Articles: respiratory-distress-syndrome.
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Semin Respir Infect · Sep 1990
ReviewHost responses in mediating sepsis and adult respiratory distress syndrome.
Despite significant advances in intensive care unit technology and mechanical ventilatory support, mortality due to adult respiratory distress syndrome (ARDS) or multiorgan failure (MOF) has not changed significantly within the past two decades. The key to improving survival requires understanding and modifying (or eliminating) factors that may initiate (or modulate) these syndromes. Infection, and the host responses to infection, are major etiological factors responsible for the induction and perpetuation of the injury to the lung and microvasculature in ARDS and MOF, and contribute to late mortality. ⋯ Interactions between these humoral and cellular mediators appear to set in motion an amplified cascade of events culminating in cellular and tissue injury. In this article, several of these putative inflammatory mediators are discussed in detail, and the importance of cytokine networking and the possible role of nonimmune cells in the orchestration of the inflammatory response associated with ARDS and MOF are explained. Finally, future therapeutic strategies aimed at blocking or suppressing the release or effects of endogenous mediators may be the key to improving the outcome of these disorders.
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Critical care medicine · Sep 1990
Adult respiratory distress syndrome: roles of leukotriene C4 and platelet activating factor.
The relationship between leukotriene C4 (LTC4), platelet activating factor (PAF), and adult respiratory distress syndrome (ARDS) was studied in nine patients and 84 control subjects. A leukocyte adherence inhibition (LAI) assay induced by each of the ligands was used to monitor the subjects for 3 consecutive days or until clinical recovery was noted. LAI was considered to be positive if the nonadherence index (NAI) was greater than 30 for LTC4 or greater than 20 for PAF. ⋯ The mean NAI (52.2 +/- 18) of LTC4-induced LAI in ARDS patients was significantly (p less than .05) higher when compared with the control group (-5 +/- 6.4), whereas that of PAF-induced LAI was less than 20 in both groups, indicating that LTC4 is a more specific ligand than PAF. All three patients in whom ARDS was caused by sepsis responded to both LTC4 and PAF, but results of specific receptor-antagonist experiments indicated that each compound acted independently. The mean NAI for LTC4 (58.5 +/- 10) and PAF (49.1 +/- 12) in patients with septic ARDS were significantly (p less than .05) higher when compared with those of patients with sepsis alone (0.5 +/- 9.9 and 4.4 +/- 17, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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Long-term respiratory therapy with high pressure levels in case of ARDS can lead to several symptoms requiring surgical treatment. Various forms of manifesting barotrauma predominate (bronchopleural fistula, pneumothorax, pneumatocele and soft tissue emphysema), while hematothorax, infected necrosis of parenchyma or esophagotracheal fistula are rare. Most of the operations became necessary because of bronchopleural fistula resp. pneumothorax, and with this indication the number of reoperations was especially high. Of 21 patients 13 (62%) survived.