Respiratory distress syndrome acute

In low doses, inhaled NO may have a beneficial therapeutic effect, since NO in the inspired air leads to pulmonary vasodilation. In persistent pulmonary hypertension of the newborn, NO inhalation has already been used with some success. NO inhalation as the treatment for acute respiratory distress syndrome, however, has been disappointing. Only transient improvements of oxygenation were detected and the outcome of placebo-controlled trials did not show any improvement... 

Phagocyte-derived ROMs have been implicated in the pathogenesis of a number of pulmonary diseases, including emphysema, acute respiratory distress syndrome, and various environmental diseases such as asbestos-related fibrosis and cancer (Mossman and Marsh, 1985). The relatively high oxygen tension in pulmonary tissue renders the lung prone to oxidative stress (Edwards and Lloyd, 1988). 

Monitor for evidence of cerebral edema, noncardiogenic (permeability) pulmonary edema, acute respiratory distress syndrome, hyperchloremic metabolic acidosis, and vascular thrombosis... 

APACHE Acute Physiology, Age, and Chronic Health Evaluation ARDS acute respiratory distress syndrome... 

Signs and symptoms New infiltration on chest, x-ray accompanied by fever, cough, dyspnea, chest pain, hypoxia, leukocytosis. Can progress to acute respiratory distress syndrome and death. 

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... 

M29. Miller, E. J., Cohen, A. B and Matthay, M. A., Increased interleukin-8 concentrations in the pulmonary edema fluid of patients with acute respiratory distress syndrome from sepsis. Crit. Care Med. 24, 1448-1454 (1996). 

Wygrecka, M., Morty, R.E., Markart, P., Kanse, S.M., Andreasen, P.A., Wind, T., Guenther, A., and Klaus, T.P. (2007) Plasminogen activator inhibitor-1 (PAI-1) is an inhibitor of factor VILactivating protease in patients with acute respiratory distress syndrome. J. Biol. Chem., 10.1074/jbc.M610748200, published online ahead of print. 

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. 

The following factors have been suggested as alternatives to consider when presented with a potential case of exposure to carbon monoxide diabetic ketoacidosis, hypothyroidism and myxedema coma, labyrinthitis, and lactic acidosis toxic exposures resulting in methemoglobinemia ingestion of alcohols or narcotics and diseases that cause gastroenteritis, encephalitis, meningitis, and acute respiratory distress syndrome. 

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. 

Suggested Alternatives for Differential Diagnosis Drug induced noncardiac pulmonary edema, acute respiratory distress syndrome, pneumonic plague, tularemia, Q fever, and viral influenza. 

Suggested Alternatives for Differential Diagnosis Acute respiratory distress syndrome, congestive heart failure, pulmonary edema, AIDS, pneumonia, cardiogenic shock, septic shock, phosgene toxicity, phosphine toxicity, salicylate toxicity with pulmonary edema, influenza, plague, tularemia, and anthrax. 

ARDS, acute respiratory distress syndrome DIC, disseminated intravascular coagulation. 

Progression of uncontrolled sepsis leads to evidence of organ dysfunction, which may include oliguria, hemodynamic instability with hypotension or shock, lactic acidosis, hyperglycemia or hypoglycemia, possibly leukopenia, disseminated intravascular coagulation, thrombocytopenia, acute respiratory distress syndrome, GI hemorrhage, or coma. 

Disease state-specific formulations are designed to meet specific nutrient requirements and to manage metabolic abnormalities. Unfortunately, scientific and clinical research supporting their efficacy is minimal, except for low carbohydrate formulations supplemented with specific fatty acids and antioxidants for patients with acute respiratory distress syndrome. Oral supplements are not intended for tube feeding. They are sweetened to improve taste and are therefore hypertonic. 

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... 

T Kobayashi, K Tashiro, X Cui, T Konzaki, Y Xu, C Kabata, K Yamamoto. Experimental models of acute respiratory distress syndrome clinical relevance and response to surfactant therapy. Biology Neonate 80 Suppl 1 26—28, 2001. 

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