PDF(Pubmed)
Abstract：
BACKGROUND: Fiberglass has a larger aerodynamic diameter and is less likely to be inhaled into the lungs. Further, it will be cleared even if it is mechanically broken into smaller pieces and inhaled into the lungs. Fiberglass lung disease has been well documented if long term exposure but was thought reversible and would not cause severe diseases. The diagnosis of fiberglass lung disease depends on exposure history and histopathological findings. However, the exact occupational exposure history is often difficult to identify because mixed substance exposure often occurs and fiberglass disease is not as well-known as asbestosis.
METHODS: A 66-year-old man had unexplained transudative pericardial effusion requiring pleural pericardial window operation twice at another medical center where asbestosis was told because of his self-reported long-term asbestosis exposure and the histopathological finding of a ferruginous body in his lung. Constrictive pericarditis developed two years later and resulted in congestive heart failure. Radical pericardiectomy combined with lung biopsy was performed following chest computed tomography imaging and the transudative nature of pericardial effusion not compatible with asbestosis. However, the histopathologic findings of his lung and pericardium at our hospital only showed chronic fibrosis without any asbestosis body. The patient\'s lung was found to be extremely fragile during a lung biopsy; histopathologic specimens were reviewed, and various fragments of fiberglass were found in the lung and pericardium. The patient\'s occupational exposure was carefully reevaluated, and he restated that he was only exposed to asbestosis for 1-2 years but was heavily exposed to fiberglass for more than 40 years. This misleading exposure history was mainly because he was only familiar with the dangers of asbestos. Since most fiberglass lung diseases are reversible and the symptoms of heart failure resolve soon after surgery, only observation was needed. Ten months after radical pericardiectomy, his symptoms, pleural effusion, and impaired pulmonary function eventually resolved.
CONCLUSIONS: Fiberglass could cause inflammation of the pericardium, resulting in pericardial effusion and constrictive pericarditis, which could be severe and require radical pericardiectomy. Exact exposure history and histopathological examinations are the key to diagnosis.
METHODS: A 66-year-old man had unexplained transudative pericardial effusion requiring pleural pericardial window operation twice at another medical center where asbestosis was told because of his self-reported long-term asbestosis exposure and the histopathological finding of a ferruginous body in his lung. Constrictive pericarditis developed two years later and resulted in congestive heart failure. Radical pericardiectomy combined with lung biopsy was performed following chest computed tomography imaging and the transudative nature of pericardial effusion not compatible with asbestosis. However, the histopathologic findings of his lung and pericardium at our hospital only showed chronic fibrosis without any asbestosis body. The patient\'s lung was found to be extremely fragile during a lung biopsy; histopathologic specimens were reviewed, and various fragments of fiberglass were found in the lung and pericardium. The patient\'s occupational exposure was carefully reevaluated, and he restated that he was only exposed to asbestosis for 1-2 years but was heavily exposed to fiberglass for more than 40 years. This misleading exposure history was mainly because he was only familiar with the dangers of asbestos. Since most fiberglass lung diseases are reversible and the symptoms of heart failure resolve soon after surgery, only observation was needed. Ten months after radical pericardiectomy, his symptoms, pleural effusion, and impaired pulmonary function eventually resolved.
CONCLUSIONS: Fiberglass could cause inflammation of the pericardium, resulting in pericardial effusion and constrictive pericarditis, which could be severe and require radical pericardiectomy. Exact exposure history and histopathological examinations are the key to diagnosis.
摘要：
背景：玻璃纤维具有较大的空气动力学直径，并且不太可能被吸入肺部。Further,即使它被机械地分解成更小的碎片并吸入肺部，它也会被清除。如果长期暴露，玻璃纤维肺病已得到充分证明，但被认为是可逆的，不会导致严重的疾病。玻璃纤维肺病的诊断取决于暴露史和组织病理学发现。然而,确切的职业暴露史通常难以确定,因为经常发生混合物质暴露,并且玻璃纤维疾病不像石棉沉滞症那样广为人知.
方法：一名66岁的男子在另一个医疗中心进行了两次不明原因的渗出性心包积液，需要进行胸膜心包窗手术，因为他的自我报告的长期石棉肺暴露和肺中有铁质体的组织病理学发现。缩窄性心包炎在两年后发展并导致充血性心力衰竭。在胸部计算机断层扫描成像和心包积液的渗出性与石棉沉着症不相容后，进行了根治性心包切除术联合肺活检。然而,在我们医院，他的肺和心包的组织病理学发现仅显示慢性纤维化，没有任何石棉沉着症。在肺活检中发现患者的肺非常脆弱；检查组织病理学标本，在肺和心包中发现了各种玻璃纤维碎片。对患者的职业暴露进行了仔细的重新评估，他重申，他只暴露于石棉沉滞症1-2年，但严重暴露于玻璃纤维超过40年。这种误导性的接触史主要是因为他只熟悉石棉的危险。由于大多数玻璃纤维肺部疾病是可逆的，并且心力衰竭的症状在手术后很快消失，只需要观察。根治性心包切除术后十个月,他的症状,胸腔积液,和受损的肺功能最终解决。
结论：玻璃纤维可引起心包炎症，导致心包积液和缩窄性心包炎，这可能是严重的，需要根治性心包切除术。确切的暴露史和组织病理学检查是诊断的关键。
方法：一名66岁的男子在另一个医疗中心进行了两次不明原因的渗出性心包积液，需要进行胸膜心包窗手术，因为他的自我报告的长期石棉肺暴露和肺中有铁质体的组织病理学发现。缩窄性心包炎在两年后发展并导致充血性心力衰竭。在胸部计算机断层扫描成像和心包积液的渗出性与石棉沉着症不相容后，进行了根治性心包切除术联合肺活检。然而,在我们医院，他的肺和心包的组织病理学发现仅显示慢性纤维化，没有任何石棉沉着症。在肺活检中发现患者的肺非常脆弱；检查组织病理学标本，在肺和心包中发现了各种玻璃纤维碎片。对患者的职业暴露进行了仔细的重新评估，他重申，他只暴露于石棉沉滞症1-2年，但严重暴露于玻璃纤维超过40年。这种误导性的接触史主要是因为他只熟悉石棉的危险。由于大多数玻璃纤维肺部疾病是可逆的，并且心力衰竭的症状在手术后很快消失，只需要观察。根治性心包切除术后十个月,他的症状,胸腔积液,和受损的肺功能最终解决。
结论：玻璃纤维可引起心包炎症，导致心包积液和缩窄性心包炎，这可能是严重的，需要根治性心包切除术。确切的暴露史和组织病理学检查是诊断的关键。
