Indium is a relatively rare element that has had limited use for decades as a metal, in alloys, and for electronics applications. During the past 15 years, global demand for indium has increased several-fold, driven by the novel use of indium-tin oxide (ITO) thin fi lms in the production of fl at-panel displays (such as liquid crystal displays [LCDs]), touch screens, and other electronic devices. 1,2 ITO is a sintered ceramic material typically consisting of 90% indium oxide (In 2 O 3 ) and 10% tin oxide (SnO 2 ). Exposures to indium metal and indium compounds (including indium hydroxide [In(OH) 3 ], indium oxide, and ITO) may occur during ITO production, ITO use for the creation of thin fi lms, and reclamation. The bulk of the ITO industry is located in Japan, with some activity in the United States, China, Taiwan, and South Korea. 3 As of May 2010, 10 clinical cases of lung disease in indium workers from three countries (Japan, United States, and China) had been reported. 2 Seven cases were described as interstitial lung disease (ILD) characterized by pulmonary fi brosis with or without emphysema. Three cases were described as pulmonary alveolar proteinosis (PAP). Individually, these 10 case reports left unclear why some workers developed ILD and others developed PAP, and the relationship, if any, between these distinct pulmonary disease processes.Background: Reports of pulmonary fi brosis, emphysema, and, more recently, pulmonary alveolar proteinosis (PAP) in indium workers suggested that workplace exposure to indium compounds caused several different lung diseases. Methods: To better understand the pathogenesis and natural history of indium lung disease, a detailed, systematic, multidisciplinary analysis of clinical, histopathologic, radiologic, and epidemiologic data for all reported cases and workplaces was undertaken. Results: Ten men (median age, 35 years) who produced, used, or reclaimed indium compounds were diagnosed with interstitial lung disease 4-13 years after fi rst exposure (n 5 7) or PAP 1-2 years after fi rst exposure (n 5 3). Common pulmonary histopathologic features in these patients included intraalveolar exudate typical of alveolar proteinosis (n 5 9), cholesterol clefts and granulomas (n 5 10), and fi brosis (n 5 9). Two patients with interstitial lung disease had pneumothoraces. Lung disease progressed following cessation of exposure in most patients and was fatal in two. Radiographic data revealed that two patients with PAP subsequently developed fi brosis and one also developed emphysematous changes. Epidemiologic investigations demonstrated the potential for exposure to respirable particles and an excess of lung abnormalities among coworkers. Conclusions: Occupational exposure to indium compounds was associated with PAP, cholesterol ester crystals and granulomas, pulmonary fi brosis, emphysema, and pneumothoraces. The available evidence suggests exposure to indium compounds causes a novel lung disease that may begin with PAP and progress to include fi brosis and emphysema, and, in som...
BackgroundA cluster of severe lung disease occurred at a manufacturing facility making industrial machines. We aimed to describe disease features and workplace exposures.MethodsClinical, functional, radiologic, and histopathologic features were characterized. Airborne concentrations of thoracic aerosol, metalworking fluid, endotoxin, metals, and volatile organic compounds were measured. Facility airflow was assessed using tracer gas. Process fluids were examined using culture, polymerase chain reaction, and 16S ribosomal RNA sequencing.ResultsFive previously healthy male never‐smokers, ages 27 to 50, developed chest symptoms from 1995 to 2012 while working in the facility's production areas. Patients had an insidious onset of cough, wheeze, and exertional dyspnea; airflow obstruction (mean FEV1 = 44% predicted) and reduced diffusing capacity (mean = 53% predicted); and radiologic centrilobular emphysema. Lung tissue demonstrated a unique pattern of bronchiolitis and alveolar ductitis with B‐cell follicles lacking germinal centers, and significant emphysema for never‐smokers. All had chronic dyspnea, three had a progressive functional decline, and one underwent lung transplantation. Patients reported no unusual nonoccupational exposures. No cases were identified among nonproduction workers or in the community. Endotoxin concentrations were elevated in two air samples; otherwise, exposures were below occupational limits. Air flowed from areas where machining occurred to other production areas. Metalworking fluid primarily grew Pseudomonas pseudoalcaligenes and lacked mycobacterial DNA, but 16S analysis revealed more complex bacterial communities.ConclusionThis cluster indicates a previously unrecognized occupational lung disease of yet uncertain etiology that should be considered in manufacturing workers (particularly never‐smokers) with airflow obstruction and centrilobular emphysema. Investigation of additional cases in other settings could clarify the cause and guide prevention.
Based on these results, some changes have already been implemented, including decreased student-to-instructor ratios, more open scan time, and more required components. The breadth of formal assessment has increased. Multiple pilot programs for clinical rotations are being developed. There is an ongoing need for faculty development and continued assessment of ultrasound competency.
We present a case of pericardioesophageal fistula formation in a 40 year old male who 23 days after undergoing a repeat ablation procedure for atrial fibrillation developed chest pressure, chills and diaphoresis. After initial labs and tests that demonstrated no evidence for acute myocardial ischemia, the patient underwent CT angiography of the chest. The study revealed pneumopericardium and a pericardial effusion. Suspicion was raised of perforation of the posterior left atrial myocardial wall with injury to adjacent esophagus. Water soluble contrast with transition to barium sulfate esophagram subsequently performed identified a perforation further affirming the postulate of a fistulous communication between the esophagus and pericardium. Transthoracic echocardiogram confirmed pericardial effusion but did not demonstrate myocardial defect. Endoscopic management was preferred and an esophageal stent was placed. Follow up esophagram showed an intact esophageal stent without evidence of extravasation.
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