Introduction: Endobronchial valve (EBV) placement is one technique to attain bronchoscopic lung volume reduction (BLVR). This procedure has shown clinical benefits in terms of lung function, symptoms, and quality of life. A few complications have been reported including pneumothorax, dislocation or migration of the valve, hemoptysis, COPD exacerbation, and pneumonia. However, supraventricular tachycardia (SVT) was not seen as a potential complication within 45 days of the procedure. Hypothesis: SVT is a complication of EBV placement to attain BLVR. Methods: We conducted a retrospective chart review of consecutive patients who underwent EBV placement between January 2018 and December 2021. Patients who developed SVT were compared to patient who did not get SVT. Results: A total of 94 cases were identified. The incidence of SVT was 18 (19.15%) cases post EBV placement. The patients who developed SVT were older (median [IQR]: 74 [69-76], 72.2% males and all were whites (100%). The time to develop SVT ranged between 2.5 hours and 118 hours with median 40.5 hours. 13 (72.2%, P= 0.007) of patients who developed SVT had an electrolyte imbalance post EBV placement. Electrolyte imbalance was an independent factor for predicting SVT on multiple regression after controlling for age, BMI, gender, and location of valve placement (adjusted OR, [CI 95%] 4.64, [1.41 - 15.29], P = 0.012). Placement of EBV in the lingula and left upper lobe (LUL) have higher incidence of SVT (5 (27.8%, P = 0.049) and 12 (66.7%, P = 0.071), respectively). Table 1 and Table 2 further summarizes the result from the study. Conclusion: Given the results, SVT can be recognized as a potential complication of BLVR. Additional caution must be paid to patients who have EBV placed in the LUL and patients with electrolyte imbalance post procedure. Electrolyte imbalance post procedure was the only statistically significant independent predicting factor for SVT. A larger study is needed to determine the level of association.
INTRODUCTION: Pulmonary Langerhans cell histiocytosis (PLCH) is a cystic disease that makes up 3-5% of interstitial lung diseases. It is thought to be secondary to infiltration of Langerhans cells (CD1a positive histiocytes) in the lung leading to destruction of bronchiolar walls and parenchyma and the development of interstitial fibrosis and cysts with advanced disease. At least 90% of patients are current smokers. It mostly affects younger adults, with a peak at age 20-40 years. We present a case of PLCH in an elderly patient who quit smoking 13 years prior but had persistent exposure to secondhand smoke because his wife smoked.CASE PRESENTATION: A 70-year-old male former smoker with a history of emphysema and aortic abdominal aneurysm (AAA) presented for imaging abnormalities noted incidentally during surveillance for AAA. He was asymptomatic. He was noted to have ground-glass nodules measuring 1.3 cm. He was lost to follow-up until 3 years later when a repeat CT showed unchanged ground-glass opacity (GGO) with new cysts and extensive nodules associated with cavitation in the upper lobes bilaterally. Further progression was noted on CT Chest 3 months later with upper lobe predominant interstitial thickening with GGOs, tree-in-bud opacities and new cavitary solid and subsolid pulmonary nodules. Navigational bronchoscopy was performed for transbronchial biopsy of a nodule and bronchoalveolar lavage. Work-up for bacterial, viral, and fungal infections was negative. Biopsy showed zones of fibrosis containing smokers' macrophages and cells with folded and grooved nuclei highly suspicious for pulmonary Langerhans cells which stained positive for CD1a, confirming PLCH. He had a 43 pack-year history and quit 13 years prior but reported that his wife was an avid current smoker. He was counseled to avoid all exposure to tobacco smoke with regular monitoring on imaging.DISCUSSION: The natural history of PLCH is variable, ranging from spontaneous remission to end-stage fibrotic lung disease with continued smoking. Complications can include pneumothorax and pulmonary hypertension, which is independently associated with increased mortality. PLCH is a smoking-related interstitial lung disease and smoking cessation has been shown to resolve or stabilize disease in 62% of patients. While PLCH is typically seen in younger, current smokers, our case highlights the importance of maintaining a high index of suspicion for PLCH in upper lobe predominant cystic and nodular disease, even in an older patient who does not smoke as they may have continued exposure to secondhand smoke.CONCLUSIONS: Screening for exposure to secondhand smoke and stopping exposure is crucial to prevent high morbidity and poor quality of life in patients with PLCH
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