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OBJECTIVES: To determine the incidence, risk factors, and outcome of transfusion-related acute lung injury in a cohort of critically ill patients. DESIGN: In a retrospective cohort study, patients with transfusion-related acute lung injury were identified using the consensus criteria of acute lung injury within 6 hrs after transfusion. Inclusion criterion was a length of intensive care unit admission >48 hrs. Patients developing transfusion-related acute lung injury were matched (on age, sex, and admission diagnosis) to transfused control subjects and patients developing acute lung injury from another origin. SETTING: Tertiary referral hospital. PATIENTS: All first-admitted patients from November 1, 2004, until October 1, 2007, to the intensive care unit. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Of 5208 admitted patients, 2024 patients had a length of stay >48 hrs, of whom 109 were suspected transfusion-related acute lung injury cases. Compared with transfused control subjects, risk factors for transfusion-related acute lung injury were emergency cardiac surgery (odds ratio, 17.6 [1.8-168.5]), hematologic malignancy (odds ratio, 13.1 [2.7-63.8]), massive transfusion (odds ratio, 4.5 [2.1-9.8]), sepsis (odds ratio, 2.5 [1.2-5.2]), mechanical ventilation (odds ratio, 3.0 [1.3-7.1], and high Acute Physiology and Chronic Health Evaluation II score (odds ratio, 1.1 [1.0-1.1]; p < .03 for all). The volume of platelets and plasma transfused was associated with transfusion-related acute lung injury in the univariate analysis. However, this association disappeared in the multivariate analysis. Compared with acute lung injury control subjects, risk factors for transfusion-related acute lung injury were sepsis (odds ratio, 2.4 [1.1-5.3]) and high Acute Physiology and Chronic Health Evaluation II score (odds ratio, 1.1 [1.0-1.1]), whereas pneumonia (odds ratio, 0.4 [0.2-0.7]) was a negative predictive factor. Patients with transfusion-related acute lung injury had a longer duration of mechanical ventilation compared with transfused control subjects and acute lung injury control subjects (231 [138-472] vs. 71 [46-163] and 70 [42-121] hrs, p < .001). Also, 90-day survival of patients with transfusion-related acute lung injury was lower compared with transfused control subjects and acute lung injury control subjects (53% vs. 75% and 83%, p < .02). CONCLUSIONS: Transfusion-related acute lung injury is common in critically ill patients. Transfusion-related acute lung injury may contribute to an adverse outcome associated with transfusion. This study identifies transfusion-related acute lung injury risk factors, which may aid in assessing the risks and benefits of transfusion in critically ill patients. [ABSTRACT FROM AUTHOR]

Purpose: Hyperoxia may induce pulmonary injury and may increase oxidative stress. In this retrospective database study we aimed to evaluate the response to hyperoxia by intensivists in a Dutch academic intensive care unit.Methods: All arterial blood gas (ABG) data from mechanically ventilated patients from 2005 until 2009 were extracted from an electronic storage database of a mixed 32-bed intensive care unit in a university hospital in Amsterdam. Mechanical ventilation settings at the time of the ABG tests were retrieved.Results: The results of 126,778 ABG tests from 5,498 mechanically ventilated patients were retrieved including corresponding ventilator settings. In 28,222 (22%) of the ABG tests the arterial oxygen tension (PaO(2)) was >16 kPa (120 mmHg). In only 25% of the tests with PaO(2) >16 kPa (120 mmHg) was the fraction of inspired oxygen (FiO(2)) decreased. Hyperoxia was accepted without adjustment in ventilator settings if FiO(2) was 0.4 or lower.Conclusion: Hyperoxia is frequently seen but in most cases does not lead to adjustment of ventilator settings if FiO(2) <0.41. Implementation of guidelines concerning oxygen therapy should be improved and further research is needed concerning the effects of frequently encountered hyperoxia. [ABSTRACT FROM AUTHOR]

BACKGROUND: : With adaptive support ventilation, respiratory rate and tidal volume (VT) are a function of the Otis least work of breathing formula. We hypothesized that adaptive support ventilation in an open lung ventilator strategy would deliver higher VTs to patients with acute lung injury. METHODS: : Patients with acute lung injury were ventilated according to a local guideline advising the use of lower VT (6-8 ml/kg predicted body weight), high concentrations of positive end-expiratory pressure, and recruitment maneuvers. Ventilation parameters were recorded when the ventilator was switched to adaptive support ventilation, and after recruitment maneuvers. If VT increased more than 8 ml/kg predicted body weight, airway pressure was limited to correct for the rise of VT. RESULTS: : Ten patients with a mean (±SD) Pao2/Fio2 of 171 ± 86 mmHg were included. After a switch from pressure-controlled ventilation to adaptive support ventilation, respiratory rate declined (from 31 ± 5 to 21 ± 6 breaths/min; difference = 10 breaths/min, 95% CI 3-17 breaths/min, P = 0.008) and VT increased (from 6.5 ± 0.8 to 9.0 ± 1.6 ml/kg predicted body weight; difference = 2.5 ml, 95% CI 0.4-4.6 ml/kg predicted body weight, P = 0.02). Pressure limitation corrected for the rise of VT, but minute ventilation declined, forcing the user to switch back to pressure-controlled ventilation. CONCLUSIONS: : Adaptive support ventilation, compared with pressure-controlled ventilation in an open lung strategy setting, delivers a lower respiratory rate-higher VT combination. Pressure limitation does correct for the rise of VT, but leads to a decline in minute ventilation. [ABSTRACT FROM AUTHOR]