A 46-year-old man consulted our department for the chief complaint of exacerbation of respiratory distress of 2-month duration, with accompanying night sweats, fever, and weight loss. He was an electrician and had no history of dust inhalation, drug use, or pet birds. He was previously healthy with unremarkable medical history. He had been smoking 20 cigarettes per day from age 20 years. He had quit paper cigarettes 3 months before, and smoked 20 cigarettes per day using an e-cig pen. He used the e-cigs until the day before examination. Physical findings at presentation revealed pallor, body temperature 37.1 C. Chest auscultation revealed mild fine crackles in both sides of the chest with normal heart sounds.
Laboratory data at hospital arrival included white blood cell count 15,200/mm3 (77.5% neutrophils, 11.5% lymphocytes, and 4.0% eosinophils). C-reactive protein levels (11.81 mg/dL) were elevated and Krebs von den Lungen 6 (KL-6) was high at 1841 U/mL. Blood gas analysis findings in room air revealed pH 7.504, PaCO2 29.0 Torr, PaO2 52.6 Torr, HCO3 22.7 mmol/L, and base excess 0.7. Pulmonary function testing (PFT) revealed the %vital capacity of 50.6%, indicating restrictive impairment.
Chest radiography revealed opacities in the bilateral upper lung fields with extensive bilateral ground-glass opacity (GGO) predominantly around the lateral segments of the lungs (Fig. 1A). Chest computed tomography (CT) revealed GGO and traction bronchiectasis throughout the entire bilateral upper lobes; non-segmental GGO with curvilinear shadow was also observed in the middle lobe, lingula, and bilateral lower lobes (Fig. 1B).
Two days after the initial examination, BAL and TBLB were performed. Bronchoscopic examinations revealed normal airways. The BAL fluid findings included CD4/CD8 0.6, total cell count 4.0 x 105/mL, and cell fractionation of 18% macrophages, 57.5% neutrophils, 6.0% lymphocytes, and 18.5% eosinophils. Bacterial culture examination revealed normal flora. Abundant lipid-laden macrophages were observed upon Oil Red O staining of BAL fluid (Fig. 2A).
Lung histological examination revealed lesions with acute changes, alveolar septum swelling, and eosinophil and neutrophil invasion, with intra-alveolar invasion of eosinophils and neutrophils; in addition, abundant macrophages containing blackish-brown pigment and multinucleated foreign-body giant cells and intra-alveolar organization (Fig. 2B-D). These changes were considered to be caused by inhalation of foreign bodies through the airways, which led to the histopathological diagnosis of acute alveolitis with intra-alveolar fibrosis caused by e-cig use. We diagnosed e-cig-induced ALI caused by inhalation.
After bronchoscopy, methylprednisolone was administered at a dose of 1 g/day for 3 days. The patient received high-dose steroids, because at the time of treatment he had severe hypoxia. Thereafter, the patient received maintenance therapy of 1 mg/kg prednisolone. Antibiotics were not prescribed. After 2 weeks of treatment, chest radiography showed that the extensive GGO had markedly ameliorated (Fig. 1C). After 4 weeks, PFT results returned to normal range. The subject was tapered off gradually from steroid therapy with follow-up observation and discharged from the hospital on Day 30. He completely quitted e-cig smoking and no subsequent flare up of pneumonitis was observed on outpatient follow-up.