Teaching Case

Our patient had fever (38-39°C), unproductive cough and pleuritic pain. X-ray showed ill defined peripheral nodular infiltrates. CT showed multiple subpleural nodules, related to terminal branches of the pulmonary artery, some with a peripheral cavitation with crescent shape. Blood culture was positive for S. aureus and echocardiography showed tricuspid vegetation.

The patient presented to the emergency room with malaise, fever (38-39°C), unproductive cough and pleuritic chest pain with seven days of evolution. Physical examination showed: body temperature (39°C), tachycardia with normal cardiac sounds, and tachypnea with symmetric murmur on pulmonary auscultation. Laboratory data showed: Anemia (Hb- 10,7mg/dl), leukocytosis (14300cells/dl) with neutrophilia (91%), elevation of PCR (32mg/dl), and normal blood gases. Admission chest X-ray showed ill defined nodular infiltrates, predominantly in the periphery of lower lobes, some presenting a silhouette sign with the left cardiac border and diaphragm. One of the opacities, in the lower left pulmonary field, had a central hypertranslucency that was related to cavitation (Fig. 1). On CT scan we could see in all pulmonary lobes multiple subpleural nodules, closely related to terminal branches of pulmonary artery. The nodules measured less than 2cm, had well defined borders and some had a peripheral cavitation with a crescent shape (Figs. 2, 3); in the lower lung lobes, there were areas of consolidation with ill defined borders and air bronchograms (Fig. 4). The patient also had a blood culture (positive for S. aureus) and an echocardiography, which showed cardiac vegetation on the tricuspid valve. After two months of intravenous antibiotics, blood cultures became negative, cardiac vegetation disappeared and chest x-ray didn’t show any lesion.

This entity consists in thromboembolic material with septic origin causing the occlusion of small pulmonary arteries [1]. Septic thrombus can arise from endocarditis (most frequently associated with intravenous drugs abuse), infected catheter, abscess, septic thrombophlebitis, urinary and odontogenic infection. The etiological agent is usually S. aureus [2]. Prognosis is closely related to early diagnosis; establishing the diagnosis is not always straightforward since radiographic signs may be non-specific, blood cultures negative, and heart murmur undetectable [3]. Chest x-ray remains the screening test, although findings are nonspecific (multiple, bilateral, peripheral nodular lesions with ill defined borders, some with cavitation and pleural effusion) [4]. CT is more sensitive and specific. Documented findings include: multiple peripheral parenchymal nodules, a feeding vessel sign, cavitation, and wedge-shaped peripheral lesions abutting the pleura. Additional findings may be infiltrates, air bronchograms within nodules, and extension into the pleural space [3]. Diagnosis is made on the basis of characteristic imaging abnormalities in association with one or more of the following criteria: Positive blood cultures, tricuspid valve vegetations proven by echocardiography, a compatible clinical course, or other signs of septic embolization [5]. Treatment consists of intravenous large spectrum antibiotics, until blood cultures become negative and valve vegetation disappeare.