The American review of respiratory disease
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Silicone fluid injection for mammary augmentation is a well-known illegal procedure. It has been associated with many complications, including local tissue granulomatous reaction, chronic infection, and sclerosis, but pulmonary involvement in human beings has been documented in only six cases. We describe three more such cases of pulmonary embolism. ⋯ Unfortunately, one of them died and another lived with the sequelae of pulmonary fibrosis. The mortality rate of the nine total patients with pulmonary embolism induced by silicone fluid, including our three cases, is 33%. Because of this high mortality rate and long-term sequelae of pulmonary fibrosis, no silicone fluid injection should be given for cosmetic reasons, especially in mammary augmentation in which a large volume of silicone fluid is more likely to be used, and the early use of corticosteroid therapy may be helpful.
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Am. Rev. Respir. Dis. · May 1993
Randomized Controlled Trial Clinical TrialPEEP does not improve pulmonary mechanics in infants with bronchiolitis.
Positive end-expiratory pressure (PEEP) may improve pulmonary mechanics, work of breathing, and gas exchange in some patients with respiratory failure. These beneficial effects do not occur consistently, however, and side effects, such as gas trapping due to expiratory flow limitation, may be exacerbated. We determined the effects of PEEP (0, 3, 6, and 9 cm H2O applied in random order) on the expiratory airway resistance and static compliance of nine infants mechanically ventilated for acute bronchiolitis. ⋯ Increases in end-expiratory lung volumes ranged from 18 to 40% of the tidal volume at maximal PEEP. Although all infants had PEEPi (5 +/- 2 cm H2O), PEEPi had no influence on the response of mechanics to applied PEEP other than that peak inspiratory pressures increased when PEEP > PEEPi. We conclude that the routine use of PEEP in infants with bronchiolitis does not consistently improve passive expiratory pulmonary mechanics and may increase the risk of barotrauma from gas trapping.
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Am. Rev. Respir. Dis. · May 1993
Four markers of collagen metabolism as possible indicators of disease in the adult respiratory distress syndrome.
During the adult respiratory distress syndrome (ARDS), an irreversible fibrotic process can occur extremely rapidly. To establish indices of ARDS in pneumonia as well as the severity of the lung fibrosis, we have undertaken for the first time a study of four markers of collagen metabolism obtained from both bronchoalveolar lavage fluid (BALF) and serum: Type I (CI), Type III (CIII), N-terminal peptide of Type III procollagen (PIIINP), and galactosylhydroxylysylglucosyltransferase activity (GGT). We studied 61 patients (13 coma controls, 29 with pneumonia, and 19 with ARDS). ⋯ Molecular mass determinations demonstrated that CI- and CIII-related antigens in BALF were essentially intact triple helices of collagens or procollagens. Among patients with histologically defined interstitial fibrosis, the level of PIIINP in BALF was significantly higher for those with an additional intraalveolar fibrosis. In conclusion, measurements of these collagen markers may be useful for assessing disease activity and reflecting the flux of collagen molecules in the lung.
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Am. Rev. Respir. Dis. · May 1993
Limited contribution of emphysema in advanced chronic obstructive pulmonary disease.
Previous studies on autopsy specimens or surgically resected lobes or lungs have reached varying conclusions regarding the importance of small airways disease and emphysema in causing fixed expiratory airflow limitation in patients with chronic obstructive pulmonary disease (COPD). We obtained high resolution CT scans of the lung and lung function in 56 consecutive patients with fixed expiratory airflow limitation. There was poor correlation between CT emphysema score and either FEV1/FVC% (r = -0.36) or FEV1 % predicted (r = -0.20). ⋯ A strong negative correlation between diffusing capacity % predicted and diffusing capacity per alveolar volume and CT emphysema score was found only in patients with FEV1 > or = 1 L (r = -0.75, p < 0.0001). Thus, emphysema does not appear to be primarily responsible for expiratory airflow limitation in COPD. A low diffusing capacity may be spuriously misleading in patients with FEV1 < 1 L and no or trivial emphysema.