Acute respiratory distress

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... 

Mr. Potter, age 57 years, is admitted to the pulmonary unit in acute respiratory distress. The primary health care provider orders IV aminophylline. In developing a care plan for Mr. Potter, you select the nursing diagnosis Ineffective Airway Clearance. Suggest Jiursing interventions that would be most important in managing this problem. 

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. 

Signs and Symptoms Characterized by sudden onset of fever, discharges from the nose and eyes, and drooling (ptyalism). Animals have a loss of appetite and show a reluctance to move. Pox lesions appear on the skin but are most obvious on face, eyelids and ears, perineum, and tail. Lesions begin as an area of reddening, then progressing to papules, vesicles, pustules with exudation, and finally to scabs. Lesions also appear on the mucous membranes of the nostrils, mouth, and vulva. Animals suffer acute respiratory distress. Healing is very slow. Mortality peaks about 2 weeks after the onset of the skin lesions. 

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. 

Kelly, D.F., D.G. Morgan, and V.M. Lucke. 1979. Acute respiratory distress in dogs with paraquat poisoning. Pages 297-308 in Animals as Monitors of Environmental Pollutants. Natl. Acad. Sci., Washington, D.C. 

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

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