We present a case of a 47-year-old woman with a past medical history of actinic keratosis, seborrheic dermatosis, anxiety, deep vein thrombosis, and depression, who presented with a 4-day history of progressively worsening shortness of breath, nasal congestion, fevers, chills, cough, lower extremity swelling, and generalized body aches. There was no history of sick contacts, TB exposure, or recent travel. She was on the following medications: alprazolam, amlodipine, buspirone, clonazepam, dicyclomine, losartan, ondansetron, warfarin, escitalopram oxalate, ibuprofen, methadone, and topical tretinoin.
While in the emergency room, she was unable to maintain adequate oxygenation and required endotracheal intubation. Bilateral crackles and rhonchi were heard on chest examination. Patient was treated empirically with multiple antibiotics. After no significant improvement, she was placed on steroids as well as azathioprine and managed with supportive care. CBC with differential showed a WBC count of 9.97, hemoglobin 9.9, hematocrit 35.8, and platelet count of 266. Blood culture showed no growth. Influenza A and B Antigen and cryptococcal antigen were negative. Bronchoalveolar lavage culture showed no growth and gram stain was negative. Serology for rheumatoid factor was normal and histoplasma antigen was not detected. Electrolytes, blood urea nitrogen, and creatinine were normal. Echocardiogram revealed elevated right ventricular systolic pressure (81-90 mmHg) with subsequent right heart catheterization confirming pulmonary hypertension. Chest CT with contrast revealed bilateral diffuse predominant ground glass attenuation with scattered alveolar opacities of the lungs. Due to clinical deterioration, a repeat chest CT without contrast done 9 days after showed multifocal consolidation in bilateral lungs which had worsened when compared to previous CT. Small trace pleural effusions were present but no pneumothorax.
CT Angiogram pulmonary embolism protocol with contrast was done 5 days after the second chest CT and it showed no filling defect within the pulmonary arterial system to indicate any significant pulmonary embolus but revealed small partial occlusive filling defect in the right internal jugular vein. The heart and pericardium were unremarkable. Extensive multifocal airspace opacities were seen in the bilateral lungs which worsened compared to the prior exam. These were greater in the bilateral upper lobes.
Due to lack of clinical improvement, a video assisted thoracoscopic surgery (VATS) with biopsy of the right middle and lower lung lobes was performed which revealed a diffuse alveolar septal thickening, due to combination of fibroblastic proliferation and alveolar lining cell hyperplasia. Scattered eosinophilic hyaline membranes were also present and these findings were supportive of diffuse alveolar damage. Several fibrinous thrombi were also noted in the small arteries. No viral inclusions were identified and biopsy cultures showed no growth.
Patient had significant improvement with continued supportive treatment and was discharged 20 days after admission to a long-term care center, advised to stop e-cigarette smoking, and to follow up with the pulmonologist and the primary care physician in the clinic on outpatient basis. Patient adhered to lifestyle modification and clinic visits and a repeat chest CT scan done about 3 months following discharge showed significant improvement in the previously seen infiltrates with complete resolution in the upper lung zones.