Acute respiratory distress syndrome ARDS

Outcome parameters for VAP, HAP, and HCAP are similar to those with CAP. Clinical improvement should occur within 48 to 72 hours of the start of therapy. If a patient is not responding to therapy, then, again, consider infectious and noninfectious reasons. Infectious explanations are the same as for CAP, but noninfectious reasons are not. They include atelectasis, acute respiratory distress syndrome (ARDS), pulmonary embolism or hemorrhage, cancer, empyema, or lung abscess. 

One formula, Oxepa , has been studied specifically in critically ill patients with acute respiratory distress syndrome (ARDS).29 This high-fat formula contains high quantities of the C0-3 fatty acids (EPA) and y-linolenic acid (GLA). y-Linolenic... 

Lung tissue injury is also mediated by reactive oxygen and nitrogen species in another inflammatory lung disease, acute respiratory distress syndrome (ARDS) [267], Lamb et al. 

Suggested Alternatives for Differential Diagnosis Scarlet fever, cellulitis, cat scratch disease, gas gangrene, necrotizing fasciitis, tick-borne diseases such as Rocky Mountain spotted fever, pneumonia, septic shock, acute respiratory distress syndrome (ARDS), disseminated intravascular coagulation. 

Treatment of acute respiratory distress syndrome (ARDS), lipoprotein-releasing activity, in biomaterials as nonthrom-bogenic surfaces Inhibitor of human immunodeficiency virus (HIV) binding to T-lymphocytes 1, 30-31... 

Polymorphonuclear neutrophils (PMN) have been implicated in the pathogenesis of post-traumatic and sepsis-related complications such as acute lung injury and acute respiratory distress syndrome (ARDS), a prominent form of end-organ damage that... 

Pulmonary - rales from acute respiratory distress syndrome (ARDS) in severe exposure... 

In particular, excessive proteolysis of elastin by HLE has been implicated in pulmonary emphysema [19]. In this case, the imbalance appears to result from reduced levels of active extracellular alpha,-proteinase inhibitor (a,-PI), the primary plasma inhibitor of HLE. This decrease is caused either by a genetic disorder (PiZZ phenotype individuals) or by reduction in the elastase inhibitory capacity (EIC) of ai-PI due to its oxidative inactivation by tobacco smoke [20]. The detailed evidence supporting the potential role of elastase in the development of emphysema has been extensively reviewed [21] and will not be repeated here. The fact that HLE is also a potent secretagogue [22] may play a role in several disease states, including cystic fibrosis [23], chronic bronchitis [24], and acute respiratory distress syndrome (ARDS) [25]. The mechanism of the secretagogue activity is not known, but, since the HLE-induced secretion can be blocked by specific HLE inhibitors, it appears to require catalytic activity by the enzyme [26]. 

Many chemicals cause irritation of the eyes, skin, and respiratory tract. In severe cases respiratory tract irritation can progress to acute respiratory distress syndrome (ARDS)/acute lung injury, which may be delayed in onset for up to 24-72 h in some cases. 

In adults, a severe form of lung injury can develop in association with sepsis, pneumonia, and injury to the lungs due to trauma or surgery. This catastrophic disorder is known as acute respiratory distress syndrome (ARDS) and has a mortality rate of more than 40%. In ARDS, one of the major problems is a massive influx of activated neurophils which damage both vascular endothelium and alveolar epithelium and result in massive pulmonary edema and impairment of surfactant function. Neutrophil proteinases (e.g., elastase) break down surfactant proteins. A potential therapeutic strategy in ARDS involves administration of both surfactant and antiproteinases (e.g., recombinant a I -antitrypsin). 

Mustard gas exposure also causes inflammatory lung diseases, including acute respiratory distress syndrome (ARDS) (Calvet et al., 1994 Sohrabpour, 1984). A defective secretion of surfactant by alveolar type 11 cells has been implicated as one of the causative factors for the development of ARDS (Ansceschi, 1989). A major component of lung surfactant is DPPC (Stith and Das, 1982). The precursor of DPPC is normally l-pahnitoyl-2-oleolyl PC. DPPC is produced by deacylation and subsequent reacylation with palmitic acid at 2-position of glycerol moiety of the unsaturated phospholipid. 

Acute respiratory distress syndrome (ARDS) is a syndrome presenting with bilateral pulmonary infiltrates, high oxygen requirements (Pao2/Fi02 <200 mm Hg), and noncardiogenic pulmonary edema. 

This chapter addresses the problems of acute respiratory distress syndromes in neonates, children, and adults. Abbreviations are used throughout the text, and a glossary for physiology, diseases, and drugs is presented in Table 28-1. Descriptions of ventilator-related terms are provided in Tables 28-2 and 28-3. Because the physiology of neonatal respiratory distress syndrome (RDS) and acute respiratory distress syndrome (ARDS) has some differences, these diseases will be discussed separately. 

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