Articles: respiratory-distress-syndrome.
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Review
Endotoxin, septic shock and acute lung injury: neutrophils, macrophages and inflammatory mediators.
The treatment of septic shock remains a major problem in surgical practice. Current research on the pathogenesis of the sepsis syndrome focuses on the effects of the lipopolysaccharide constituents of bacterial endotoxin. Evidence suggests that endotoxin induces a whole-body inflammatory response that in turn mediates organ damage, eventually leading to multiorgan failure. ⋯ This review summarizes current experimental work on how endotoxin leads to lung injury, based on its effects in animals and patients. Present knowledge suggests that future treatment of septic shock might involve inhibiting the body's inflammatory response to endotoxin. Possible ways of doing this are discussed.
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In recent years, we have experienced advances in treatments for severe ARDS. One that holds promise for these critically ill adult patients is ECMO, which can provide gas exchange and lung rest for the patient in severe reversible respiratory failure. Advances in ECMO techniques, appropriate patient selection and the development of heparinized tubing will all improve the potential for survival in patients who are placed on ECMO therapy in the future.
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An imbalance of proteolytic enzymes and protease inhibitors may contribute to the development of bronchopulmonary dysplasia. We studied secretory leukocyte protease inhibitor (not previously addressed), and alpha 1-antitrypsin, alpha 1-antichymotrypsin, alpha 2-macroglobulin and elastase. Albumin was used as an internal reference. ⋯ A decreased concentration of alpha 1-antitrypsin was found in the second and third postnatal weeks (p = 0.002). Further detailed studies of the balance between proteases and protease inhibitors and of the importance of pulmonary infections in the pathogenesis of bronchopulmonary dysplasia are suggested. Secretory leukocyte protease inhibitor is important both as an elastase inhibitor of bronchial mucus and as a marker of infection in the bronchi.
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The relationship between oxygenation and lung volume during high frequency oscillatory ventilation (HFOV) was studied. We ventilated anesthetized, tracheostomized adult rabbits that were rendered surfactant-deficient by lung lavage. Lung volume was measured by the 'disconnection technique'. ⋯ However, there was little improvement in PaO2 despite the use of repeated SI and the increase in MAP. We conclude that oxygenation has a linear relationship to lung volume during HFOV, and that secondary lung injury due to long-term CMV impairs the response to HFOV. Therefore, it is important to minimize the risk of such secondary injuries before instituting HFOV.
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The effect of dead space reduction was studied in 10 VLBW infants (GA 26-31 wks, mean BW 1100 grms) on mechanical ventilation using a constant flow ventilator with a flow sensor device (Draeger Babylog 8000, Lubeck, Germany). Shortening of the endotracheal tube and removal of the flow sensor resulted in a calculated 50% reduction of dead space (-2.3 ml) and in a fall of tcpCO2 from (mean and range) 45 (40-49) to 35 (31-36) mmHG. ⋯ Besides a routinely performed shortening of the ET tube this means of ventilation was used with success in two VLBW infants with desperate respiratory situations who both survived, in an older infant with high-grade tracheal stenosis to wean him from the respirator and in three neonates with congenital diaphragmatic hernia in conjunction with delayed operative repair who could be weaned from respiratory support 4, 13 and 20 days post surgery. We conclude that dead space reduction is a means to achieve gentle ventilation and to reduce lung damage from artificial ventilation.