Atelectasis pulmonary

Atelectasis—Pulmonary parenchymal collapse due to alveolar or bronchial obstraction. 

An estimated oral dose of 260 mg endosulfan/kg caused severe seizures in a 43-year-old man, and brain death from cerebral herniation and massive cerebral edema occurred within 4 days of exposure (Boereboom et al. 1998) there were no signs of myocardial infarction and only slight congestion of the heart, but pulmonary congestion and atelectasis were evident at autopsy. 

Human once Resp 260 M (pulmonary congestion, atelectasis) Boereboom et al. 1998 Technical... 

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. 

Infant respiratory distress syndrome (IRDS), also known as hyaline membrane disease, is one of the most common causes of respiratory disease in premature infants. In fact, it occurs in 30,000 to 50,000 newborns per year in the U.S. — most commonly in neonates bom before week 25 of gestation. IRDS is characterized by areas of atelectasis, hemorrhagic edema, and the formation of hyaline membranes within the alveoli. IRDS is caused by a deficiency of pulmonary surfactant. Alveolar type II cells, which produce surfactant, do not begin to mature until weeks 25 to 28 of... 

The therapy for IRDS includes mechanical ventilation with continuous positive airway pressure. This maintains adequate ventilation and prevents airway collapse between breaths with the formation of atelectasis. Therapy also includes administration of exogenous pulmonary surfactant. Two types of surfactants are used to prevent and treat IRDS in the U.S. These include surfactants prepared from animal sources as well as synthetic surfactants. Exogenous pulmonary surfactants are administered as a suspension (in saline) through the endotracheal tube used for mechanical ventilation. 

Mucolytic Adjuvant therapy for abnormal, viscid, or inspissated mucus secretions in chronic bronchopulmonary disease (chronic emphysema, emphysema with bronchitis, chronic asthmatic bronchitis, tuberculosis, bronchiectasis, primary amyloidosis of lung) acute bronchopulmonary disease (pneumonia, bronchitis, tracheobronchitis) pulmonary complications of cystic fibrosis tracheostomy care pulmonary complications associated with surgery use during anesthesia posttraumatic chest conditions atelectasis due to mucus obstruction diagnostic bronchial studies (bronchograms, bronchospirometry, bronchial wedge catheterization). 

Respiratory Pneumonia pharyngitis sinusitis hyperventilation rhinitis apnea aspiration pneumonia asthma dyspnea atelectasis increased cough/sputum epistaxis hypoxia pneumothorax hemoptysis bronchitis chest pain pulmonary fibrosis. 

Aerosol - Several serious adverse events occurred in severely ill infants with life-threatening underlying diseases, many of whom required assisted ventilation. Additional reports of worsening of respiratory status, bronchospasm, pulmonary edema, hypoventilation, cyanosis, dyspnea, bacterial pneumonia, pneumothorax, apnea, atelectasis, and ventilator dependence have occurred. Sudden deterioration of respiratory function has been associated with initiation of aerosolized ribavirin use in infants. If ribavirin aerosol treatment produces sudden deterioration of respiratory function, stop treatment and reinstitute only with extreme caution, continuous monitoring, and consideration of coadministration of bronchodilators. 

Aerosol Adverse reactions may include anemia and hemolytic anemia apnea atelectasis bacterial pneumonia bigeminy bradycardia bronchospasm cardiac arrest conjunctivitis cyanosis digitalis toxicity dyspnea hypotension hypoventilation pneumothorax pulmonary edema rash reticulocytosis tachycardia ventilator dependence worsening of respiratory status. 

Respiratory - Coughing, dyspnea, pulmonary edema (5% or more) abnormal breath sounds, atelectasis, congestion, hypoxia, pharyngitis, pleural effusion, rales, rhinitis (2% to less than 5%). 

In animals, acute oral exposure to doses of 4,000 mg/kg has been observed to cause respiratory edema, atelectasis and hemorrhage (Gould and Smuckler 1971). This is accompanied by marked disruption of subcellular structure in most pulmonary cell types, including granular pneumocytes, capillary endothelial cells and Clara cells (Boyd et al. 1980 Gould and Smuckler 1971 Hollinger 1982). It has been shown that Clara cells were most severely injured because they are the most active in metabolic activation of carbon tetrachloride. Injury to capillary endothelial cells is dose-... 

Diller, 1985 Ohio et al, 1991). Pulmonary injury is exacerbated by elevated levels of leukotrienes and neutrophil chemotactic agents. The neutrophils release cytokines and other reactive mediators worsening pulmonary injury (Ohio et al, 1991 Sciuto et al, 1995). Localized emphysema and partial atelectasis occur. Death is from anoxia secondary to pulmonary edema (Borak and Diller, 2001 Proctor and Hughes, 2004). 

Lung/tracheal congestion, fluid in the pleural cavity, atelectasis, emphysema, and/or pulmonary edema and lung hemorrhaging were observed in rats... 

In animals, HCl is a severe irritant of the eyes and respiratory system. The 30 min LC50 values in rats and mice are 4701 and 2644 ppm, respectively. Animals exposed to high concentrations of HCl gas developed necrosis of the tracheal and bronchial epithelium, pulmonary edema, atelectasis, emphysema, and damage to the pulmonary blood vessels and liver. Chronic exposure to 10 ppm for 6hday for life did not cause neoplastic lesions or serious irritant effects in the nasal epithelium of rats. In experimental animals, exposure to a concentration of 1350 ppm hydrogen chloride gas caused clouding of the cornea after 1.5 h and exposure to 3000 ppm for 6 h caused slight erosion of the corneal epithelium. 

Postexposure survival remains a perplexing problem. In the early work, death was probably due to many factors such as exhaustion from the work of breathing, contamination of lungs by urine, feces, and skin oils, atelectasis due to loss of pulmonary surfactant, hyaline membrane, and possibly electrolyte imbalances, especially in the lung parenchyma. However, Kylstra and Lanphier devised techniques to obviate the difficulties en-... 

At postmortem examination, most monkeys had similar gross pulmonary lesions. Lungs were diffusely heavy and wet, with multifocal petechial hemorrhages and areas of atelectasis. Clear, serous-to-white, frothy fluid often drained freely from the laryngeal orifice. The small and large intestines frequently had petechial hemorrhages and mucosal erosions. Typically, monkeys had mildly swollen lymph nodes, with moist and bulging cut surfaces. 

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