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Pulmonary Vascular Disease |

Chronic Left Lower Lobe Pulmonary Infiltrates During Military Deployment FREE TO VIEW

John Hunninghake, MD
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San Antonio Uniformed Services Healthcare Education Consortium, Windcrest, TX


Chest. 2014;146(4_MeetingAbstracts):882A. doi:10.1378/chest.1991753
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Abstract

SESSION TITLE: Pulmonary Vascular Disease Student/Resident Case Report Posters I

SESSION TYPE: Medical Student/Resident Case Report

PRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PM

INTRODUCTION: Airborne hazards for the deployed military population such as geologic dusts, burn pits, or air pollution are reported to increase respiratory symptoms, may exacerbate pre-existing asthma, and are linked to AEP. Development of obstructive or interstitial diseases is less common; etiologies are not well established. The development of chronic pulmonary infiltrates during deployment in this patient was initially thought to be exposure-related.

CASE PRESENTATION: This patient is a 58 y.o. active duty male referred for chronic LLL infiltrates after a 24 month Afghanistan deployment. Past medical history was notable for atrial fibrillation s/p ablation in April 2010, HTN, and GERD. He developed acute respiratory symptoms in December 2010 (while deployed) with productive cough, fevers, and mild hemoptysis. He received 2 courses of azithromycin for presumed pneumonia based on LLL infiltrates. Follow-up CT chest demonstrated isolated LLL infiltrates; he was referred to Landstuhl Regional Medical Center in April 2011. Bronchoscopy identified mild interstitial fibrosis, hemosiderin-laden macrophages, and few multinucleated giant cells. After returning from deployment, he had stable symptoms of mild exertional dyspnea and wheezing. Repeat evaluation showed normal PFTs and negative methacholine. The isolated LLL abnormalities gradually improved from 2011 until 2013 when increased infiltrates were noted. Repeat FOB with biopsy demonstrated normal pathologic findings and cell counts. Two months later, he was admitted for cardioversion of recurrent atrial fibrillation. Cardiac CT angiography revealed complete occlusion of the left inferior pulmonary vein. Comparison with prior CT from January 2011 showed a complete pulmonary vein stenosis eight months after undergoing initial ablation therapy. Ventilation/perfusion scanning noted LLL perfusion of 5.5% compared to 30.7% in the RLL.

DISCUSSION: Pulmonary vein stenosis is a known complication of radiofrequency ablation for atrial fibrillation. Severe stenosis or complete occlusion was noted in 3.4% of patients and may be associated with cough, dyspnea, or hemoptysis. V/Q scanning can define the functional significance.

CONCLUSIONS: Despite the chronic infiltrates and symptoms, the CT findings in this patient were unrelated to deployment exposures.

Reference #1: Saad EB, et al. Pulmonary vein stenosis after radiofrequency ablation of atrial fibrillation: functional characterization, evolution, and influence of the ablation strategy. Circulation. 108(25):3102-7, 2003 Dec 23.

Reference #2: Packer DL, et al. Clinical presentation, investigation, and management of pulmonary vein stenosis complicating ablation for atrial fibrillation. Circulation. 111(5):546-54, 2005 Feb 8.

Reference #3: Barrett CD. Di Biase L. Natale A. How to identify and treat patient with pulmonary vein stenosis post atrial fibrillation ablation. Current Opinion in Cardiology. 24(1):42-9, 2009 Jan.

DISCLOSURE: The following authors have nothing to disclose: John Hunninghake

No Product/Research Disclosure Information


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