Articles: respiratory-distress-syndrome.
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ARDS is the pulmonary manifestation of both direct and indirect insults to the lung. Trauma patients are at particular risk for ARDS from the direct effects of their injuries, as well as from complications that may occur during their hospital courses. ARDS prevention can be enhanced through diverse areas of medical focus. ⋯ Newer modes of mechanical ventilation may help us to avoid ventilator-induced exacerbation of lung injury. As we define the role of nonconventional therapies, such as anti-inflammatory and anticytokine therapies, our ability to actively interrupt and reverse the progression of the inflammatory cascade will be enhanced. As yet, ARDS continues to be a challenging disease process to both fully understand and successfully treat in our critically ill patients.
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Critical care medicine · May 1997
Clinical TrialAdditive beneficial effects of the prone position, nitric oxide, and almitrine bismesylate on gas exchange and oxygen transport in acute respiratory distress syndrome.
To test the hypothesis that prone position ventilation, nitric oxide, and almitrine bismesylate, each acting by a different mechanism to improve arterial oxygenation, could exert additive beneficial effects when used in combination in patients with severe acute respiratory distress syndrome (ARDS). ⋯ In ARDS patients with severe hypoxemia, arterial oxygenation can be improved by combining the prone position, nitric oxide, and almitrine bismesylate, without deleterious effects.
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Systemic inflammatory response syndrome (SIRS) and infections are frequently associated with the development and progression of acute respiratory distress syndrome (ARDS) and multiple organ dysfunction syndrome (MODS). We investigated, at onset and during the progression of ARDS, the relationships among (1) clinical variables and biological markers of SIRS, (2) infections defined by strict criteria, and (3) patient outcome. Biological markers of SIRS included serial measurements of inflammatory cytokines (IC)-tumor necrosis factor-alpha (TNF-alpha) and interleukins (IL) 1 beta, 2, 4, 6, and 8-in plasma and BAL fluid. ⋯ Sepsis as a precipitating cause of ARDS was associated with higher plasma IC levels. However, NIs were not associated with an increase in SIRS composite scores, individual SIRS criteria, or plasma IC levels above patients' preinfection baseline. SIRS composite scores over time were similar in S and NS. SIRS criteria, including fever, were found to be nonspecific for NI. Irrespective of etiology of ARDS, plasma IC levels, but not clinical criteria, correlated with patient outcome. These findings suggest that final outcome in patients with ARDS is related to the magnitude and duration of the host inflammatory response and is independent of the precipitating cause of ARDS or the development of intercurrent NIs.
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This study was designed to investigate the pathogenesis of chlorine gas (Cl2) induced acute lung injury and oedema. Isolated blood-perfused rabbit lungs were ventilated either with air (n=7) or air plus 500 parts per million (ppm) of Cl2 (n=7) for 10 min. Capillary pressure, measured by analysing the pressure/time transients of pulmonary arterial, venous and double (both arterial and venous) occlusions, was unchanged in both groups. ⋯ No changes were observed in the control lungs. The extravascular lung water/blood-free dry weight ratio was 8.6+/-1.6 in the Cl2 group and 4.0+/-0.5 in the control group (p<0.001), confirming that the increase in lung weight was related to accumulation of extravascular fluid. Although the alveolar flooding by oedema is explained, in part, by the Cl2-induced epithelial injury, our results suggest that Cl2 exposure induces acute lung injury and oedema due to an increased microvascular permeability.
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To evaluate the effect of nitric oxide (NO) on acute pulmonary hypertension and right ventricular function in patients with acute respiratory distress syndrome. ⋯ NO did not relieve the acute pulmonary artery hypertension associated with acute respiratory distress syndrome. As a consequence of this, right ventricular function failed to improve during the administration of NO.