Articles: respiratory-distress-syndrome.
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Case Reports
Combined pressure control/high frequency ventilation in adult respiratory distress syndrome and sickle cell anemia.
Acute chest syndrome complicating sickle cell anemia may progress to adult respiratory distress syndrome despite appropriate therapy. Extra-alveolar air leaks may complicate the care of these patients as conventional mechanical ventilation becomes increasingly difficult. We successfully treated a child with sickle cell anemia, acute chest syndrome, adult respiratory distress syndrome, and severe extra-alveolar air leaks using a new combined mode ventilatory approach: pressure control with high-frequency ventilation.
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To identify serial changes in the appearances of the lungs on computed tomography (CT) in patients with established adult respiratory distress syndrome (ARDS). Second, to evaluate any relationship between the extent of morphologic abnormalities on CT anatomic and physiologic derangement using a numeric score of the severity of lung injury. ⋯ The CT appearances of patients with ARDS who survive are variable and relate to the pattern of disease in the acute phase. Furthermore, the extent of CT abnormalities correlates strongly with LIS in both the acute phase and at follow-up.
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Cytokine networks between immune and nonimmune cells of the alveolar-capillary membrane are necessary for cellular communication during pulmonary inflammation. The subsequent events of these cellular/humoral interactions are pivotal to the initiation and propagation of the inflammatory response leading to pulmonary injury. The studies cited in this paper underscore the interrelationship of early response cytokines, adhesion molecules, and the chemokine IL-8 that orchestrate the recruitment of neutrophils into the lung. ⋯ The participation of IL-8 and potentially other C-X-C chemokines in the inflammatory response appears to be critical for the orchestration of the directed migration of inflammatory leukocytes into the lung. After arriving in the lung, these activated leukocytes can respond to noxious stimuli or induce pulmonary injury through the release of reactive oxygen metabolites, proteolytic enzymes, and additional cytokines. Our current knowledge and future investigations regarding the mechanisms involved in neutrophil elicitation may allow us to employ clinical interventional strategies that will attenuate neutrophil-dependent acute lung injury, such as ARDS.
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We investigated the impact of right ventricular performance on oxygen kinetics in 15 consecutive patients with acute respiratory distress syndrome. Six hundred and twenty-two complete assessments of haemodynamics, right ventricular function and oxygenation were used for evaluation. Patients were grouped as survivors (n = 8) and nonsurvivors (n = 7) and studied during four phases of lung failure. ⋯ No clinically relevant differences in right ventricular function or oxygenation were observed between periods of moderate or severe pulmonary hypertension. Nonsurvivors have depressed cardiac function caused by reduced contractility and not by inadequate right ventricular end-diastolic volume (preload) or increased pulmonary artery pressure (afterload). Maintenance of oxygen delivery in ARDS is predominantly a function of cardiac performance and not of pulmonary gas exchange.