Chest imaging
Case TypeClinical Cases
Authors
Claudia Roncella 1, Chiara Romei 2, Maria Letizia Mazzeo 3, Fabio Falaschi 4, Davide Caramella 5
Patient28 years, male
A 28-year-old male intravenous drug user presented to the emergency department with fever, dyspnoea, chest pain and cough.
On auscultation fine crackles at the pulmonary bases and a right systolic parasternal murmur were detected.
Blood tests revealed increased leukocytes, C-reactive protein and procalcitonin. Blood culture was positive to methicillin-resistant Staphylococcus aureus.
The patient underwent supine chest X-rays, which showed bilateral poorly marginated nodules (Fig. 1). Consequently, a contrast-enhanced chest computed tomography (CT) was performed, which confirmed the presence of multiple bilateral nodular and wedge-shaped parenchymal lung consolidations, characterised by a predominant peripheral distribution and heterogeneous in dimensions (smaller than 3 cm) and appearance (solid and cavitated) (Fig. 2).
After contrast injection, the wedge-shaped consolidations did not show any enhancement, while some of the nodules presented a peripheral rim enhancement and a necrotic center (Fig. 3).
In maximum intensity projection (MIP) reconstructions, the “feeding vessel sign” was seen, hinting their haematogenous origin (Fig. 4).
Other findings were: pericardial effusion, a small amount of bibasilar pleural effusion, disventilatory parenchymal bands and enlargement of hilar and subcarinal lymph nodes (Fig. 5).
An echocardiogram was performed, and tricuspid insufficiency with endocardial vegetations were found.
Septic pulmonary embolism is caused by fragments of thrombi containing pathogens, mobilised from an infectious site and transported in the pulmonary arterial circulation where they get implanted, leading to infarctions and micro-abscesses [1-2].
The microorganisms most often involved are bacteria (i.e. methicillin-resistant and methicillin-sensitive S.aureus, K.pneumoniae and Fusobacteria), fungi (i.e. Candida and Aspergillus in immunocompromised patients) and parasites [1-3].
Causes of septic pulmonary embolism include right-sided endocarditis (caused by S. aureus in intravenous drug users), infected indwelling catheters and pacemaker wires, skin, dental and bone infections, septic thrombophlebitis (i.e. Lamierre’s syndrome) and liver abscesses [1-3].
Common risk factors are intravenous drug use, alcoholism, diabetes and immunologic deficiencies [1-2].
Clinical findings are aspecific and include fever, dyspnoea, chest pain and cough [3].
Complications of septic pulmonary embolism are: lung abscesses, broncho-pleural fistulas, pleural empyema, pneumothorax, septic shock and multiple organ failure [1-3].
Consequently, a prompt diagnosis is essential and imaging techniques, especially chest CT, play an important role [4].
Chest X-ray can be negative or non-specific, showing bilateral, peripheral, poorly marginated lung nodules, which may present cavitation (1-3 cm) [1-4].
CT findings consist of multiple parenchymal lung lesions (5-35 mm) involving all the lung lobes, represented by nodules, wedge-shaped consolidations (broad base against the pleura) and infiltrates [1-4]. They have a vascular, peripheral distribution, since the septic emboli have a small size and get implanted in peripheral pulmonary vessels [1-5]. The lesions progressively evolve into cavitations [1, 4, 5].
The simultaneous presence of solid, subsolid and cavitated lesions with different dimensions reflects repeated episodes of embolic shower [1-5]. For this reason the number of the lesions may vary on sequential chest CTs [6].
After contrast administration, the lesions may not show contrast enhancement (pulmonary infarcts) or may present a strong peripheral rim-enhancement and a necrotic center [5, 6].
In limited cases, the “feeding vessel sign” is present. It is a non-specific finding, characteristic of all nodules of haematogenous origin (septic emboli, metastases, etc.) and consists of a pulmonary vessel that penetrates into a nodule. Recent studies have shown that most frequently the “feeding vessel sign" is due to a venous branch [7].
The treatment includes the eradication of the infection through antimicrobial drugs.
In tricuspid valve endocarditis, cardiac surgery may be necessary in selected cases (i.e. right heart failure, resistant microorganisms, and long-lasting bacteraemia) (Fig. 6) [8].
Written informed patient consent for publication has been obtained.
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[8] Panduranga P1, Al-Mukhaini M, Sulaiman K, Al-Abri S (2010) Tricuspid valve endocarditis in an intravenous drug abuser masquerading as pulmonary tuberculosis. Heart Views 11(3):121-4 (PMID: 21577381)
URL: | https://www.eurorad.org/case/16404 |
DOI: | 10.35100/eurorad/case.16404 |
ISSN: | 1563-4086 |
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