A Hybrid Approach in Treating a Mycotic Aneurism Caused by MRSA: A Case Report

Introduction

An infectious or mycotic aneurysm is an abnormal focal dilation of the arterial wall resulting from infection-induced degeneration, first described by William Osler in the context of infective endocarditis [1]. Mycotic aortic aneurysm (MAA) is a particularly challenging entity due to its rapid progression and high risk of rupture, leading to significant mortality [2,3].

We present the case of a woman with end-stage renal disease (ESRD) on hemodialysis who developed methicillin-resistant Staphylococcus aureus (MRSA) bacteremia and a MAA with a fatal outcome despite multidisciplinary management.

Case Report

A 58-year-old Hispanic woman with insulin-dependent type 2 diabetes mellitus, hypertension, and ESRD on hemodialysis through an arteriovenous (AV) fistula for 3 years presented to the Emergency Department with 1 week of fever, vomiting, and diarrhea, and 3 days of cough and dyspnea. She had missed 2 dialysis sessions due to malaise.

On examination, she was lethargic, tachypneic, febrile, mildly desaturated, and had a blood pressure of 138/70 mmHg. Chest auscultation revealed decreased breath sounds bilaterally, the abdominal examination was unremarkable, and there was grade 2 bilateral pitting edema in the lower limbs. A chest X-ray (Figure 1) revealed a left paratracheal opacity extending from the hilum of the lung to the apex, suggestive of upper-lobe atelectasis; and a right lower-lobe opacity with air bronchograms and pleural effusion. Admission laboratory findings are shown in Table 1.

The patient was admitted to the intensive care unit (ICU), where empiric vancomycin and cefepime were initiated and hemodialysis was resumed. Blood cultures and pleural fluid cultures were positive for MRSA. Antibiotics were escalated to ceftaroline and daptomycin.

Due to MRSA bacteremia in a dialysis patient, a transesophageal echocardiogram (TEE) was performed to evaluate for infective endocarditis. TEE (Figure 2, Video 1) showed preserved left ventricular ejection fraction and no evidence of vegetations or valvular dysfunction. At 50 mm from the esophageal probe insertion, the study revealed a saccular formation in the descending thoracic aorta measuring 4.3×2.3 cm, with a 2-cm neck. Color Doppler imaging confirmed flow into the aneurysmal sac. The surrounding aortic wall appeared thickened and irregular, with decreased echogenicity of the underlying periaortic tissue. The aortic root appeared normal, and several calcified plaques (up to 3 mm) were noted in the thoracic aorta.

Thoracic computed tomography angiography (CTA) (Figures 3, 4) revealed a saccular, lobulated aneurysm in the posterior wall of the descending thoracic aorta distal to the diaphragmatic hiatus, measuring 4.7 cm in length and 2.7 cm in diameter, with a neck of 2.4×2 cm). Periaortic fat stranding and a 77-ml perianeurysmal fluid collection were also observed.

Based on imaging and laboratory findings, a diagnosis of MAA was considered. Despite appropriate antibiotic therapy, the patient’s condition worsened, with persistent bacteremia and vasopressor requirement. A multidisciplinary team opted for surgical intervention.

Under general anesthesia in a hybrid operating room, endovascular aneurysm repair (EVAR) was performed via bilateral femoral access. Four endoprostheses (2 ALPHA ZTA-P-105, 1 ZDEG-P-25-117 PF, and 1 ALPHA ZTA-P-26-105) were deployed from the origin of the left subclavian artery to the celiac trunk. A balloon catheter was used to ensure graft apposition. Completion angiography confirmed aneurysm exclusion and preserved flow in aortic branches. Femoral access sites were closed with percutaneous closure devices.

Subsequently, thoracotomy was performed to drain a left empyema and periaortic collection. Upon opening the aneurysmal sac, 2000 cc of pulsatile bleeding occurred. Hemostasis was attempted using packing and vacuum-assisted closure (VAC). The patient required a massive transfusion and returned to the ICU intubated and on dual vasopressors.

Her clinical course further deteriorated with refractory metabolic acidosis, hyperlactatemia, hyperkalemia, and death 4 days after surgery. Cultures from the aortic wall confirmed MRSA infection.

Discussion

ETIOLOGY AND PATHOPHYSIOLOGY:

MA arise from either hematogenous seeding of a previously damaged arterial wall – often at atherosclerotic plaques – or direct extension from adjacent infected tissues [2,5]. This leads to inflammation, necrosis, and weakening of the arterial wall, resulting in pseudoaneurysm formation: a contained rupture surrounded by a fibrous capsule or adjacent structures. Pseudoaneurysms carry a high risk of rupture, frequently with fatal outcomes. Less commonly, true aneurysms can form if the wall is weakened without rupture. The descending thoracic and abdominal aorta are the most commonly affected sites [6–9].

The microbiological profile varies by region. In Asia, Salmonella enterica (eg, S. enteritidis, S. choleraesuis) predominates. In Europe and North America, Staphylococcus aureus, Streptococcus species, and Enterococcus are more frequent. Rare pathogens include Candida, Aspergillus, Mycobacterium tuberculosis, and anaerobes, particularly in immunocompromised patients [4,5,10]. Risk factors for MA include ESRD, hemodialysis, diabetes, and intravenous drug use. Persistent bacteremia – especially with S. aureus – should raise concern for vascular involvement [2,5].

CLINICAL MANIFESTATIONS AND DIAGNOSIS:

The presentation of MAA is often nonspecific, which can delay diagnosis. Symptoms typically include fever (in up to 75% of cases), localized thoracic, abdominal, or back pain, and occasionally a pulsatile mass or signs of rupture. Septic shock or thromboembolic events can also occur [9,11].

Laboratory workup usually shows elevated inflammatory markers, but there is no pathognomonic test. Blood cultures are positive in 50–90% of cases, though sensitivity decreases after antibiotic initiation [1,12].

Our patient presented with fever, respiratory and gastrointestinal symptoms, and signs of volume overload after missed hemodialysis sessions. Laboratory findings included leukocytosis, hyperkalemia, and metabolic acidosis. Persistent MRSA bacteremia prompted further imaging to identify cardiac or vascular seeding.

IMAGING STUDIES:

Multimodal imaging is essential for diagnosing MAA. TEE is valuable for evaluating patients with bacteremia, with over 90% sensitivity for valvular and proximal aortic lesions. It is particularly useful in critically ill patients, in whom CTA or MRA may not be feasible. TEE findings suggestive of MAA include saccular pseudoaneurysms with Doppler flow, irregular wall thickening, and periaortic echolucent areas indicating inflammation [13].

CTA is the preferred imaging modality due to its speed, resolution, and ability to detect aneurysm morphology, periaortic inflammation, pre-existing wall calcification, and complications such as rupture or fistula [6,14]. A typical finding is a saccular lobulated dilation with adjacent fat stranding or soft-tissue attenuation.

Magnetic resonance angiography (MRA) offers high-resolution imaging without radiation and is useful when iodinated contrast is contraindicated [15]. Positron emission tomography/computed tomography (PET/CT) with 18F-FDG is increasingly used to identify metabolically active infection and is especially helpful in the context of equivocal CTA findings or post-EVAR follow-up to assess persistence of infection [14].

In our case, chest X-ray showed consolidation and pleural effusion, raising a suspicion of infection. TEE excluded endocarditis and detected the aortic aneurysm. CTA confirmed the diagnosis, providing detailed anatomy that guided intervention. These imaging modalities were critical to timely diagnosis and management.

TREATMENT STRATEGIES:

Management of MAA requires a multidisciplinary approach combining antimicrobial therapy with surgical or endovascular intervention. Empiric antibiotics should be started promptly and tailored to culture results. In our case, MRSA was isolated. Treatment options for this organism include vancomycin, daptomycin, linezolid, and rifampin (particularly in biofilm-associated infections). Duration typically ranges from 6 weeks to 6 months, but lifelong suppressive therapy may be needed in select cases (eg, high-risk or non-surgical) [2,3,5].

Open surgical repair (OSR) involves debridement and revascularization, but is associated with high morbidity, especially in frail or comorbid patients. EVAR offers a less invasive option with lower perioperative risk, but can lead to residual infection due to lack of debridement [3]. In a systematic review of 1358 patients, EVAR showed lower intraoperative (1.0% vs 1.8%) and early mortality (6.5% vs 15.9%) than OSR, but higher rates of late sepsis (5.7% vs 0.9%) and reintervention (17.6% vs 7.3%) [10].

Treatment choice must be individualized, considering aneurysm location, patient clinical status, rupture risk, and surgical candidacy. In our case, due to hemodynamic instability, persistent infection, comorbidities, and aneurysm anatomy, a hybrid strategy was selected – EVAR followed by thoracotomy for drainage of the periaortic collection and empyema. Despite initial procedural success, the patient developed hemorrhagic shock and multiorgan failure, dying 4 days postoperatively.

The prognosis of MAA depends on rupture, pathogen virulence, comorbidities, and timing of intervention. Long-term clinical and imaging (CTA or PET/CT) post-EVAR follow-up is essential to detect graft complications or persistent infection [3,12,14].

Conclusions

MAA are rare but highly lethal if not promptly diagnosed and treated. Clinicians should suspect MAA in patients with persistent bacteremia and risk factors such as ESRD or immunosuppression.

Multimodal imaging – particularly CTA, TEE, and PET/CT – is essential for diagnosis and monitoring. Management requires prolonged antibiotics, individualized surgical or endovascular intervention, and close follow-up. While OSR remains the standard method, EVAR is increasingly used in high-risk patients with suitable anatomy.

Despite aggressive treatment, prognosis remains poor in complex cases, as illustrated by this case of fatal MRSA-associated thoracic MAA in a hemodialysis patient. Further research is needed to guide treatment strategies and improve outcomes in this challenging condition.