Atrial fibrillation and concomitant left subclavian, axillary and brachial artery embolism after fiberoptic bronchoscopy: A case report

BACKGROUND Fiberoptic bronchoscopy has been widely used in the diagnosis and treatment of respiratory diseases.Numerous major and minor complications have been reported following this procedure.The incidence of major postoperative complications is approximately 0.5%and includes respiratory depression,pneumothorax,pulmonary edema,pneumonia,airway obstruction and cardiorespiratory arrest.Minor complications include vasovagal reactions,cardiac arrhythmias,hemorrhage,pneumothorax,aphonia,nausea,vomiting and fever.However,to our knowledge,a case of atrial fibrillation(AF)concomitant with fatal arterial embolism in the upper extremities following diagnostic bronchoscopy has never been reported.CASE SUMMARY A 70-year-old female patient presented with a history of rheumatic heart disease beginning at 10 years of age and an approximately 10-year history of hypertension.The patient was transferred from the cardiology department to the respiratory department due to recurrent coughing,pneumonia,and fever.She underwent fiberoptic bronchoscopy in the respiratory department.Approximately 2 h after completion of bronchoscopy,she complained of left arm numbness and weakness.Physical examination detected cyanosis of the left upper extremity,grade III weakened limb muscle strength,and undetectable left brachial artery pulsation.Auscultation indicated AF.B-mode ultrasound examination of the blood vessels showed hyperechoic material in the left subclavian,axillary and brachial arteries,and parallel veins.As our hospital has no vascular surgery capability,the patient was transferred to a specialized hospital for emergency thrombectomy that day.A tracking investigation found that the patient’s conditions improved after successful thrombectomy.CONCLUSION Thromboembolism following bronchoscopy is rare,and only a few cases of cerebral air embolism after bronchoscopy have been reported.

Role of various imbalances centered on alveolar epithelial cell/fibroblast apoptosis imbalance in the pathogenesis of idiopathic pulmonary fibrosis

There have been recent extensive studies and rapid advancement on the pathogenesis underlying idiopathic pulmonary fibrosis(IPF),and intricate pathogenesis of IPF has been suggested.The purpose of this study was to clarify the logical relationship between these mechanisms.An extensive search was undertaken of the PubMed using the following keywords:"etiology,""pathogenesis,""alveolar epithelial cell(AEC),""fibroblast,""lymphocyte,""macrophage,""epigenomics,""histone,"acetylation,""methylation,""endoplasmic reticulum stress,""mitochondrial dysfunction,""telomerase,""proteases,""plasminogen,""epithelial-mesenchymal transition,""oxidative stress,""inflammation,""apoptosis,"and"idiopathic pulmonary fibrosis."This search covered relevant research articles published up to April 30,2020.Original articles,reviews,and other articles were searched and reviewed for content;240 highly relevant studies were obtained after screening.IPF is likely the result of complex interactions between environmental,genetic,and epigenetic factors:environmental exposures affect epigenetic marks;epigenetic processes translate environmental exposures into the regulation of chromatin;epigenetic processes shape gene expression profiles;in turn,an individual’s genetic background determines epigenetic marks;finally,these genetic and epigenetic factors act in concert to dysregulate gene expression in IPF lung tissue.The pathogenesis of IPF involves various imbalances including endoplasmic reticulum,telomere length homeostasis,mitochondrial dysfunction,oxidant/antioxidant imbalance,Th1/Th2 imbalance,M1-M2 polarization of macrophages,protease/antiprotease imbalance,and plasminogen activation/inhibition imbalance.These affect each other,promote each other,and ultimately promote AEC/fibroblast apoptosis imbalance directly or indirectly.Excessive AEC apoptosis and impaired apoptosis of fibroblasts contribute to fibrosis.IPF is likely the result of complex interactions between environmental,genetic,and epigenetic factors.The pathogenesis of IPF involves various imbalances centered on AEC/fibroblast apoptosis imbalance.