Articles: respiratory-distress-syndrome.
-
The justification for restricting fluid administration, or more directly, for actively trying to lower pulmonary capillary pressures during pulmonary edema, is embodied in the familiar "Starling equation." This model predicts that pulmonary edema will develop if lymph flow or changes in other so-called "safety factors" cannot compensate for increases in pulmonary capillary pressures. Numerous experimental studies support the logical extension of this paradigm, namely that reduced capillary pressures and/or reduced perfusion to acutely injured lung units will result in reduced extravascular lung water accumulation. ⋯ Furthermore, although a strategy of fluid restriction/diuresis could potentially increase the risk of either cardiac or renal dysfunction, currently available data suggest that this management strategy in euvolemic (and certainly in hypervolemic) ARDS patients can be pursued without clinically important deterioration in either type of organ function. Thus, on balance, a strategy of fluid restriction/diuresis should be pursued during the first few days of ARDS, while carefully monitoring and supporting the perfusion of vital organs.
-
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.
-
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.
-
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.
-
Case Reports
Increased blood pressure during inverse ratio ventilation in two patients with adult respiratory distress syndrome.
Inverse ratio ventilation (IRV) is increasingly used in the supportive treatment of patients with hypoxemic respiratory failure. A recent study suggests that IRV reduces cardiac output with minimal effect on mean arterial pressure. We report two cases in which IRV led to reproducible increases in mean arterial pressure. Concomitant hemodynamic measurements suggest that these responses occurred as a result of increased vascular resistance.