A 55-year-old Caucasian female with past medical history of gastroesophageal reflux disease, mild intermittent asthma, anxiety and panic attacks, moderately large hiatal hernia, primary hypothyroidism, and chronic low back pain presented to the emergency department with complaints of increasing dyspnea since the last 6 month period. The dyspnea has started insidiously and gradually worsened. She noted a decrease in her exercise tolerance. Pt denied any orthopnea and paroxysmal nocturnal dyspnea. She also complained of chronic cough that was productive of moderate amounts of whitish sputum. Pt denied any recent fevers, hemoptysis, and weight loss. She did not have any recent history of travel or sick contacts. She had a 30 pack year of smoking history which she quit about a year before presentation. Her occupational history was noncontributory to the presentation.
At the time of presentation her vitals were: temp of 37.6 C, pulse rate of 64 beats/min regular, respiratory rate of 20 breaths/min, and oxygen saturation of 92% breathing on 2 L nasal cannula. On physical examination, she was an obese Caucasian female who looked her stated age. Notable pertinent positives on the examination included a thick neck and dry crackles with Velcro rales auscultated at the bases of both lungs. Remainder of the examination was unremarkable. Review of the previous records from our institution and other institutions indicated that the patient had multiple admissions with similar complaints in the past. Provisional diagnosis during these admissions were either community acquired pneumonia or hospital acquired pneumonia.
On this admission, the patient was also initially started on antibiotics but she only noted minimal improvement in her symptoms. Further workup was conducted to identify the cause. Human immunodeficiency virus testing was negative. Tests for other infectious processes such as tuberculosis, Streptococcal, and Legionella pneumonia were negative. Angiotensin converting enzyme level was normal and there was no evidence of pulmonary embolism on imaging. Serial computerized axial tomography scans (CAT scans) demonstrated interstitial lung involvement with patchy bilateral ground glass opacities and mediastinal lymphadenopathy. The infiltrates were progressively worsening on repeated CAT scans Fig. 1 demonstrating X- ray and Fig. 2, Fig. 3, Fig. 4 - CAT scans.
Patient finally underwent a video-assisted thoracoscopy for biopsy of the lung. Pathology revealed patchy organizing fibrosis with acute on chronic inflammation, microabscess formation, and foreign body granulomas with demonstration of frank vegetable matter in the lungs. Acid-fast stain test and Grocott's methenamine silver stain were negative. Findings were compatible with chronic microaspirations likely propagated by hiatal hernia causing idiopathic pulmonary fibrosis. The patient was referred for surgical repair of the hiatal hernia.
CT: lung windows: diffuse bilateral interstitial infiltrates, with tree in bud configuration. There re patchy ground glass changes seem throughout, with focal consolidation within the right mid to lower lung zone.