Case Presentation: A 72-year-old male with a history of tobacco use (12 pack-years) presented to the hospital with 4 months of a progressive nonproductive cough. He experienced coughing spells lasting minutes with positional changes. The patient additionally endorsed night sweats, unexpected weight loss of 11 pounds, and dyspnea on exertion. In the days prior to admission, he had visited another hospital’s emergency department (ED), where he had an x-ray of the chest performed before being sent home with cough syrup. As his symptoms persisted, the patient returned to our hospital’s ED. On exam, the patient had tachycardia with diminished breath sounds in the right middle and lower and left lower lung fields, but was otherwise unremarkable. His initial labwork was remarkable for an elevated D-dimer. On admission, computed tomography (CT) angiogram of the chest revealed bilateral pleural effusions and subsegmental pulmonary emboli with intralobular septal line thickening, diffuse groundglass opacities, and nodular consolidation in the right upper lobe. Thoracentesis was performed, and cytology of the pleural fluid revealed numerous malignant epithelial cells present in glandular clusters in a background of mesothelial cells and chronic inflammation, consistent with adenocarcinoma. PET/CT scan demonstrated extensive nodal, osseous, pulmonary, and left adrenal metastatic disease. The patient was diagnosed with stage IV NSCLC and was ultimately discharged on apixaban for his pulmonary emboli with oncology followup prior to proceeding with systemic treatment. Unfortunately, the patient returned to the hospital ~2 weeks later with worsening dyspnea and progressive hypoxia. A CT scan of the chest revealed diffuse interstitial opacities most consistent with PLC. Given the patient’s rapid deterioration, he was deemed ineligible for cancer therapy, and ultimately passed away 3 weeks after his initial diagnosis of NSCLC.
Discussion: Because PLC obstructs the pulmonary lymphatic channels, PLC can present as intra/interlobular thickening on CT. Peribronchovascular thickening, which is highly specific for PLC, and groundglass consolidations were both observed on our patient’s initial CT but mistaken for pulmonary edema versus an atypical pneumonia. In retrospect, these subtle findings may have triggered an expedited evaluation (possible bronchoscopy with BAL or transbronchial biopsy). An earlier tissue diagnosis of PLC would likely have resulted in grounded discussions with our oncologists surrounding markers influencing the patient’s prognosis, estimated life expectancy, and options for definitive or supportive treatment in the setting of advanced, complicated NSCLC.
Conclusions: This case presents select outcomes associated with a delayed diagnosis of PLC in an adult with stage IV NSCLC and pulmonary emboli. The presence of intra/interlobular thickening on CT in someone with known pulmonary malignancy should raise concern for PLC. Additionally, earlier identification of PLC could have helped bridge goals of care and quality of life conversations with patients and their families given that patients with NSCLC and PLC have a very poor baseline prognosis.