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.