Chest
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Case Reports
Management of acute respiratory failure due to pulmonary edema with nasal positive pressure support.
The management of patients with respiratory failure from cardiogenic pulmonary edema may require intubation and mechanical ventilation. This provides both ventilatory assistance as well as the beneficial hemodynamic effects of positive intrathoracic pressure. As the need for ventilation is usually short term, noninvasive ventilatory support may be adequate. We report the use of biphasic positive airway pressure by nasal mask (BiPAP system) to successfully manage two patients with respiratory failure due to pulmonary edema.
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An autopsy was performed on a patient who had chronic hypersensitivity pneumonitis that was observed for 9 years. The patient was a farmer who developed symptoms every March through July during the use of moist hay that was infected heavily with Candida. Precipitins and an inhalation challenge test to C albicans were positive. We interpret the role of C albicans in this case.
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We tested the hypothesis that maximal exercise performance in subjects with interstitial lung disease (ILD) is limited by respiratory factors. Assuming this is so, ventilatory stimulation by added dead space (VD) should impair exercise capacity. ⋯ The decrease observed in TLIM, work rate, and peak VO2 with added VD, associated with a lack of change in VI or oxygen desaturation at end-exercise, suggests that exercise limitation in ILD is primarily due to respiratory factors.
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The aim of the study was to identify risk factors for early onset pneumonia (EOP) in trauma patients, in order to seek possible intervention strategies. ⋯ In a trauma population, a combined severe abdominal and thoracic trauma represents a major risk factor for EOP. Mechanical ventilation administered during the first days after trauma seems to reduce the risk of EOP. As reported in previous studies, mechanical ventilatory support lasting more than 5 days is associated with an increased risk of LOP.
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The lung injury in adult respiratory distress syndrome (ARDS) has been associated with increased expiratory hydrogen peroxide (H2O2) concentrations. Furthermore, patients with sepsis and ARDS are reported to have greater serum scavenging of H2O2 than patients with ARDS only. We hypothesized that the systemic presence of H2O2 would be detectable in the urine of these two groups of patients and that, in the case of ARDS sepsis, the relative contribution of each disease to the production this analyte would be discernible. Accordingly, we used an in vitro radioisotope assay to follow the weekly course of urine H2O2 levels in ARDS patients with and without sepsis, and in samples from control non-ARDS patients with sepsis with indwelling urinary catheters and in samples provided by healthy volunteers. ⋯ Lung injury scores did not differentiate patients with ARDS and sepsis from patients with ARDS only during the first 10 days in the ICU; however, urine H2O2 levels were significantly greater in the patients with ARDS and sepsis. Moreover, despite no initial difference in lung injury, patients who did not survive ARDS and sepsis had consistently greater urine H2O2 concentration than patients who survived sepsis. The urine H2O2 level in the ARDS-only group was about 70 percent of the level in the survivor ARDS and sepsis group, suggesting that ARDS alone is the major contributor to the H2O2 oxidant processes during combined ARDS and sepsis. Furthermore, these studies demonstrate that urine H2O2 may be a useful analyte to differentiate the severity of oxidant processes in patients with ARDS and sepsis albeit the prognosis appears to be survival or nonsurvival.