Infectious aortitis (IA) is a rare, life-threatening cardiovascular disease for which early diagnosis can be missed due to a lack of specific clinical, radiological, and laboratory features. IA’s common sign is a mycotic aortic aneurysm (MAA), which manifests as a mushroom-shaped structure on a blood vessel. This manifestation does not refer to a specific pathogenic cause, such as a fungal infection (1); rather, MAAs is an acute inflammatory response to pathogenic infection, which induces neutrophilic infiltration at the arterial wall. During this process, the collagenolytic and elastolytic enzymes are activated, which is concomitant with saccular lumen dilation and rupture (2-4).
MAAs are associated with high mortality due to their increased risk of rupture, which is especially common in the abdominal aorta compared with peripheral arteries (5). Early diagnosis and timely intervention are critical in reducing the mortality of MAAs; however, early diagnosis is challenging due to nonspecific symptoms and low sensitivity of blood cultures (6-9). Furthermore, the incidence of adverse events in patients with MAAs after invasive treatment is higher than those with pseudoaneurysms associated with other causes, such as trauma and atherosclerosis. The endovascular stenting of MAAs may be associated with a high risk of stent infection, endoleak, reinfection, and potential rupture (10,11).
The diagnosis of MAAs requires awareness of the spectra of computed tomography (CT), magnetic resonance imaging (MRI), and 18F-fluorodeoxyglucose (FDG) positron emission tomography (PET)/CT. The use of CT angiography (CTA) in the assessment of aortic disease—including MAAs—is increasing, owing to its non-invasive, efficient, broad coverage and its isotropic voxel capabilities. With CT technology development and advanced dose reduction techniques, CTA is a fast and high-quality method with minimal contrast medium and radiation dose. The high tissue resolution of MRI can provide valuable anatomical and physiological information, especially in assessing abscess and tissue edema. In the latest studies, 18F-FDG-PET/CT has shown higher sensitivity and diagnostic accuracy in infected aortic aneurysms and aortic prosthetic graft infection compared to CTA (12,13).
This review provides an overview of the clinical, pathological, and radiological presentations of MAAs. The imaging findings during the period following medication, interventional, or surgical management are also described. The imaging characteristics in other infectious pathogens are highlighted for differential diagnosis, especially in patients with negative blood culture results.
MAAs usually occur in the elderly, predominantly affecting immunocompromised patients, such as diabetes mellitus, liver cirrhosis, end-stage renal disease, alcoholism, chronic glucocorticoid therapy, post-transplantation immunosuppression, human immunodeficiency virus infection, drug abuse, and malignancy (14-17). The known causative organisms of MAAs are Salmonella, Staphylococcus aureus, Klebsiella pneumoniae (KP), Escherichia coli, Mycobacterium, and Brucella melitensis. Fungi, such as Candida albicans and Aspergillus, are also rare causes of infected aneurysms.
Non-typhoidal Salmonella has been reported as the most common organism in Eastern countries, especially in the atherosclerotic abdominal aorta (8,16,18-20). Salmonella usually resides in the phagosomes of host macrophages and other antigen-presenting cells, such as dendritic cells, which participate in the formation of atherosclerotic plaques. The immunocompromised condition contributes to its reproduction and invasiveness from atherosclerotic plaques (21-23) (Figure 1).
Klebsiella pneumoniae (KP)
Klebsiella infection can occur in almost all organs but is most commonly observed in the liver and lungs. Approximately 60–93% of patients with KP have comorbid diabetes mellitus (15,24,25). KP can invade the aortic wall and induce MAAs from the location of damaged vascular endothelial walls (16). In patients suffering from aortic pseudoaneurysm and pyogenic liver abscess and who have a history of diabetes mellitus, KP should be considered as the causative organism (Figure 2).
About 75% of MAAs caused by Mycobacterium tuberculosis present as a contiguous lesion on the surrounding tissue, such as lymph node enlargement or paraspinal abscess (26,27). Constant surveillance imaging can indicate pathogenesis (Figure 3).
Pseudoaneurysm caused by Staphylococcus aureus has been reported in intravenous drug users, as well as iatrogenic or traumatic arterial wall injury patients (28,29) (Figure 4). In these patients, MAAs develop from direct infectious inoculation at the time of vascular trauma.
Brucella melitensis is a zoonotic intracellular Gram-negative coccobacillus responsible for multisystem infections, including the aorta—especially in immunocompromised patients. The common transmission route is through direct contact with infected cattle via milk or other body fluids (30).
Due to the risk of rapid expansion and consequent rupture, timely diagnosis and treatment of MAAs are paramount. Unfortunately, some patients could be clinically silent until an aneurysm rupture. The most frequent presenting symptoms of MAAs are fever and pain (16,19). MAAs localized to the thoracic aorta usually manifest as chest pain, whereas infected abdominal aortic aneurysms usually manifest as abdominal pain with or without a pulsatile mass. The laboratory abnormalities are often nonspecific and may include elevated erythrocyte sedimentation rate (ECR), C-reactive protein (CRP), and leukocytosis. Blood cultures fail to detect bacteria in approximately 25% of cases, which might contribute to broad-spectrum antibiotic therapy administration.
Life-threatening hemorrhage—such as hemoptysis, gastrointestinal hemorrhage, and sequentially shock—could result from fistulae. The poor prognosis of these patients emphasizes the importance of early diagnosis. Aortoenteric fistula is caused by aneurysm infection spreading to the enteron, which usually begins at the duodenum, adjacent to the aorta (Figure 5). Thoracic MAAs with surrounding lung parenchyma infection or compaction cause aortobronchial fistula (Figure 6), a less recognized complication of abdominal MAAs. A dramatic increase in mortality occurs in patients without clear preoperative diagnosis compared to those with clear preoperative diagnosis (100% in patients without a clear diagnosis vs. 15% in patients with clear diagnosis).
Iliopsoas abscess (IPA) is a common complication in abdominal MAAs with or without endograft infection, presenting as a direct invasive infection with purulent materials occurring within the iliopsoas muscle. The causative organisms include Mycobacterium, Salmonella, KP, other Gram-negative bacilli, and mixed bacteria. The mortality rate is as high as 100% if IPA is left untreated (31-33). IPA is reported as a major risk factor for patients with MAAs; thus, clinicians should be cautious about this potential complication. In tuberculous spondylitis patients, MAAs can involve secondary spread from spine lesions (Figure 7). The rate of mortality is high among MAA patients with combined pyogenic spondylitis (34,35).
Open surgical repair has been regarded as an effective treatment for MAA but is associated with a mortality rate of over 20% (17,29). The endovascular repair of MAAs—an expeditious temporization of MAA rupture in hemodynamic instability cases—is well-established. Kan et al. demonstrated that there was no significant difference in overall survival rate between open surgical repair and endovascular repair (20); however, the insertion of an endovascular graft in an infected field remains a major concern. Stent graft implantation is a significant independent predictor of persistent infection (20). Prolonged culture-specific antibiotic therapy, combined with open surgery or endovascular techniques, is a key component for successfully treating MAAs.
CT, MRI, and PET/CT are the most commonly used imaging modalities in the detection and assessment of clinically suspected infected aneurysms. Due to the higher quality spatial resolution of contrast-enhanced CT and MRI, these modalities can provide valuable information regarding the morphology of aortic aneurysm, aortic wall enhancement, and the relationship between the aneurysm and adjacent tissue; however, PET/CT is the most sensitive of these modalities in detecting infection, which is depicted by increased uptake of FDG. Like PET/CT, diffusion-weighted imaging (DWI) MRI is also sensitive in detecting infection with restricted diffusion manifestation. DWI and T2-weighted MRI can assist in detecting soft tissue edema and adjacent organ involvement.
Infected aortic aneurysm
An infected aortic aneurysm appears on CT and MRI as a focal, contrast-enhancing, lobulated, saccular lumen, with an indistinct, irregular aortic wall (Figure 8). CT is the most sensitive imaging modality for detecting calcification and gas bubbles. The calcification interruption indicates the location of the disrupted aortic wall. Gas bubbles that appear in and around MAAs have high diagnostic reliability of etiology (Figure 9). Rapidly progressive growth of true or false aneurysms (>5 mm in 2 weeks) is also suggestive of an infectious etiology (Figure 10). The thickened MAA wall usually appears as a high signal intensity on T2-weighted MRI and DWI (Figure 11), with increased uptake of FDG on PET/CT.
Eccentric periaortic inflammatory soft tissue usually manifests as rim or septum enhancement following the administration of contrast material (venous phase) on contrast-enhanced CT and MRI (Figure 8). Periaortic edema appears as a distinctive fat stranding on CT; lymph nodes adjacent to MAAs might also appear swollen and enhanced (Figure 1). The edema of periaortic tissue and lymph nodes have the same MRI and PET/CT findings as the thickened MAAs wall described above (Figure 11).
CT provides a definitive diagnosis of IPA and other features that involve adjacent structures. IPA's typical features on CT include enlarged iliopsoas muscle, single or multiple relatively low-density abscess cavities with rim-like contrast-enhanced walls (Figure 7), and in some cases, gas within lesions. Interestingly, MRI and PET/CT are sensitive modalities in detecting IPA with typical restricted-diffusion manifestation on MRI and increased uptake of FDG on PET/CT (Figure 11).
Primary and secondary pyogenic spondylitis manifests intervertebral disc and/or vertebral body destruction on CT and MRI (Figure 12). The diagnosis of pyogenic spondylitis can also be confirmed on PET/CT with increased metabolic manifestations. MRI and PET/CT enable spondylitis visualization without morphological changes in the early stage (Figure 11).
Contrast medium shunt from the aorta to the inferior vena cava, digestive tract, or bronchus, is a diagnostic sign for aortic fistula (36,37). The shunt usually manifests as early enhancement of the inferior vena cava well before it appears in the renal and hepatic parenchyma, with a density of the adjacent digestive tract or bronchus similar to that of the adjacent aorta. When aortacaval fistula occurs, dilated and retrograded enhanced renal or iliac veins can be seen on enhanced CT and MRI, with direct communication between the aorta and inferior vena cava (Figure 13). Aortocutaneous fistulas are extremely rare and are usually seen in cases involving prior vascular prosthetic graft insertion (Figure 14) (38). Abnormal accumulation of FDG has diagnostic significance for aortoenteric and aortobronchial fistulae.
Recognition of infection-related complications should be considered during the analysis of follow-up images. Radiological signs are important diagnostic criteria in the detection of aortic graft infection (39), including ectopic gas, peri-graft inflammation, and fluid, thickening of adjacent bowel, pseudoaneurysm formation, and increased 18F-FDG uptake at the graft anastomosis (Figure 15) (13,39). The peri-graft fluid within the first 3 months after surgery may contribute to postoperative changes (39). Considering the white blood cell count and clinical symptoms, persistent existence, or gradual increase in the peri-graft fluid should be suspected as an infection-related complication. Extraanatomic bypass procedure avoids graft placement within an infected field, lowering the risk of graft reinfection compared to in situ reconstruction with a prosthetic graft (17). The endovascular repair of MAAs should be regarded as a temporizing treatment mainly performed on hemodynamically unstable patients. Compared to surgery, the challenges of wide debridement and effective drainage of suppuration brings risks of stent infection (Figure 16), endoleak (Figure 17), aortic fistulas, and potential rupture (8) (Figure 18). Spondylitis and IPA secondary to reinfection occur after both open surgery and endovascular repair (Figures 10,19). A prospective study—including 35 patients with suspected aortic graft infection—showed high concordance between 18F-FDG-PET/CT and expert consensus criteria from the Management of Aortic Graft Infection Collaboration (MAGIC) for detecting aortic graft infection (13). Further, 18F-FDG-PET/CT can also be used to monitor the response of MAAs and aortic graft infection to antibiotic treatment.
Diagnosis of life-threatening MAAs is challenging due to the non-specific symptoms and negative blood cultures associated with prior antibiotic use. CT, MRI, and FDG-PET/CT allow early identification of MAAs, which is crucial for improving patient outcomes. Surveillance imaging permits assessment and promotes treatment efficacy. Figure 20 summarizes both clinical and radiological features that can assist in the diagnosis of MAAs. Clinicians—especially cardiologists, vascular surgeons, and radiologists—should be familiar with the clinical features and common manifestations of MAAs to ensure appropriate evaluation and management of the disease.
The authors would like to thank Drs. Fengqiang Wang, Huaiping Yuan and Jin Cheng for their assistance in providing some cases that were used in this study.
Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at http://dx.doi.org/10.21037/qims-20-941). Dr. ZS serves as an unpaid associate editor of Quantitative Imaging in Medicine and Surgery. The other authors have no conflicts of interest to declare.
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