Articles: respiratory-distress-syndrome.
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Long-term extracorporeal support for acute lung failure was introduced in 1972. In the 1970s, much effort was concentrated on technical improvements. However, a multicenter study comparing continuous positive-pressure ventilation and continuous positive-pressure ventilation plus extracorporeal circulation failed to show improvement in survival rates. ⋯ The main complication of the technique was bleeding due to systemic heparinization. However, the technology used in that period was the same as in the 1970s. Recently, technological improvement--such as percutaneous cannulation and surface-heparinized artificial lungs--has allowed clinical performances to improve substantially. "Lung rest" philosophy, coupled with safe technology, may provide a rational basis to test this technique in a randomized fashion for widespread use.
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In 1987, nitric oxide was reported to be an endothelium-dependent relaxing factor. When inhaled as a gas at low levels, nitric oxide selectively dilates the pulmonary circulation. Significant systemic vasodilation does not occur because nitric oxide is inactivated by rapidly binding to hemoglobin. ⋯ Tachyphylaxis to nitric oxide inhalation has not been observed. While additional chronic toxicology studies need to be performed, significant pulmonary toxicity has not been observed at low inhaled concentrations (< 80 parts per million by volume). Potentially, inhaled nitric oxide may be a valuable therapy in patients with adult respiratory distress syndrome.
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Oxygen therapy is administered to decrease tissue hypoxia and to relieve arterial hypoxemia. High concentrations of oxygen are often used in patients with adult respiratory distress syndrome. Supplying oxygen to animals has been known to produce tissue damage, with toxicity increasing with the increase of oxygen concentrations and exposure pressures. ⋯ Lung damage may occur as a result of normobaric hyperoxia. A severe retinopathy (retrolental fibroplasia) occurs in neonates during oxygen exposures. For all of these reasons, the lowest possible concentration of oxygen that relieves tissue hypoxia is recommended in patients with adult respiratory distress syndrome.
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Adult respiratory distress syndrome (ARDS) and multiple organ failure (MOF) occur as a result of an unbridled systemic inflammatory response (i.e., severe systemic inflammatory response syndrome [SIRS]). Early epidemiologic studies concluded that infection with systemic sepsis was the common pathway for the development of ARDS and eventual MOF. As a consequence, research investigation from 1977 to 1987 focused on later clinical events (e.g., immunosuppression, persistent hypercatabolism, and bacterial translocation). ⋯ The traditional infection models of ARDS and MOF are applicable to current research and patient care efforts. However, the inflammatory models emphasize the pivotal role of the initial traumatic insult. Moreover, while ARDS occurs earlier than other types of overt organ failure, it is now believed that simultaneous organ injury is occurring, presumably via similar inflammatory mechanisms.
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Bronchopleural fistula occurring as a complication in patients with the adult respiratory distress syndrome typically appears after 1 to 2 wks of illness, and is associated with a poor prognosis. Whether the bronchopleural fistula per se worsens outcome is not known because of the lack of studies on its natural history. ⋯ Controlled studies are lacking, however, and the application of sound, general management principles is of primary importance. The great majority of patients can be managed satisfactorily without resort to unfamiliar, labor-intensive, potentially hazardous measures.