Case presentation:
A 34 years old Mauritanian gentleman with no past medical history presented with a history of fever and productive cough from 2 weeks. Fever was intermittent, a high grade in nature with no diurnal variation. It was associated with productive cough with mild streaks of hemoptysis from one week. There was no history of night sweats, joint pains, or significant unintentional weight loss. Family history was unremarkable for any disease. There was no drug abuse, recent travel, or sick contact.
On clinical examination, the patient was in mild distress due to cough and high-grade fever of 39.3 C. His blood pressure at presentation was normal; however, he had mild tachypnea from 20-24/min, tachycardia of 102/min with normal oxygen saturation at room air. On auscultation of the chest, there was bronchial breathing in the right lung’s middle zone and crackles in the lower zone, respectively. The left side of the lung revealed decreased air entry in the middle zone. The rest of the systemic examination was unremarkable. A Chest XR showed extensive non-homogenous infiltrates in the right lung and left middle zone of the lung, respectively, as shown in the figure: 1. Due to the ongoing COVID 19 pandemic, he was kept under airborne isolation and screened for SARS- CoV-2 virus by real time reverse transcriptase-polymerase chain reaction (rRT-PCR) from the nasopharyngeal sample using gene Xpert technology. It was inconclusive initially. Sepsis workup including blood cultures, urine cultures, respiratory viral panel PCR was negative. There was a clinical suspicion of PTB; therefore, sputum for Acid Fast Bacillus (AFB) PCR, smear, and culture was sent. His sputum for AFB came positive for active PTB. And was immediately started on anti TB medications.
His fever started to settle down but the patient had persistent sinus tachycardia and tachypnea. ECG and cardiac markers were normal. An urgent CT pulmonary angiogram (CTPA) was ordered to rule out PE. CTPA revealed lung air space disease with new consolidation areas suggestive of an underlying infective process like pulmonary tuberculosis or COVID 19. An acute filling defect was identified in the left lower lobe anterior and lateral segments of the pulmonary arteries impressive of pulmonary embolism, as shown in the figure: 2. Repeat COVID 19 screening test was negative. Family history did not reveal any thromboembolic disease in the first-degree relative. Thrombophilia workup, including protein C and S, anti-thrombin activity, Factor V Leiden, and prothrombin gene mutations, was unremarkable. Based on clinical presentation and further investigations, he was labeled and treated as a case of active PTB complicated with PE. He was started immediately on therapeutic anticoagulation with low molecular weight heparin (LMWH) as an inpatient and was discharged on Rivaroxaban, a new oral anticoagulant (NOAC), with follow-up of 6 weeks. During the follow-up period, he remained stable.