Version July 2025
INTRODUCTION —
An aneurysm is an abnormal focal arterial dilation. Pre-existing aneurysms can become secondarily infected, but aneurysmal degeneration of the arterial wall can also be the result of infection that may be due to bacteremia or septic embolization, as in the case of mycotic aneurysms. The name mycotic aneurysm was coined by Osler to describe aneurysms associated with bacterial endocarditis [1]. These were noted to have the appearance of "fresh fungus vegetations"; however, the majority of mycotic aneurysms are caused by bacteria. Although some authors use the term "mycotic" to describe infected aneurysms regardless of etiology, we will limit the use of this term to those aneurysms that develop when material originating in the heart causes arterial wall infection and, subsequently, dilation [2].
Aneurysms are classified into true aneurysms and false aneurysms (or pseudoaneurysms). True aneurysms involve all three layers of the arterial wall (intima, media, and adventitia). A false, or pseudo-, aneurysm is a collection of blood or hematoma that has leaked out of the artery but is then confined by the surrounding tissue.
Infected aneurysm is a serious clinical condition that is associated with significant morbidity and mortality. Treatment consists of antibiotic therapy combined with aggressive surgical debridement of the infected tissue and vascular reconstruction, as needed. Endovascular therapies may have a role in the treatment of ruptured infected aneurysms and the treatment of patients at prohibitive risk for open surgery.
The pathogenesis, microbiology, clinical manifestations, diagnosis, and treatment of infected arterial aneurysm are reviewed. (See "Clinical features and diagnosis of abdominal aortic graft or endograft infection" and "Open surgical repair of abdominal aortic aneurysm", section on 'Graft infection'.)
The diagnosis and management of noninfected aneurysms are discussed in separate topic reviews. (See "Unruptured intracranial aneurysms" and "Extracranial carotid artery aneurysm" and "Management of thoracic aortic aneurysm in adults" and "Overview of aneurysmal disease of the aortic arch branches or upper extremity arteries in adults" and "Management of asymptomatic abdominal aortic aneurysm" and "Overview of visceral artery aneurysm and pseudoaneurysm" and "Iliac artery aneurysm" and "Femoral artery aneurysm" and "Popliteal artery aneurysm".)
RISK FACTORS —
Risk factors for infected aneurysm include:
●Arterial injury – Arterial injury is an important risk factor for an infected aneurysm. Artery injury resulting in infected femoral artery pseudoaneurysm is commonly due to intravenous drug use, but predisposing factors (such as invasive monitoring, percutaneous access for cardiac catheterization, use of extracorporeal membrane oxygenation, or other interventions) can also lead to infected aneurysm [3-6]. Arterial injury may result from other mechanisms, such as gastrointestinal perforation [7,8] or peripheral nerve block [9]. (See 'Direct bacterial inoculation' below.)
●Antecedent infection – In a retrospective review, nearly half of 43 patients with an infected aortic aneurysm were found to have an antecedent infection that included pneumonia, cholecystitis, urinary tract infection, endocarditis, diverticulitis, soft tissue infection, and osteomyelitis. In the pre-antibiotic era, the majority of infected aneurysms were due to endocarditis. More contemporary series identify endocarditis as the likely etiology in 17 to 29 percent of cases [10,11]. The rapid development of an infected aortic aneurysm associated with periodontal infection and oral surgery has also been reported [12-15]. (See 'Septic emboli (mycotic aneurysm)' below.)
●Impaired immunity – Immunosuppressive states predispose the patient to infection, which may present with atypical clinical features. Immunosuppressive disorders were found in 70 percent of patients with infected aneurysms in a review of 43 patients [16]. Diabetes, alcoholism, chronic glucocorticoid therapy, chemotherapy, and malignancy have been identified as possible risk factors for infected aneurysms [16-20]. Immune mechanisms may play a role in the development of infected aneurysm in a variety of other circumstances, such as in patients with cancer [21], cirrhosis [22], those undergoing hemodialysis [23], following gastrointestinal endoscopy [24], posttransplant, those with human immunodeficiency virus (HIV) infection [25-27], and following trauma or near drowning [28]. (See 'Bacteremic seeding' below.)
●Atherosclerosis – Patients with atherosclerosis, particularly older adults, are at risk for bacteremic seeding of atheromatous plaques. (See 'Bacteremic seeding' below.)
●Pre-existing aneurysm – Pre-existing aneurysms are at risk for secondary infection due to bacteremia or spread from a contiguous infection. The prevalence of infection in a pre-existing aneurysm is overall low(See 'Bacteremic seeding' below and 'Contiguous infection' below.)
ETIOLOGY
Direct bacterial inoculation — Direct inoculation of bacteria into the arterial wall can occur at the time of vascular injury. An arterial injury may be self-inflicted, iatrogenic, accidental, or due to assault (gunshot, stab). Infected pseudoaneurysms following arterial injury have become one of the most common forms of infected aneurysms. The femoral artery is the most commonly involved arterial site.
Infected pseudoaneurysms can result from injection drug use wherein users inadvertently inoculate themselves via contaminated needles into the arterial wall (they are aiming for the adjacent veins) or a surrounding hematoma. Infected pseudoaneurysms of the common femoral artery are the most common, but infections involving the external iliac, carotid, brachial, axillary, and subclavian arteries have also been reported.
Bacteremic seeding — Bacteremic seeding of a pre-existing intimal injury, atherosclerotic plaque, or aneurysm can lead to arterial wall infection.
The intima is normally highly resistant to infection, but when diseased, it allows bacteria to pass through it into deeper layers of the arterial wall. Once a local infection is established, suppuration, localized perforation, and pseudoaneurysm can result. The aorta is the most common location affected primarily since it is the most frequent site of atherosclerosis, but peripheral arteries can also be affected. Infected aneurysms can occur in the absence of significant atherosclerosis [29].
In a similar manner, pre-existing aneurysms may become secondarily infected, which may predispose to rupture. In a study of 80 patients undergoing open aortic repair, a greater number of positive cultures were found in patients with ruptured aneurysms compared with asymptomatic and symptomatic aneurysms (38 versus 9 and 13 percent, respectively) [30]. Rupture of abdominal aortic aneurysms is discussed elsewhere. (See "Management of symptomatic (non-ruptured) and ruptured abdominal aortic aneurysm", section on 'Introduction'.)
Contiguous infection — A focus of infection can extend to the arterial wall. Extension of a postoperative infection can lead to an infected aneurysm and has been described in the setting of appendectomy [31], cholecystectomy [32], colorectal surgery [33,34], as a result of pancreatic pseudocyst [35], and following knee or hip replacement surgery [36-38]. Extension of infection not related to surgery can also occur, as seen in vertebral osteomyelitis [39-41].
Septic emboli (mycotic aneurysm) — In endocarditis, septic emboli from the heart valve can occlude the vasa vasorum of the vessel or the vessel lumen, leading to vascular wall infection and mycotic aneurysm formation. Embolism is estimated to occur in between 25 and 50 percent of patients, but only about 1 to 5 percent develop symptomatic mycotic aneurysm [42]. Because of their embolic nature, mycotic aneurysms tend to be multiple, but they can also be solitary [43]. Spontaneous resolution with antibiotic therapy for endocarditis has been reported [44-46]. As such, the true prevalence of mycotic aneurysm is unknown.
Mycotic aneurysms can develop anywhere but are most commonly seen in the intracranial arteries, followed by visceral arteries and upper or lower extremity arteries, typically occurring at arterial bifurcations [42]. Rarely, mycotic aneurysms of coronary arteries have also been described [47].
In a report including 4518 patients with endocarditis, 85 (1.9 percent) had a mycotic aneurysm, 46 patients had an intracranial site, and 39 patients had an extracranial site [48]. Aneurysm rupture occurred in 39 patients; in addition, rupture also occurred in another 9 patients who initially had an unruptured aneurysm. In a review including 922 cases of definite infective endocarditis, symptomatic peripheral mycotic aneurysm was observed in 2 percent of cases [43]. Six peripheral artery aneurysms were identified: two in the popliteal artery and one each in the ulnar artery, brachial artery, hepatic artery, and coronary artery [43].
MICROBIOLOGY —
Blood cultures are positive in 50 to 85 percent of cases [49,50]. Organisms have been isolated from aneurysmal tissue in up to 76 percent of patients [30,49]. In one case series, multiple organisms were isolated in 8 percent, and no pathogen was identified in 25 percent of cases [10]. Identification of the causative organism using molecular methods (bacterial 16S ribosomal ribonucleic acid [rRNA]) has been described [51].
●Bacteria – The organisms with the greatest affinity for the arterial wall are Staphylococcus spp and Salmonella spp [52-54].
•Gram-positive bacteria
-Staphylococcus aureus – S. aureus is the most common pathogen reported in 28 to 71 percent of cases [10,49]. In several reports of infected aneurysms, methicillin-resistant S. aureus (MRSA) predominated [55-57]. In one series of pre-existing aneurysms, Staphylococcus epidermidis was the most prevalent organism [30]. Infected aneurysms due to vancomycin-intermediate S. aureus (VISA) have also been described [58].
-Other Gram-positive organisms - Streptococcus pneumoniae was a frequent etiology of infected aneurysms in the pre-antibiotic era but became rare with the advent of penicillin; however, S. pneumoniae may be re-emerging as a cause of infected aneurysms [59,60].
Other gram-positive organisms associated with mycotic aneurysm include non-pneumococcal Streptococcus [61], Clostridium [62], Corynebacterium [63], Rothia dentocariosa [64], Listeria [27,65-67], Lactococcus cremoris [68], Nocardia [69], and Staphylococcus lugdunensis [70]).
•Gram-negative bacteria
-Salmonella spp - Salmonella is reported in 15 to 24 percent of cases [10,52,71]. The diseased aorta appears to be vulnerable to Salmonella, and this pathogen is frequently isolated in infected aneurysms due to bacteremic seeding of atherosclerotic plaque [72].
-Other Gram-negative organisms – Besides Salmonella spp, other Gram-negative organisms are also associated with bacteremic seeding [33,73-75]. In one study, Gram-negative organisms were observed in 35 percent of cases and were associated with a higher incidence of aneurysm rupture (84 versus 10 percent) and mortality (84 versus 50 percent) compared with gram-positive organisms [75].
Other gram-negative organisms associated with mycotic aneurysms include Pseudomonas [73], Klebsiella [76], E. coli [74], Yersinia [77,78], Brucella [79,80], Haemophilus influenzae [81], Acinetobacter [82], Burkholderia pseudomallei [melioidosis] [83-88]) and Campylobacter [89,90]).
•Other bacteria
-Syphilis - Syphilis (T. pallidum) once caused up to 50 percent of infected aneurysms (image 1) [91]. The incidence of aneurysms secondary to syphilis seems to parallel the increase in syphilis incidence (figure 1) .
-Coxiella burnetti - Coxiella burnetii can also be the cause of an infected aneurysm [92-96]. A C. burnetii–infected aneurysm can occur without other manifestations of chronic Q fever [92]. (See "Chronic Q fever, including endocarditis", section on 'Vascular infection'.)
-Anaerobes – Anaerobes associated with mycotic aneurysms include Bacteroides [97], Eikenella [98], and Clostridium septicum [99,100]).
●Mycobacteria – Tuberculosis is a rare cause of infected aneurysms and is most often due to erosion of periaortic lymph nodes into the aortic wall [101-105]. One review of cases of infected aneurysms caused by Mycobacterium tuberculosis reported 41 cases between 1945 and 1999 [106].
●Fungi – Fungal arterial infections are rare but may occur in patients with immune suppression, diabetes mellitus, or following treatment of a disseminated fungal disease. In addition, the risk of perforation of the digestive tract (eg, aortoenteric fistula) appears to be increased in those with fungal infection [107]). Pathogens include Candida [108], Cryptococcus [109], Aspergillus [110], Pseudallescheria boydii [28], and Scedosporium apiospermum [111].
CLINICAL MANIFESTATIONS
Classic presentation — The classic presentation of an infected aneurysm is a painful, pulsatile, and enlarging mass together with systemic features of infection, such as fever and chills or sweats. This presentation is more likely to be found for infected aneurysms that are superficial in location (eg, common femoral artery). In one series of 52 infected aneurysms among people who inject drugs, a tender indurated mass was palpated in 92 percent of cases; these were pulsatile in 52 percent of cases [49]. A bruit was heard in 50 percent of cases, fever was observed in 48 percent, and there was bleeding at the injection site in 15 percent of cases. In some cases, infected aneurysm may be masked by overlying inflammation. Thus, the presence of a soft tissue infection in association with a major blood vessel should raise suspicion for an infected aneurysm. Infected aneurysms can be easily misdiagnosed as cellulitis, abscess, or thrombophlebitis.
For deeper sites, the aneurysm may not be palpable and may be apparent only on imaging studies. Infected aneurysms involving the aorta or iliac arteries may be accompanied by abdominal or back pain. On the other hand, patients with infected aortic aneurysms may manifest only with a fever of unknown origin, some of whom will remain undiagnosed until rupture. (See "Clinical features and diagnosis of abdominal aortic aneurysm".)
Infected aortic aneurysm must be distinguished from inflammatory aortic aneurysm, which can have similar clinical features, such as fever, weight loss, nonspecific abdominal pain, and elevated erythrocyte sedimentation rate [112]. Inflammatory aneurysms are characterized by an inflammatory infiltrate in the aortic adventitia associated with adventitial fibrosis. Diagnostic signs on abdominal computed tomography help to differentiate these. (See 'Differential diagnosis' below.)
Infected aneurysm of the intracerebral vessels may present as stroke or subarachnoid hemorrhage, particularly in the setting of endocarditis.
Other presentations — Undiagnosed, infected aneurysms can lead to progressive infection, sepsis, hemorrhage, or thrombosis, leading to ischemic symptoms, the manifestations of which depend on location. Some of these include:
●Gastrointestinal bleeding – Although gastrointestinal bleeding is more commonly caused by an infected aortic graft, a primary aorto-duodenal fistula may be due to an infected aortic aneurysm by erosion of the vessel into the third portion of the duodenum [55,113,114]. Rupture of an infected aneurysm into other gastrointestinal structures, such as the appendix [115] or esophagus [116], can also occur. (See "Aortoenteric fistula: Recognition and management".)
●Heart failure – As with noninfected aneurysms, rupture of an infected aneurysm into a vein results in an arteriovenous fistula [117]. If a sufficiently large artery and vein are involved (eg, aortocaval fistula), high-output heart failure may result. (See "Causes and pathophysiology of high-output heart failure".)
●Acutely expanding hematoma – For superficial infected aneurysms, the hematoma will be easily seen. Retroperitoneal hematoma from infected aortic or iliac aneurysm rupture may lead to hypovolemic shock. (See "Management of symptomatic (non-ruptured) and ruptured abdominal aortic aneurysm", section on 'Introduction'.)
●Acute or chronic mesenteric ischemia – Infected aneurysms of the superior mesenteric artery may acutely thrombose or embolize into the terminal mesenteric branches, leading to symptoms of intestinal ischemia. (See "Overview of intestinal ischemia in adults" and "Acute mesenteric arterial occlusion" and "Chronic mesenteric ischemia".)
●Peripheral ischemia – Infected aneurysm of the peripheral arteries may acutely thrombose or embolize distally. (See "Clinical features and diagnosis of acute arterial occlusion of the lower extremities" and "Embolism to the lower extremities".)
●Dysphagia and hoarseness – Enlarging or ruptured carotid or subclavian artery aneurysm may compress the structures of the neck, leading to stenosis or deviation of the trachea [118] or impingement of the laryngeal nerves. (See "Extracranial carotid artery aneurysm" and "Overview of aneurysmal disease of the aortic arch branches or upper extremity arteries in adults".)
●Hemoptysis – A mass due to a pulmonary artery aneurysm may be seen during bronchoscopy [119]. Rupture of pulmonary artery aneurysm may lead to massive hemoptysis [120]. (See "Evaluation and management of life-threatening hemoptysis".)
●Osteomyelitis/Discitis – Infection of the aorta may extend to the thoracic or lumbar spine [121]. (See "Vertebral osteomyelitis in adults: Clinical manifestations and diagnosis", section on 'Clinical features'.)
●Psoas abscess – Extension of infection from an aortic or iliac aneurysm to the psoas muscle may cause flank pain, inguinal pain, and limping [76]. (See 'Clinical manifestations' above and "Psoas abscess".)
●Neuropathy – Infected aneurysms can impinge on the nerves supplying the extremities [122]. (See "Overview of upper extremity peripheral nerve syndromes" and "Overview of lower extremity peripheral nerve syndromes".)
DIAGNOSIS
Clinical approach — The suspicion of an infected aneurysm based on history and physical findings should be followed up on by laboratory and imaging studies. The diagnosis of an infected aneurysm is based on suggestive imaging findings, and infection is confirmed by culturing an organism from the blood. Computed tomography (CT) angiography definitively diagnoses the aneurysm, specific features suggest infection, and CT also simultaneously evaluates the status of the circulation [123]. (See 'Vascular imaging' below.)
On laboratory examination, an increased white blood cell count is found in 64 to 71 percent of patients [52,124,125]. Inflammatory markers, including C-reactive protein and erythrocyte sedimentation rate, are generally elevated.
Cultures — Blood cultures (aerobic, anaerobic, fungal) should be obtained in any patient with a suspected infected aneurysm. Because blood cultures may be negative in 25 to 50 percent of patients, negative blood cultures alone are not sufficient to rule out infected aneurysms.
An infected aneurysm may be first suspected in the operating room based on purulence in association with a pre-existing aneurysm [126]. Tissue samples of the aneurysm wall should be sent for culture (aerobic, anaerobic, fungal) and Gram stain. In the operating room, a negative Gram stain is not sufficient to exclude a diagnosis of an infected aneurysm [124]. Conversely, positive tissue cultures in the absence of clinical findings do not confirm an infected aneurysm in the absence of appropriate clinical findings. In one study, 69 percent of patients had positive preoperative blood cultures, and 92 percent had positive aneurysm wall cultures, but the operative Gram stain was positive in only 50 percent of patients with ruptured infected aneurysms and 11 percent of unruptured but infected aneurysms [124].
Molecular methods for the identification of the causative organism from operative aneurysm tissue have been described [127,128]. Such methods warrant pursuit if initial cultures are negative.
Vascular imaging — Imaging studies for the detection of intracranial mycotic aneurysms include CT angiography, magnetic resonance (MR) angiography, and digital subtraction angiography (DSA) [42]. Of these, CT angiography is the most useful for diagnosing infected aneurysms [129]. MR angiography is an alternative diagnostic study when intravenous contrast is contraindicated [130]. When vascular imaging is consistent with an infected aneurysm, we prefer to perform additional imaging of the remainder of the vasculature to identify multifocal disease. In the setting of high clinical suspicion for intracranial mycotic aneurysm with negative imaging results, conventional angiography is reasonable [42].
Findings on CT angiography suggestive of an infected aneurysm include the following [129,131-135] :
●Saccular, eccentric aneurysm or multilobulated aneurysm
●Soft tissue inflammation or mass around a vessel
●Aneurysm with intramural air or air collection around the vessel
●Perivascular fluid collection
●Involvement of the visceral segment of the aorta
In the mesenteric circulation, indistinct fat planes may be indicative of vascular inflammation [136,137]. If a diagnosis of an infected aneurysm remains in doubt, a repeat scan can be performed after a short interval to evaluate for rapid enlargement or changes to the aneurysm that suggest infection [132-134].
Ultrasound is useful for diagnosing the presence of an aneurysm; however, findings on ultrasound are not reliable for delineating the presence or extent of infection. (See "Clinical features and diagnosis of abdominal aortic aneurysm", section on 'Diagnosis'.)
DSA is not reliable for identifying infected aneurysms; it is also invasive and associated with potential hazards. Nuclear medicine studies, including fluorodeoxyglucose-positron emission tomography (FDG-PET) and gallium scanning, are alternative modalities for evaluating infected aneurysms [138-144]. Case series have described the use of FDG-PET/CT in the diagnosis of infected aneurysms [93,138].
Imaging studies for the detection of extracranial mycotic aneurysms include CT or multislice CT angiography with 3D reconstruction. Transesophageal echocardiography (TEE) is useful for identifying mycotic aneurysms of the sinus of Valsalva and thoracic aorta [42].
DIFFERENTIAL DIAGNOSIS —
Infected aneurysms need to be differentiated from inflammatory vascular changes (eg, Takayasu arteritis, giant cell arteritis, other forms of aortitis, or another large vessel vasculitis, idiopathic [eg, inflammatory abdominal aortic aneurysm (AAA)]). Patients with inflammatory aneurysms often have findings suggestive of perivascular fibrosis with adhesions to adjacent structures. Inflammatory aneurysms are not associated with periaortic air or fluid and are not infected.
As an example, an inflammatory AAA is defined as an aneurysm with a ≥1 cm thickness inflammatory rind surrounding the aorta on abdominal computed tomography. The periaortic soft tissue density is sometimes enhanced with intravenous contrast, and the ureters may be deviated medially [112]. Periaortic fibrosis may result in adhesions between the aorta and the ureters or duodenum, leading to indistinct retroperitoneal tissue planes on imaging studies. (See "Clinical features and diagnosis of abdominal aortic aneurysm", section on 'Infected versus inflammatory AAA'.)
Other differential diagnostic considerations include:
●Lemierre syndrome (septic thrombophlebitis of the internal jugular vein) can mimic an infected aneurysm, as it presents with bacteremia, embolism, and neck swelling. (See "Lemierre syndrome: Septic thrombophlebitis of the internal jugular vein".)
●Behçet disease (a disease characterized by oral aphthae, venous thrombosis, and other systemic manifestations) may present with arteritis, mimicking myotic aneurysm [139]. (See "Clinical manifestations and diagnosis of Behçet syndrome".)
MANAGEMENT —
There are no randomized trials to guide the management of infected aneurysms. Management strategies are primarily based on clinical experience guided by case series. The standard treatment for most infected aneurysms is antibiotic therapy combined with surgical debridement with or without revascularization [124]. Revascularization procedures are performed as needed, depending upon the affected vascular bed and the status of distal perfusion. For patients who refuse surgery or who have significant medical comorbidities that preclude surgical intervention, antibiotic therapy alone is an option. Endovascular techniques are emerging as a treatment alternative for infected aneurysms, most commonly for infected aortic aneurysms [123,140-151]. (See 'Role of endovascular techniques' below.)
Antibiotic therapy — The initial choice of antibiotic therapy should be guided by the organism most likely infecting it based on clinical circumstances. Prior to the availability of culture results, we favor treatment with a combination of vancomycin and an agent with activity against gram-negative organisms, especially Salmonella and enteric gram-negatives; reasonable choices include ceftriaxone, a fluoroquinolone, and piperacillin-tazobactam. Antibiotics should be tailored to culture and susceptibility results when they become available.
The optimal duration of antibiotic therapy is uncertain and depends on factors, including the immune competence of the patient, location of the infection, specific bacteria, autogenous versus prosthetic grafts, in situ versus extra-anatomic reconstruction, and response to treatment (fever, white count, hemodynamic stability). In general, at least six weeks of parenteral and/or oral antimicrobial therapy is administered for the treatment of infected aneurysms. If surgical drainage is performed, this time period commences from the day of surgery. In some circumstances, particularly for cases in which autologous vein grafting is used, a shorter duration may be sufficient. A longer duration of treatment may be warranted in the setting of antibiotic-resistant organisms, persistently positive cultures, and/or inflammatory markers that are slow to normalize [152]. Suppressive oral antibiotics following completion of intravenous therapy may be warranted for patients reconstructed with prosthetic graft material in situ during active infection [10,153,154].
Surgery — Management of infected aneurysms follows the general principles of managing vascular graft infection. The main surgical aim is the removal of all necrotic and infected tissue and the management of any ensuing ischemia. The decision to pursue vascular reconstruction depends primarily upon the patient's underlying vascular status and the anatomic site of the aneurysm (which determines the likelihood of ischemia distal to the site following aneurysm excision) but also on the availability of autologous graft material [153,155-161]. In many cases, the approach may need to be changed during the course of surgical exploration.
Aneurysm excision and ligation without arterial reconstruction — Following proximal and distal control of the involved artery, the infected aneurysm and surrounding infected tissue are excised. The major inflow and outflow vessels to the aneurysm should be dissected back to normal tissue. These vessels are oversewn with permanent sutures and ligated 1 to 2 cm more proximally to prevent blowout of the arterial stump. Smaller branches can be suture ligated. Antegrade instillation of heparin into the ligated artery may help preserve arterial collaterals, but ongoing anticoagulation therapy is generally not needed.
Excision with immediate reconstruction — Some form of immediate arterial reconstruction will be required in patients who are likely to develop acute ischemia with arterial ligation. The disadvantage of immediate reconstruction is the potential for recurrent infection or hemorrhage due to the breakdown of the anastomoses. The decision to perform in situ repair or extra-anatomic bypass depends upon a variety of factors, including the anatomic site and presence and severity of peripheral artery disease, but the nature and virulence of the infection also play a role. Many successful in situ reconstructions using autogenous vein and antibiotic-impregnated grafts have been performed for primary arterial infections, including those due to Salmonella [153,162] and Staphylococcus epidermidis [163]. (See 'Thoracic aorta' below and 'Abdominal aorta and iliac arteries' below.)
In some cases, it may be preferable to perform an extra-anatomic bypass prior to the excision of the aneurysm to minimize the duration of ischemia. In situ, reconstruction may be necessary for some anatomic sites (eg, thoracic aorta, suprarenal abdominal aorta). On the other hand, a limited infection that is effectively cleared following debridement may be a candidate for in-line autogenous vein reconstruction, but this practice is debated. The selection of patients, timing, and methods of reconstruction, particularly when the infected aneurysm involves the aorta or the carotid or femoral artery, remain controversial. (See 'Specific anatomic sites' below.)
When an autogenous superficial vein (eg, great saphenous vein, small saphenous vein, or arm vein) is not available or is inadequate (diameter, length, quality), options include femoral-popliteal deep vein [164,165], cryopreserved homograft [166-170], and prosthetic grafts with or without antibiotic impregnation [157,171]. The vascular anastomotic sites and conduit should be covered by healthy tissue, which may require coverage using an omental pedicle when the aneurysm is located in the abdomen, and when it is located in the extremities, rotation of a local muscle flap (eg, sartorius flap, rectus, or gracilis) [172]. The use of prosthetic grafts is associated with higher rates of reinfection.
Excision with interval reconstruction — When possible, an alternative strategy involves aneurysm excision and debridement with an interval of treatment with antibiotics prior to vascular reconstruction. This option should be considered for patients who are expected to develop only mild to moderate limb ischemia. Unfortunately, it is sometimes difficult to predict intraoperatively whether ischemia will become progressive.
Role of endovascular techniques — Endovascular therapy may be most suitable for the management of infected aneurysms in high-risk patients for whom mortality rates for open surgery would be prohibitive. Endovascular management may also be beneficial for patients with aneurysm rupture as a temporizing measure until definitive debridement and reconstruction can be performed under more "elective" circumstances [173-178]. Lastly, endovascular embolization techniques may be appropriate in managing some infected pseudoaneurysms [179,180]. (See "Endovascular repair of the thoracic aorta" and "Endovascular repair of abdominal aortic aneurysm" and "Open surgical repair of abdominal aortic aneurysm".)
Thoracic endovascular graft repair of infected aneurysm has been reported in case reports and small case series [141-143,181-186]. The largest of these series involved thoracic endovascular infected aneurysm repair in 20 patients with etiologies that included one fusiform aneurysm and 18 pseudoaneurysms [182]. Three patients died perioperatively. Three additional deaths were attributed to recurrent infection that appeared to be related to infection of the endograft. Overall mortality was 65 percent, with a mean survival of 39 ± 9 months, with many deaths related to underlying comorbidities. For patients who have significant comorbidities, thoracic endovascular repair may be an appropriate palliative option, given the even higher mortality associated with open surgery in a subset of patients.
A systematic review evaluated the endovascular management of 91 infected aortic aneurysms (thoracic and abdominal aorta), finding a 90 percent 30-day survival rate and an 82 percent two-year survival [142]. Logistic regression identified aneurysm rupture and fever as independently associated with persistent infection and mortality. Even when long-term antibiotic therapy has been provided, persistent or recurrent infections occur. In a multicenter study that included 123 patients with infected aneurysms and treated using endovascular stent-grafts, infection-related death occurred in 23 patients (19 percent), 9 after the discontinuation of antibiotics [140]. Reoperation is associated with high rates of morbidity and mortality [142,147,187,188]. Given that debridement of the infected tissues is not accomplished, the reinfection and late failure rates are not surprising. In a later nationwide study from Sweden, 132 patients were identified as having infected abdominal aortic aneurysms based upon a combination of clinical, laboratory, and radiologic features [189]. The preferred operative technique shifted from open surgery to endovascular repair after 2001, with the proportion of endovascular repairs increasing from 0 to 60 percent between 1994 and 2014. Overall, open repair was performed in 62 patients (47 percent), and endovascular repair was performed in 70 patients (53 percent); no intraoperative deaths occurred. Survival at 3 months was significantly higher for endovascular compared with open repair (96 versus 74 percent) but not significantly different at later follow-up (1 year: 84 versus 73 percent; 5 years: 58 versus 60 percent). There were also no significant differences in infection-related complications (24 versus 18 percent) or reoperation (24 versus 21 percent). It is possible that improvements in intensive care and antimicrobial therapy may explain the improved outcome for more recent cases treating infected aneurysms with endovascular aortic repair, regardless of the type of surgery.
Specific anatomic sites
Intracranial — Cerebral mycotic aneurysms tend to occur in the more distal segments of the middle cerebral artery involving the secondary and tertiary branches near the brain surface. This characteristic pattern helps to distinguish them clinically from berry aneurysms, which tend to occur near the base of the brain and the circle of Willis [190]. In one review including 820 patients, 63 percent of cerebral mycotic aneurysms involved the middle cerebral artery [191]. (See "Unruptured intracranial aneurysms".)
Intracranial mycotic aneurysms may be more likely to rupture than extracranial aneurysms. In addition, one study reported a rupture rate of 16 percent in aneurysms that were unruptured at the time of diagnosis; based on these findings, consideration for endovascular management may be warranted for unruptured intracranial mycotic aneurysms [48].
A review of intracranial infected aneurysms complicating endocarditis found that the most important factor when considering the treatment of cerebral aneurysms is whether the aneurysm has ruptured [192]. Treatment-related mortality was higher in patients with ruptured aneurysms than in patients with unruptured aneurysms (24 versus 9 percent, respectively). Among patients with ruptured aneurysms, mortality was higher in those treated with antibiotics alone compared with those treated with both antibiotics and surgery (49 versus 12 percent). Such studies have resulted in recommendations that unruptured aneurysms may be managed with antibiotics alone, but whenever possible, ruptured aneurysms should be managed with a combination of antibiotics and surgery [193]. Several studies report obliterating infected cerebral aneurysms using endovascular techniques [194-196]. Increasingly, endovascular management is being used for infected intracranial aneurysms [197].
Thoracic aorta — Infected aneurysm of the thoracic aorta is rare [198]. Most reported series have fewer than 50 patients [199-204]. In one of the larger case series involving 32 primary infected aneurysms, the morphology was primarily pseudoaneurysm [201], equally distributed between the aortic arch and descending aorta.
Thoracic endovascular aortic repair is becoming the preferred treatment (provided there is no aero-digestive communication) for patients with infected thoracic aortic pseudoaneurysm, given the high morbidity and mortality associated with open surgical repair in these patients, who tend to be older and have significant cardiovascular risk factors. (See "Endovascular repair of the thoracic aorta".)
Debridement and in situ, reconstruction of the thoracic aorta remains the preferred approach for thoracic aortic graft infection. Following debridement, surgical reconstruction techniques are similar to those used to repair noninfected aneurysms. (See "Overview of open surgical repair of the thoracic aorta".)
In the above-mentioned series, clinical symptoms consisted of fever, chest pain, hemoptysis, respiratory failure, hoarseness, loss of consciousness, and stroke [201]. The most common microorganisms were nontyphoid Salmonella (57 percent) and S. aureus (14 percent). Among patients who underwent surgery (debridement and in situ reconstruction), morbidity and one-year mortality rates were the highest for patients with infected arch aneurysms (70 and 50 percent, respectively) compared with infected proximal descending (33 and 16 percent, respectively) or distal descending aneurysms (56 and 33 percent, respectively). Mortality among patients who were managed with antibiotics alone without surgery was 85 percent, with two-thirds of these due to in-hospital rupture. In another series that included an aortic aneurysm, no patient who had a ruptured infected aneurysm survived [205].
Abdominal aorta and iliac arteries — Mortality related to infected aortic aneurysm is lower when medical and surgical therapies are combined (38 versus 96 percent) compared with medical treatment alone.
Following debridement of an infected infrarenal aortic aneurysm, placement of prosthetic graft material into the infected retroperitoneum is associated with a 25 percent reoperation rate that increases to 63 percent when the infecting organism is a gram-negative organism [156,206]. As an alternative, an autogenous vein can be used. The incidence of reinfection is low when neoaortic iliac system (NAIS) reconstruction is used [207]. Extraanatomic reconstruction (eg, axillo(bi)femoral bypass) is another option. In one study of 28 patients with primary infection of the infrarenal aorta, mortality was similar for patients undergoing in situ reconstruction compared with extra-anatomic bypass [162]. However, few patients with primary aortic infection have sufficient normal infrarenal aorta to allow safe ligation [155,208-210]. Another disadvantage of extra-anatomic bypass is the greater potential for graft thrombosis compared with in situ reconstruction. (See "Open surgical repair of abdominal aortic aneurysm".)
For infected suprarenal aneurysms, in situ repair is generally performed to preserve visceral flow, though, in some cases, in situ reconstruction is not possible - [148,161,211-213]. In these cases, an antibiotic-impregnated graft with omental coverage can be placed, if possible.
For infected aortic aneurysms, perioperative mortality is 15 to 20 percent. The morbidity and mortality of infected aneurysms are related to the inability to clear the infection and the development of end-organ ischemia [16,52,124,125]. Survival is better for infrarenal abdominal aortic aneurysms (96 versus 57 percent) compared with juxta- and supra-infrarenal aneurysms. Late complications are common, occurring in 30 to 70 percent of patients, and are frequently a cause of death [162,201].
Extracranial carotid artery — The innominate artery and common carotid artery may tolerate ligation without reconstruction; however, ligation of the internal carotid artery is associated with a 30 to 40 percent incidence of stroke [214-216]. To reduce the occurrence of stroke, a test occlusion of the internal carotid artery can be performed, and reconstruction performed selectively for those who develop signs of cerebral ischemia [217]. However, most surgeons favor immediate reconstruction with autogenous veins [218]. A case report detailed the repair of a ruptured infected carotid arterial pseudoaneurysm using a superficial femoral artery graft [219]. (See "Extracranial carotid artery aneurysm", section on 'Open surgical repair'.)
Lower extremity — Infected aneurysms of the lower extremity arteries most commonly involve the vessels in the groin. The popliteal or peroneal arteries can be affected, but infected aneurysm of the vessels below the knee is generally rare [220,221]. Lower extremity-infected aneurysm presents as a painful pulsatile mass, acute limb ischemia due to aneurysm thrombosis, rupture, or distal embolization, similar to noninfected lower extremity aneurysm. (See "Femoral artery aneurysm", section on 'Clinical presentation' and "Popliteal artery aneurysm", section on 'Clinical presentation'.)
In general, ligation of the arteries in the groin may be tolerated if ligation is limited to a single vessel (common femoral artery, superficial femoral artery, or deep femoral artery) and provided that collateral flow is adequate (figure 2) [222,223]. Lower extremity ischemia is more likely if the femoral bifurcation needs to be excised completely.
Options for surgical revascularization of the lower extremity include interposition graft (autogenous graft) [224,225], obturator bypass (autogenous or prosthetic graft), lateral femoral bypass (autogenous or prosthetic graft), and axillary to distal femoral bypass (prosthetic graft). Although prosthetic graft material may be needed for extra-anatomic reconstruction, it should be avoided in patients with a history of active intravenous drug use [157,226-233]. (See "Lower extremity surgical bypass techniques".)
As with infected aortic aneurysms, the exclusion of infected popliteal aneurysms has been managed with endovascular stenting [234,235]. (See 'Role of endovascular techniques' above.)
Amputation following management of infected femoral artery pseudoaneurysm is required in 11 to 25 percent of patients. The amputation rate in patients with intravenous substance use disorder is higher at approximately 30 percent.
Visceral arteries — Mycotic aneurysms of the visceral vessels most commonly involve the superior mesenteric artery [236]. Infected aneurysms of the splenic and renal artery have also been described [178,237]. The clinical presentation of symptomatic visceral aneurysm is abdominal pain, which can be due to aneurysm rupture.
Aneurysm excision and autogenous, in situ reconstruction is the preferred treatment. Simple ligation and debridement may be appropriate for selected small aneurysms in well-collateralized vascular beds (eg, pancreaticoduodenal arcade).
[136,238]. The management of visceral artery aneurysms is discussed in detail elsewhere. (See "Overview of visceral artery aneurysm and pseudoaneurysm" and "Treatment of visceral artery aneurysm and pseudoaneurysm".)
Upper extremity — In the upper extremity, the brachial artery is the most commonly affected site, primarily due to intravenous substance use disorder [239]. These superficial aneurysms are usually readily apparent clinically. Subclavian aneurysms can compress the surrounding neurovascular structures, leading to symptoms of venous thrombosis or brachial plexopathy [122]. (See "Overview of aneurysmal disease of the aortic arch branches or upper extremity arteries in adults".)
Upper extremity vessels, including the subclavian and brachial vessels, often tolerate ligation without ischemic consequences owing to the low metabolic rate of the upper extremity musculature and collateral circulation around the shoulder (figure 3) and elbow.
SOCIETY GUIDELINE LINKS —
Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Intestinal ischemia".)
SUMMARY AND RECOMMENDATIONS
●Definition and etiology - An infected aneurysm is a localized dilation of an artery due to the destruction of the vessel wall by infection. An infected aneurysm can develop when infection of the arterial wall causes the development of a new aneurysm or when a pre-existing aneurysm becomes secondarily infected. (See 'Etiology' above.)
●Microbiology - The organisms with the greatest affinity for the arterial wall and more likely to cause infected aneurysms are Staphylococcus spp and Salmonella spp. Other organisms include Streptococcus pneumoniae, Treponema pallidum, and Mycobacterium tuberculosis, as well as other bacterial, fungal, or anaerobic pathogens. (See 'Microbiology' above.)
●Risk factors - Infected aneurysms can occur in any artery but are most commonly seen in the cerebral, visceral, and extremity circulations, often at points of the vessel bifurcation. Risk factors for infected aneurysm include trauma, endocarditis, impaired immunity, and advanced age. (See 'Risk factors' above.)
●Clinical manifestations - The clinical manifestations depend upon the site of the aneurysm. The classic presentation is a painful, pulsatile, and enlarging mass together with systemic features of infection, such as fever and malaise. The mass may be palpable or demonstrable only by imaging. In the setting of an aneurysm involving the aorta, patients may complain of back or abdominal pain. Infected aneurysms can rupture, presenting as an expanding hematoma or, if an intracerebral vessel is affected, such as stroke or subarachnoid hemorrhage. (See 'Clinical manifestations' above.)
●Diagnosis
•The diagnosis of an infected aneurysm is based on imaging findings, and infection is confirmed by culturing an organism from the blood and/or from the aneurysm wall. If cultures are negative, the pursuit of molecular methods is warranted. (See 'Diagnosis' above.)
•Computed tomography (CT) angiography definitively diagnoses the aneurysm and simultaneously evaluates the status of the circulation. Findings on CT angiography suggestive of infected aneurysm include the following (see 'Vascular imaging' above):
-Saccular, eccentric aneurysm, or multilobulated aneurysm
-Soft tissue inflammation or mass around a vessel
-Aneurysm with intramural air or air collection around the vessel
-Perivascular fluid collection
●Management
•Antibiotic therapy - Prior to the availability of culture results, we favor treatment with a combination of vancomycin and an agent with activity against gram-negative organisms, especially Salmonella and enteric gram-negatives; reasonable choices include ceftriaxone, a fluoroquinolone, and piperacillin-tazobactam. Antibiotics should be tailored to culture and susceptibility results when they become available. The duration of therapy is individualized. (See 'Antibiotic therapy' above.)
•Surgery - At extracranial sites in patients with an acceptable surgical risk, surgical excision of the aneurysm and wide debridement of infected tissues is the treatment of choice. Revascularization is performed as needed, preferably using autogenous material passed through tissue planes remote from the site of infection. Patients with high surgical risk and at some anatomic sites (eg, nonruptured intracerebral) may be best managed with antibiotic therapy alone. (See 'Management' above and 'Surgery' above.)
•Endovascular techniques - For nonruptured infected true aneurysms in patients who are not at high risk for surgery, we prefer open surgical over endovascular methods as the primary mode of treatment. Endovascular stenting does not remove the infected focus of infection, and recurrent infection is frequent and associated with increased morbidity and mortality compared with primary surgical intervention. Endovascular techniques may be useful as a palliative measure for patients who refuse surgery, those with a prohibitive risk for surgery, and possibly for patients with ruptured infected aneurysm as a means to contain the rupture, thus allowing definitive treatment under more elective circumstances. (See 'Role of endovascular techniques' above.)
