A 60-year-old female with a medical history of essential hypertension, type 2 diabetes mellitus, epilepsy, and normocytic anemia was brought to our emergency department (ED) due to four weeks of progressive dyspnea. One-month prior, she had presented to an urgent care facility with a productive cough of one-month duration. A chest x-ray (CXR) (Fig. 1) demonstrated a significant right upper lobe consolidation concerning for community-acquired pneumonia and she was prescribed levofloxacin for seven days.
She had a follow-up appointment with her primary care provider two weeks later without improvement of symptoms and was prescribed another course of antibiotics with amoxicillin-clavulanate and azithromycin. Two weeks later, she was brought to our ED for persistent cough, dyspnea, and hypoxia on a portable pulse oximeter noticed by a family member.
On presentation, vitals were the following: temperature 97.2  F, tachycardia to 104 beats per minute, blood pressure 124/63 mmHg, respiratory rate 20 per minute, and oxygen saturation of 87% on room air. Due to a moderately elevated Well's score of 4.5 (high suspicion for PE and heart rate >100) and markedly elevated d-dimer 5672 ng/mL (normal <500 ng/mL), a computed tomography (CT) pulmonary angiogram was performed which revealed a saddle PE with a large proximal clot burden (modified miller score 16) (Fig. 2).
Right ventricle (RV) ischemia and pressure overload were also evident from elevated cardiac biomarkers (troponin I 0.29 ng/mL (normal <0.03 ng/mL) and brain-natriuretic peptide 888 pg/mL (normal <100 pg/mL)) confirming a diagnosis of sub-massive intermediate-high risk PE. A 2D-transthoracic echocardiogram revealed a left ventricle (LV) ejection fraction of 65%, an increase in the RV to LV ratio at 1.4 (normal 0.8), and normal RV systolic function (tricuspid annular plane systolic excursion 21 mm (normal >=17 mm) (Fig. 3).
Venous duplex ultrasound of the lower extremities found no evidence of deep venous thrombosis. The patient was started on supplemental oxygen and therapeutic enoxaparin. Interestingly, in addition to PE, there were innumerable nodular and patchy tiny areas of consolidations bilaterally concerning for multifocal infection (Fig. 4).
Differential diagnosis included COVID-19 pneumonia, community acquired pneumonia, fungal infection, and miliary TB. On further interviewing, she reported a remote exposure to a homeless population and current excavating construction near her job. She also endorsed a thirty-pound unintentional weight loss over the last five months. She was immediately placed into airborne isolation.
Infectious workup was remarkable for positive tuberculin purified protein derivative test at 15 mm induration, positive sputum acid-fast bacilli (AFB) culture, and positive sputum polymerase chain reaction (PCR) for mycobacterium tuberculosis. The rest of the infectious workup was negative including fungal culture and COVID-19 PCR. She was started on an anti-tuberculosis regimen of rifampin, isoniazid, pyrazinamide, and ethambutol (RIPE). After two weeks of treatment and three negative AFB sputum cultures, she was deemed non-contagious and was discharged home on enoxaparin and RIPE therapy. Enoxaparin was selected for anticoagulation to avoid the interaction of direct-oral anticoagulants and warfarin with rifampin. She had frequent telehealth follow up over the next two months with a resolution of her dyspnea and cough. The local authority was informed within 24 h of TB diagnosis and contact tracing was initiated as well.
CT Pulmonary Angiogram: Saddle pulmonary embolism seen on CT pulmonary angiogram demarcated by the red arrow. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article. ).