microscopy revealed capillary endothelial damage with activated granulocytes in contact with the alveolar basement membranes. These findings provide direct support for the proposed model of transfusion-related acute lung injury pathogenesis.
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PMID:The pathology of transfusion-related acute lung injury. 1043 2

Transfusion-related acute lung injury is a life-threatening complication of hemotherapy associated with the transfusion of plasma-containing blood products. It is characterized by acute respiratory distress, pulmonary edema and hypoxemia. Although its frequency is unknown, Food and Drug Administration data suggest that it is the third most common cause of transfusion-associated deaths, representing 9% of reported cases. Males and females of all ages are at equal risk. To date, there is no recognized profile of individuals who are at increased risk for this complication. Although there are two purported mechanisms of injury, the preponderance of evidence suggests that passively transfused complement-activating antibodies (either granulocyte or HLA-specific) act as mediators, which result in granulocyte aggregation, activation, and microvascular pulmonary injury. With appropriate respiratory intervention, most patients recover within 96 hours of the original insult and without permanent pulmonary sequelae.
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PMID:Transfusion-related acute lung injury. 1105 15

Transfusion-related acute lung injury (TRALI) is a second most serious complication of the blood transfusion. It is a group of symptoms and signs such as dyspnoea, hypotension, cyanosis, cough, elevated temperature, fever and lung oedema that usually develops within an hour or two after transfusion. The full stage clinical presentation is developed between 4th and 6th hours after transfusion. The syndrome is caused by leucoagglutinins or by other lymphocytotoxic antibodies specific for some antigens present on the donor's leukocytes. Alveoles of the lung are the main place of the pathological changes such as intra-alveolar oedema, haemorrhage, hyaline membrane formation, alveolar cell hypertrophy and scant interstitial inflammation. Chest X-ray showed bilateral pulmonary infiltrates but without vascular congestion and with normal cardiac silhouette comparing to the status before transfusion. The syndrome has to be distinquished from pulmonary oedema caused by acute cardial insufficiency, overhydration, trauma and sepsis.
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PMID:[Acute lung injury related to blood transfusion]. 1143 32

The respiratory tree has been viewed as an infrequent site of injury arising as a complication of transfusion. In recent years, this view has changed as investigators have shown that two complications--circulatory overload and transfusion-related acute lung injury--are relatively frequent events. Circulatory overload is a result of hypertransfusion to individuals at risk, the very young or old recipient. The reaction is due to fluid infusion which overwhelms the capacity of the left ventricle, resulting in pulmonary edema. While rarely fatal, studies have shown that such incidents result in intensive care and extended hospitalization. In the setting of orthopedic surgery, 1% of elderly patients undergoing hip or knee surgery experience circulatory overload. These events are associated with autologous, as well as allogeneic red blood cells (RBC) and fresh frozen plasma. Transfusionists need to be vigilant with transfusion therapy in this population. Phlebotomy and supplemental oxygen are the key therapies. Transfusion-related acute lung injury (TRALI) is the adult respiratory distress syndrome due to transfusion. It is associated with a significant morbidity and mortality of 5-14%, making it the third most common cause of death from transfusion in developed countries. It is characterized by the onset of acute respiratory distress, bilateral pulmonary edema and hypoxemia. It occurs within 1-2 hours of transfusion of a plasma-containing blood product. All blood components have been associated with the reaction, and rarely, intravenous immune globulin. There is no recognized profile of individuals at increased risk for TRALI. There are two purported mechanisms of injury; the vast majority of cases are associated with passively transfused complement-activating antibodies. These antibodies are either HLA (Class I or II) or granulocyte-specific. These antibodies appear to act as mediators, which result in granulocyte aggregation, activation, and microvascular pulmonary injury. With appropriate respiratory intervention, 80% of patients recover within 96 hours of the original insult. There are no permanent pulmonary sequelae.
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PMID:Transfusion and lung injury. 1149 76

Transfusion-related acute lung injury (TRALI) is a severe reaction between leukocyte antigen and antibody during transfusion of plasma-containing components. Recently, biologically active lipids have been also suggested to cause the disorder. It is a rare, but rather benign pulmonary edema. We report a postoperative pulmonary edema, which was temporally and clinically compatible with TRALI. Because the patient received blood products from 3 or 4 donors and the disorder was not recognized right away, the laboratory task for the definite diagnosis was difficult. Nevertheless, the patient had fully recovered in 36 hours after supportive therapies. Without identifying the blood donor implicated in the disorder, transfusion reactions or TRALI will be inevitable.
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PMID:Postoperative pulmonary edema, transfusion-related?--a case report. 1274 47

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 underdiagnosed serious complication of blood transfusion characterized by the rapid onset of respiratory distress, hypoxia, and noncardiogenic pulmonary edema during or soon after blood transfusion. The presence of anti-HLA and/or antigranulocyte antibodies in the plasma of donors is implicated in the pathogenesis of TRALI. We report 2 cases of TRALI that were caused by designated blood transfusion between mothers and their daughters; one in a 4-month-old girl who received designated packed RBCs donated by her mother and the second in a 78-year-old mother who received blood from her daughter. In both cases, examination of mother's serum revealed panel-reactive cytotoxic HLA antibodies. It is most likely that the mothers were sensitized from earlier pregnancy and produced HLA antibodies against the daughters' paternally derived HLA antigens. Designated blood transfusion between multiparous mothers and children might add an additional transfusion-related risk owing to the higher likelihood of the HLA antibody-antigen specificity between mother and child.
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PMID:Transfusion-related acute lung injury resulting from designated blood transfusion between mother and child: a report of two cases. 1508 Mar 12


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