Lesión pulmonar aguda producida por transfusión / Transfusion-related acute lung injury

El término TRALI (transfusion related acute lung injury ‘lesión pulmonar aguda producida por transfusión’) fue acuñado en 1985. Es un síndrome clínico relativamente raro, que puede constituir una amenza para la vida y que se caracteriza por insuficiencia respiratoria aguda y edema pulmonar no cardiogénico durante o después de una transfusión de productos hemáticos. Aunque su verdadera incidencia es desconocida se le ha atribuido un caso por cada 5.000 transfusiones de cualquier producto hemático y ha sido la causa más frecuente de muerte relacionada con la transfusión durante 3 años en Estados Unidos. Se han propuesto 2 etiologías. La primera es un episodio mediado por anticuerpos debido a la transfusión de anticuerpos contra el antígeno leucocitario o anticuerpos antigranulocito a pacientes cuyos leucocitos presentan antígenos afines. La segunda es un modelo en el que se precisan 2 eventos: el primero está relacionado con el cuadro clínico del receptor (sepsis, trauma, etc.) que produce activación endotelial y secuestro de neutrófilos, y el segundo es la transfusión de sustancias con capacidad de modificar la respuesta biológica que activa los leucocitos adheridos que produce daño endotelial y aumento de permeabilidad capilar. El tratamiento es de soporte en función de la gravedad del cuadro clínico, y la prevención se centra en 3 estrategias: selección de donantes, actuación sobre el almacenamiento de los productos hemáticos y evitar las transfusiones innecesarias (AU)

The term Transfusion-Related Acute Lung Injury (TRALI) was coined in 1985. It is a relatively rare, life-threatening clinical syndrome characterized by acute respiratory failure and non-cardiogenic pulmonary edema during or following a blood transfusion. Although its true incidence is unknown, a rate 1 out of every 5000 transfusions has been quoted. TRALI has been the most common cause of transfusion-related fatalities during three years in the USA. Two different etiologies have been proposed. The first is a single antibody-mediated event involving the transfusion of anti-HLA or antigranulocyte antibodies into patients whose leukocytes express the cognate antigens. The second is a two-event model: the first event is related to the clinical condition of the patient (sepsis, trauma, etc.) resulting in pulmonary endothelial activation and neutrophil sequestration, and the second event is the transfusion of a biologic response modifier that activates these adherent polymorphonuclear leukocytes resulting in endothelial damage and capillary leak. The patient management is support as needed based on the severity of the clinical picture and strategies to prevent TRALI are focused on: donor-exclusion policies, product management strategies and avoidance of unnecessary transfusions (AU)

[Transfusion-related acute lung injury]. / Lesión pulmonar aguda producida por transfusión.

The term Transfusion-Related Acute Lung Injury (TRALI) was coined in 1985. It is a relatively rare, life-threatening clinical syndrome characterized by acute respiratory failure and non-cardiogenic pulmonary edema during or following a blood transfusion. Although its true incidence is unknown, a rate 1 out of every 5000 transfusions has been quoted. TRALI has been the most common cause of transfusion-related fatalities during three years in the USA. Two different etiologies have been proposed. The first is a single antibody-mediated event involving the transfusion of anti-HLA or antigranulocyte antibodies into patients whose leukocytes express the cognate antigens. The second is a two-event model: the first event is related to the clinical condition of the patient (sepsis, trauma, etc.) resulting in pulmonary endothelial activation and neutrophil sequestration, and the second event is the transfusion of a biologic response modifier that activates these adherent polymorphonuclear leukocytes resulting in endothelial damage and capillary leak. The patient management is support as needed based on the severity of the clinical picture and strategies to prevent TRALI are focused on: donor-exclusion policies, product management strategies and avoidance of unnecessary transfusions.

Acute venous thromboembolism in patients with recent major bleeding. The influence of the site of bleeding and the time elapsed on outcome.

BACKGROUND: Patients with major bleeding who subsequently develop clinically apparent venous thromboembolism (VTE) present a particularly difficult therapeutic dilemma. METHODS: RIETE is a prospective registry of consecutive patients with symptomatic, objectively confirmed, acute VTE. We retrospectively studied those who had experienced recent major bleeding (<30 days prior to VTE) to assess the influence of the site of bleeding and the time elapsed to VTE on their 3 month outcome. RESULTS: Of 12,294 patients enrolled up to July 2005, 306 (2.5%) had recent major bleeding: gastrointestinal (GI) tract, 116 (38%); intracranial, 94 (31%); other, 96 (31%). During the study period, 19 patients [6.2%; 95% confidence interval (CI) 3.5-8.9] with recent bleeding rebled (eight died): 13 of them (68%) during the first 2 weeks. Multivariate analysis confirmed that patients with recent GI bleeding had an increased risk for both major rebleeding (hazard ratio 2.8; 95% CI 1.4-5.3) and death (hazard ratio 1.9; 95% CI 1.2-3.1) compared to those with no recent bleeding. Those who bled in other sites had an increased risk only for death (hazard ratio 2.0; 95% CI 1.2-3.3). An elapsed time of <2 weeks from bleeding to the index VTE event was also associated with an increased risk for major rebleeding (hazard ratio 2.4; 95% CI 1.2-5.0) and death (hazard ratio 2.8; 95% CI 1.8-4.5). CONCLUSION: The incidence of new bleeding or death depends on the site of prior bleeding and the time elapsed until VTE. This information may help to identify the best therapeutic approach for these high-risk patients.

Low levels of vitamin B12 and venous thromboembolic disease in elderly men.

OBJECTIVES: Hyperhomocysteinaemia is a well-known risk factor for venous thromboembolic disease (VTD). However, it is not clear whether homocysteine (Hc) itself or a related metabolite or a cofactor is primarily responsible for VTD. We carried out a case-control study to investigate whether vitamin concentrations that are involved in the Hc metabolism are associated or not with an elevated risk of VTD. DESIGN: Case-control study. METHODS: We measured serum vitamin B12, folate, creatinine and albumin concentrations and plasma Hc concentrations in 101 consecutive patients with VTD, diagnosed by image tests and 101 control subjects, matched for age and sex. RESULTS: Serum vitamin B12 concentrations were significantly lower in VTD patients than in the control subjects. There were no differences in plasma Hc or serum folate concentrations between the groups. Among the male subgroup aged more than 70 years, serum vitamin B12 concentrations were significantly lower (240.88 +/- 103.07 vs. 421.20 +/- 314.31 pmol L(-1); P = 0.03) and plasma Hc concentrations were significantly higher (13.1 +/- 4.18 vs. 10.56 +/- 3.06 micromol L(-1); P =0.04) in VTD patients than in the control group. On multivariate analysis, in patients aged more than 70 years, serum vitamin B12 concentrations were independently associated with VTD. Compared with the highest quartile of vitamin B12 (>512.6 pmol L(-1)) the odds ratio (OR) for VTD in the lowest quartile (<230.9 pmol L(-1)) was 3.8 (95% CI 1.44-10.18; P = 0.01). In the VTD group, lowest vitamin B12 concentrations (percentile 10 <152.8 pmol L(-1)) were associated with the factor V Leiden mutation (OR = 6.07, 95% CI 0.93-38.55; P = 0.04). CONCLUSIONS: Measuring vitamin B12 concentrations in elderly males may help in identifying people at risk of venous thromboembolism in our population.