Mycotic pulmonary artery aneurysms and septic pulmonary emboli in infective endocarditis: A rare case report and review of imaging findings

Abstract

Within the heterogeneous spectrum of pulmonary vascular disorders, pulmonary artery aneurysms and pseudoaneurysms remain among the least frequently encountered yet most clinically consequential entities. Despite their low incidence, they carry a significant risk of life-threatening complications and pose a considerable diagnostic and therapeutic challenge requiring timely clinical intervention. This report describes the clinical presentation of an 18-year-old female patient with a previously established diagnosis of congenital ventricular septal defect, who developed a mycotic pulmonary artery aneurysm in the context of infective endocarditis complicated by septic emboli.

Introduction

Aneurysms and pseudoaneurysms of the pulmonary arteries represent uncommon vascular abnormalities. Despite their low incidence, they carry the potential for life-threatening complications and pose a substantial challenge for prompt diagnosis and appropriate clinical management. A pulmonary artery aneurysm is defined as an abnormal localized enlargement of the pulmonary arterial lumen beyond its physiological caliber [1].

Mycotic aneurysms (MA) represent 1%-3% of all arterial aneurysms and the most common localization of primary mycotic aneurysms is the femoral artery, the abdominal and thoracic aorta; only 39 cases have been documented in the literature from 1949 to 2018 [2].

The simultaneous development of multiple bilateral mycotic pulmonary artery aneurysms within a given patient is exceedingly rare, with only isolated cases reported in the published literature [3]. The case hereby reported describes multiple bilateral pulmonary artery mycotic aneurysms along with septic emboli in a patient with a history of bacterial endocarditis.

Case report

An 18-year-old female patient with a known congenital ventricular septal defect was brought to the emergency room 48 hours after symptom onset, presenting with signs of systemic sepsis, including fever, tachycardia, tachypnea, and hypotension, together with progressive respiratory distress.

Microbiology assessment identified Staphylococcus aureus sensitive to methicillin as the causative bacteria in the blood culture. Echocardiography showed evidence of infective endocarditis by revealing multiple hyperechoic mobile masses consistent with intracavitary vegetations (Fig. 1).

Fig. 1.

(A) Transthoracic echocardiography, 2D grayscale, apical view, showing a mobile, irregular, hyperechoic mass attached to the tip of a valve leaflet, consistent with a vegetation (orange arrow). (B) Transthoracic echocardiography, 2D grayscale (left) and corresponding color Doppler (right), showing a turbulent, mosaic-pattern flow jet adjacent to the vegetation, findings in keeping with the diagnosis of infective endocarditis with associated valvular regurgitation (orange arrow).

Contrast-enhanced chest CT (Computed tomography) with angiography protocol for the pulmonary arteries demonstrated multiple basal pulmonary nodules and masses with central necrosis in the majority of the lesions. These lesions displayed a spectrum of wall appearances, ranging from thin-walled to thickened, irregular walls surrounding the necrotic contents, with the thickened walls measuring up to 6.5 mm in maximal thickness at the level of the right lung base.

A minority of lesions had solid morphology. This finding is typically consistent with hematogenous septic thromboembolic dissemination.

Besides this, the CT scan also showed multifocal aneurysmal dilatation of the pulmonary arterial branches of both lobes, a finding suggestive of mycotic aneurysms, measuring 30.86 mm on the right and 28.15 mm on the left in maximal diameter (Fig. 2), most conspicuously affecting the lobar pulmonary arterial branches.

Fig. 2.

(A) Contrast-enhanced axial CT image of the chest, mediastinal window, showing aneurysmal dilatation of the right and left lobar pulmonary arterial branches, findings suggestive of mycotic aneurysms. (B) Contrast-enhanced axial CT image at a more caudal level, showing mild aneurysmal dilatation of a left subsegmental pulmonary arterial branch, indicating that involvement extends to the subsegmental level on the left side as well (orange arrow).

Eccentric filling defects were seen inside the aneurysmal parts of the pulmonary arterial branches, mostly on the right side. The most extensive endoluminal filling defects were noted in the right inferior lobar arterial branch, along with minimal but detectable involvement of the subsegmental branches of the left lower lobe (Fig. 2). These imaging findings were highly suggestive of endoluminal material, likely representing either septic emboli or bland thromboembolic disease (Fig. 3).

Fig. 3.

Contrast-enhanced axial CT image of the chest, mediastinal window, showing eccentric intraluminal filling defects within the aneurysmal segments of both the right and left pulmonary arterial branches, more pronounced on the right side, consistent with the presence of endoluminal material (green arrow).

Several cavitary pulmonary lesions exhibited the “feeding vessel sign,” an imaging finding defined by a discrete pulmonary vessel coursing directly into the center of a lesion, which is a feature suggestive of, but not specific for, haematogenous spread and embolic origin. In this clinical context, this finding further supported septic pulmonary embolism as the underlying cause (Fig. 4).

Fig. 4.

(A and B) Axial CT images of the chest, lung window, showing multiple cavitary lesions in the right lower lobe, some of which demonstrate thick, irregular walls (green arrow), findings consistent with septic pulmonary emboli. (C) Axial CT image showing the feeding vessel sign, with a discrete pulmonary vessel coursing directly toward one of the lesions (orange arrow), supporting an embolic etiology.

A repeated CT angiogram performed 2 weeks after the start of treatment showed partial resolution of the septic emboli; however, the changes in the mycotic aneurysms remained morphologically stable compared with the earlier study.

She was then discharged on prolonged antibiotic therapy, with surgical repair of the ventricular septal defect deferred electively to a subsequent admission.

Discussion

Pulmonary arterial aneurysms are far less common than aneurysm locations in other major vascular territories, such as the thoracic aorta and the intracranial circulation. Their development has been associated with a wide variety of conditions that can predispose to it, including congenital cardiovascular anomalies, infectious causes, trauma, systemic vasculitides, and pulmonary arterial hypertension [4]. Epidemiologically, among infectious etiologies, pyogenic bacteria, have become increasingly recognized as a major cause for pulmonary arterial pseudoaneurysm formation in today's clinical practice [5].

In general terms, a mycotic aneurysm is one in which the infectious agent causes destruction of the mural layers of the arterial wall, including the intima, media, and adventitia, resulting in a focal irreversible dilatation of the lumen of the affected arterial segment [6]. This case illustrates the described pathological event through multifocal aneurysmal dilatations of bilateral pulmonary arterial branches emanating from microbiologically confirmed infective endocarditis, thereby fulfilling the classic definition of mycotic aneurysm.

Three different mechanisms have been proposed to explain the origin of mycotic pulmonary aneurysms: the transmural extension of an intraluminal septic thromboembolus from a systemic hematogenous infection, direct spread from a pulmonary infectious focus to the arterial wall, and the intravascular spread of infectious microemboli to the microvasculature of the arterial wall, which results in an outside-in pattern of transmural destruction and progressive aneurysmal dilatation [7].

The synthesis of clinical, microbiological, and radiological findings observed in our patient is most consistent with the first of these mechanisms. Specifically, it is postulated that septic thromboemboli originating from intracardiac vegetations—in the setting of S aureus endocarditis complicating a congenital ventricular septal defect—underwent hematogenous dissemination to the pulmonary arterial tree, with subsequent transmural invasion and aneurysmal degeneration of the affected vessel walls.

The clinical presentation of pulmonary mycotic aneurysms is variable and largely non-specific. The most frequently documented manifestations include hemoptysis, productive cough, and fever [8]. Of these, hemoptysis carries particular clinical significance, as it may herald impending aneurysmal rupture and warrants urgent investigation [9,10]. In the event of rupture, the clinical consequences are catastrophic and may include massive hemorrhage, asphyxiation, exsanguination, and sudden death [11]. Clinically, hemoptysis was not observed in our patient, despite multifocal mycotic aneurysmal involvement of the pulmonary arterial system. Her presentation was instead characterized by systemic sepsis and progressive respiratory compromise, a clinical phenotype that underscores the diagnostic challenge posed by this condition and emphasizes that the absence of hemoptysis should not preclude consideration of mycotic pulmonary aneurysm in the appropriate clinical setting.

Additional respiratory manifestations may arise from extrinsic bronchial compression by voluminous aneurysmal sacs and can include chronic cough, worsening dyspnea, cyanosis, or secondary pneumonia [[10], [11], [12], [13]]. Progressive dyspnea as the main respiratory symptom in this case would be most likely due to the total embolic burden over bilateral pulmonary territories and not due to direct mechanical bronchial compression—a distinction that may have implications for clinical management.

CT angiography constitutes the reference imaging technique to find out for pulmonary arterial aneurysms. It usually shows focal or multifocal aneurysmal dilatations of the pulmonary arterial tree [3]. The pathognomonic CT appearance consists of a well-circumscribed, elliptical, contrast-enhancing structure whose attenuation characteristics are isodense with adjacent opacified vessels [[4], [5], [6], [7]]. This presentation was faithfully reproduced in our case, wherein CT angiography not only established the diagnosis of multifocal mycotic aneurysms with high diagnostic confidence but also delineated the full extent of the associated septic embolic disease, thereby serving as an indispensable guide for therapeutic decision-making.

On CT, septic pulmonary embolism manifests as bilateral nodular opacities and peripheral pleural-based consolidations of variable morphology, with or without central necrosis, alongside the feeding vessel sign [[14], [15], [16]]. The latter—defined as a discrete pulmonary vessel oriented directly toward the center of a parenchymal nodule—has been established as a highly specific imaging indicator of septic embolism, with a reported prevalence ranging from 67% to 100% across published series [[14], [15], [16]]. In our patient, all of these imaging findings were readily identified, including bilateral cavitary and noncavitary nodules, peripheral consolidative opacities, and a distinct feeding vessel sign associated with several cavitary lesions. Taken together with the clinical presentation and microbiological results, these radiological features strongly pointed toward septic pulmonary embolism and played a key role in supporting the diagnosis.

Magnetic resonance imaging (MRI), though less commonly employed than CTA for pulmonary arterial evaluation, represents a viable alternative in patients with contraindications to iodinated contrast material, such as documented allergy or renal insufficiency. Its role in the assessment of the pulmonary arterial system has been well established in the literature [17,18]. T1-weighted sequences provide adequate delineation of pseudoaneurysms, while fast spin echo and gradient echo sequences allow morphological evaluation of the pulmonary arterial tree [17]. Gadolinium-enhanced MR angiography additionally improves delineation of distal pulmonary arterial branches [19].

Additionally, MRI offers the advantage of characterizing arterial wall abnormalities in connective tissue disorders and providing hemodynamic flow information in post-stenotic dilatation secondary to pulmonary valve disease [1].

Conservative management consisting of targeted intravenous antibiotic therapy has been documented as a viable and successful strategy in a carefully defined subset of patients—namely those harboring small, morphologically stable aneurysms without clinical or radiological evidence of rupture or those in whom operative intervention is precluded by comorbidity or surgical risk [2,20,21]. Given her preserved hemodynamic status, sustained clinical improvement with organism-directed antibiotic therapy, and the radiological stability of the aneurysmal sacs observed in serial imaging, a nonoperative strategy was wisely chosen. The 2-week follow-up CT angiogram gave objective evidence of the effectiveness of treatment in terms of partial regression of the septic embolic burden and morphological stability of the mycotic aneurysms, thereby justifying continued conservative management.

In that context, serial CT angiography serves as a valuable surveillance tool to monitor aneurysmal size and morphological stability over time. Although no formally standardized follow-up interval has been established, imaging reassessment following treatment completion and clinical stabilization—approximately 8-12 weeks after therapy initiation—appears clinically reasonable [1].

The extent of infection at diagnosis largely dictates the morbidity and mortality associated with mycotic pulmonary aneurysms [22]. Early clinical suspicion and prompt diagnostic evaluation are therefore essential to optimize patient outcomes. The absence of standardized management guidelines further contributes to outcome variability, reinforcing the need for a formal professional consensus [22].

Conclusion

Although mycotic aneurysms of pulmonary arteries constitute a very rare vascular entity and are quite challenging to diagnose, it is imperative that every radiologist who is in practice should be able to recognize the clinical and imaging features of this disorder to promptly initiate therapeutic measures appropriate to the severity of the disease and thus contribute to the success of the patient outcome. Whatever the cause of death, delayed diagnosis can certainly be one of the factors; thus it is imperative to recognize the disorder early.

Patient consent

Written informed consent was obtained from the patient for the anonymized information to be published in this article.