New horizons (Baltimore, Md.)
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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.
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Late adult respiratory distress syndrome (ARDS) refers to the clinical stage of ARDS when the lung attempts to repair the initial or persistent injury to the endothelial and epithelial lining of the respiratory units. Histologically, it is characterized by the replacement of damaged epithelial cells and the striking accumulation of mesenchymal cells (fibroproliferative phase) and their connective tissue products in the air spaces and walls of the intra-acinar microvessels. Unfortunately, this reparative process is frequently ineffective, leading directly or indirectly to the patient's death. ⋯ Prolonged mechanical ventilation predisposes the patient to the development of pulmonary and extrapulmonary infections. Moreover, release of inflammatory cytokines from the lung with fibroproliferation causes fever and leukocytosis, making clinical distinction from pulmonary or extrapulmonary infections difficult, if not impossible. Anecdotal reports suggest that corticosteroid treatment may accelerate recovery in late ARDS.