Severe acute respiratory distress syndrome

Unlabeled Uses Cardiopulmonary bypass surgery hemodialysis pulmonary hypertension associated with acute respiratory distress syndrome, systemic lupus erythematosus, or congenital heart disease refractory CHF severe community-acquired pneumonia... 

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. 

Inhalation is the major route of exposure. Diphosgene is extremely damaging to mucous membranes, eyes, skin, and the respiratory tract, and may cause minor irritation to severe tissue damage and death. Toxicity effects vary with the concentration of vapor and the length of exposure. Signs and symptoms of toxicity may be immediate or delayed. The delayed (up to 6h) acute respiratory distress syndrome is characteristic of chocking agent inhalation. 

Furfural can cause skin sensitization and has been shown to cause irritant dermatitis which may become eczematous. It can be absorbed through the skin or by inhalation and it is an irritant to the eyes, skin, and respiratory system. No throat or eye irritation was noted in humans exposed to 10 ppm for 8h or 20 ppm for 4h. No data are available relative to reproductive or developmental effects in humans exposed to furfural. When air concentrations reach from 2 to 14 ppm, headaches, itching of the throat, and red/weeping eyes occurred in exposed humans. If exposures are severe, respiratory tract irritation can progress to acute respiratory distress syndrome, which may be delayed in its onset by up to 72 h. The National Institute for Occupational Safety and Flealth has indicated that 100 ppm in air is a concentration immediately dangerous to life or health. 

Lam C-F, van Heerden PV, Sviri S, Roberts BL, Ilett KF. 2002. The effects of inhalation of a novel nitric oxide donor, DETA/NO, in a patient with severe hypox-aemia due to acute respiratory distress syndrome. Anaesth. Intensive Care 30 472-76... 

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). 

Multiple studies have addressed the role of thyroid supplementation in critically ill patients with cardiac disease, sepsis, pulmonary disease (e.g., acute respiratory distress syndrome), or severe infection, or with burn and trauma patients. In spite of a very large number of published studies, it is very difficult to form clear recommendations for treatment with thyroid hormone in the intensive care unit. 

Indications for renal replacement therapy in the acute setting and for other disease processes are different from those for ESRD. A common mode of ESRD therapy in the outpatient setting is intermittent hemodialysis (IHD) where a patient receives intense treatment over the course of a few hours several times a week. Acute renal failure in the inpatient setting is often treated with continuous renal replacement therapy (CRRT), which is applied for the entire duration of the patient s clinical need and relies upon hemofiltration to a higher degree than IHD (Meyer, 2000). Other nonrenal indications for CRRT are based on the theoretical removal of inflammatory mediators or toxins and elimination of excess fluid (Schetz, 1999). These illnesses include sepsis and systemic inflammatory response syndrome, acute respiratory distress syndrome, congestive heart failure with volume overload, tumor lysis syndrome, crush injury, and genetic metabolic disturbances (Schetz, 1999). 

Respiratory Mild dyspnea is common and affects about 10% of patients [44 , 45 J. Grade 3 or 4 dyspnea is uncommon (1.2% and 0.1% of patients respectively) [46 ]. Acute respiratory distress syndrome (ARDS) is extremely rare, affecting 0.002% of patients [47 ]. Patients present with progressive dyspnea, severe hypoxemia, and bilateral... 

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