https://orcid.org/0000-0002-2915-9045
Abstract
Infection of the native aorta or after previous open or endovascular repair of the thoracic aorta is associated with high risks for morbidity and mortality. We analysed the outcome after surgical management of a native mycotic aneurysm or of prosthetic graft infection of the descending aorta.
From June 2000 to May 2019, a total of 39 patients underwent surgery in our centre for infection of the native descending aorta (n = 19 [49%], group A) or a prosthetic descending aorta [n = 20 (51%), group B]. In the 20 patients in group B, a total of 8 patients had prior open aortic repair with a prosthesis and 12 patients had a previous endovascular graft repair.
The cohort patients had a mean age of 57 ± 14; 62% were men (n = 24). The most common symptoms at the time of presentation included fever, thoracic or abdominal pain and active bleeding. Emergency surgery was performed in 11 patients (28%); 3 patients had emergency endovascular stent grafts implanted during thoracic endovascular aortic repair for aortic rupture before further open repair. The 30-day mortality was 42% in group A and 35% in group B. The 90-day mortality was 47% in group A and 45% in group B. Pathogens could be identified in approximately half of the patients (46%). The most commonly identified pathogens were Staphylococcus aureus in 6 patients (15%) and Staphylococcus epidermidis in 4 patients (10%). Survival of the entire group (including patients with both native and prosthetic graft infections) was 44 ± 8%, 39 ± 8% and 39 ± 8% at 1, 2 and 3 years after surgery. The percentage of patients who survived the initial perioperative period was 81 ± 9%, 71 ± 9% and 71 ± 10% at 1, 2 and 3 years after surgery.
Patients with infection of the descending aorta, either native or prosthetic, are associated with both high morbidity and mortality. However, patients who survive the initial perioperative period have an acceptable long-term prognosis. In emergency situations, thoracic endovascular aortic repair may help to stabilize patients and serve as bridge to open repair.
INTRODUCTION
An infected thoracic aortic aneurysm is a relatively rare condition, comprising 0.65% to 1.3% of all aortic aneurysms [1, 2]. Its aetiology has changed since the first description by Sir William Osler in 1851 of a 30-year-old man with multiple aneurysms at the aortic arch after endocarditis [3].
An infected thoracic aneurysm carries an extremely poor prognosis due to its rapid expansion and high risk of rupture [4]. Despite improvements in antimicrobial therapy and perioperative management, surgical treatment is still associated with high mortality of up to 75% [5–7]. Until recently, there were no standard surgical guidelines for handling an infected thoracic aneurysm [8, 9]. Traditionally, the standard therapy of choice comprised control of infection, radical surgical resection, revascularization and prevention of recurrent infection [5, 10, 11]. This year, the European Society for Vascular Surgery has published guidelines on the treatment of vascular graft and endograft infections in the thoracic, thoraco-abdominal or abdominal aorta [12].
In addition to native infected aneurysms, a prosthetic graft infection after a previous open or endovascular aortic repair is another devastating complication. Endovascular aneurysm repair has become widely accepted in the last 2 decades as the treatment of choice for patients with high comorbidities. Furthermore, endovascular stent grafts [implanted during thoracic endovascular aortic repair (TEVAR)] have also been used to treat mycotic aneurysms. However, there is no clear evidence that this treatment option yields a sound outcome. Kan et al. [13] used endovascular repair to treat a mycotic aneurysm; although the 30-day mortality was only 10.4%, the 1-year survival was only 39%. Therefore, one has to question whether or not endovascular repair is a useful approach in such cases.
Furthermore, the clinical application of an endovascular treatment in an infected area of the aorta is associated with a high risk of complications such as infection of the graft itself, especially in the presence of a fistula to the gastrointestinal or respiratory tract [14–16].
This study describes our experiences and the outcomes after surgical intervention for a native mycotic aneurysm and prosthetic graft infection of the descending aorta in a single centre over 19 years.
MATERIALS AND METHODS
Ethical statement
This is a retrospective analysis, and our institution does not require ethical approval for such studies.
Study design
We retrospectively analysed our electronic hospital records to identify patients with an infected thoracic aorta or with an infected prosthetic graft. Our study focuses exclusively on the descending and/or thoraco-abdominal aorta. A computerized database was generated by analysing patient records, medical charts and operative reports.
From June 2000 to May 2019, a total of 39 patients with a mean age of 57 ± 14 years underwent surgery in our hospital for infection of the descending aorta. These patients were assigned to 1 of the 2 following groups: group A includes patients with infection of the native thoracic aorta (mycotic aneurysm) [n = 19 (49%)]. The diagnosis of a mycotic aneurysm was established by the presence of 2 or more of the following criteria: symptoms of infection (fever, positive haematologic test and culture results, abdominal or back pain), imaging evidence of an infected aorta (periaortic mass or oedema, periaortic gas or gas in the aneurysm thrombus and rapid progress of the aneurysm) (Fig. 1). Negative blood culture test results were not used as exclusion criteria if signs of infection and positive radiological findings were present. These criteria for establishing a diagnosis of mycotic aneurysm have been described previously by other groups [4, 17].
Radiological images of a mycotic aneurysm. These images show a computed tomographic scan of a patient with a mycotic aneurysm. (A) A transverse section. (B) A coronary view. The arrows mark periaortic oedema, suggestive of inflammation.
The second group (group B) includes patients with prosthetic graft infection of the descending aorta [group B; n = 20 (51%)]. In group B, 8 patients (21%) underwent prior open aortic repair and 12 patients (31%) had previous TEVAR. The diagnosis of prosthetic graft infection was made from the presence of both clinical signs (fever, positive inflammatory blood test and/or culture results, abdominal or back pain) and imaging findings of infection.
Of note, 14 patients (74%) in group A and 8 patients (40%) in group B were referred to our centre from peripheral hospitals with a diagnosis of mycotic aneurysm or infected aortic prosthesis. In group B, 12 patients underwent initial surgery at our centre between 1976 and 2014.
We excluded patients who underwent only long-term antibiotic therapy without surgical intervention.
Diagnosis of aortic infection
Diagnosis of thoracic aortic infection (native or prosthetic) was based on clinical and radiological findings. Positron emission tomography/computed tomography was also used to make the diagnosis (Fig. 2).
Radiological and operative images of prosthetic graft aortic infections. (A) The positron emission/computed tomographic scan of a patient who underwent previous thoracic endovascular aortic repair. Both clinical and radiological findings are strongly suggestive of prosthetic graft infection. (B) The infected material explanted intraoperatively. (C) The self-sewn xenopericardial tube. (D) The final result of the descending aorta after replacement with a pericardial tube.
Negative blood culture test results and the absence of pyrexia were not regarded as exclusion criteria, especially in patients who had already received antibiotic treatment, if other criteria including radiological findings, were typical for aortic infection.
We retrospectively searched the demographic details, clinical findings, anatomical location of the infection, leucocytosis, fever, results of blood cultures (pre- and postoperatively), surgical and antibiotic therapy, postoperative complications and morbidity and mortality, including survival.
Perioperative management and surgical technique
All patients received preoperatively empirical broad-spectrum antibiotics or directed antibiotic treatment if positive blood culture test results were available. All patients underwent open replacement of the descending or thoraco-abdominal aorta via a left lateral thoracotomy or thoraco-phreno-laparotomy approach. We used the following grafts for aortic reconstruction: silver-coated polyester prostheses, cryopreserved homograft or pericardial tube xenografts. In patients with previous open repair or TEVAR, we extracted the previous (endo-)graft (Fig. 3). We did not use muscle flap as a surgical technique to reduce risk of infection after resection and wide debridement to aortic and periaortic tissue. The defect and graft were covered with omentum or biological pericardial patches.
Intraoperative images of the infected prosthesis. (A) The opened descending aorta. The prosthesis is fractured during explantation. Complete excision could be achieved. (B) The aorta after removal of the infected material. The infected material caused irritation in the aorta, leading to a significant lesion. (C) The fractured but completely excised infected area. (D) The final result of the descending aorta after replacement with a self-made pericardial xenotube.
Microbiological samples were taken for identification of the causative pathogens. Afterwards, the operative field was thoroughly irrigated. Postoperatively, all patients underwent long-term treatment for at least 6 weeks with the appropriate antibiotics. If cultures were available, patients received specific antibiotics targeting the cultured organism. If cultures did not show any bacterial growth, patients received broad-spectrum antibiotics.
Postoperative follow-up
Computed tomography scans were done postoperatively. Individual consent was obtained from patients to allow for follow-up examinations. Follow-up imaging was performed by computed tomography angiography scan or magnetic resonance imaging angiography at 3 months, 6 months and annually thereafter.
Patients were contacted by telephone and seen in our clinic. Primary care physicians were contacted to obtain examination results.
Statistical analyses
Data analysis was performed using SPSS 26 Statistics software (2019) (IBM SPSS Statistics for Windows, Version 26.0., Armonk, NY, USA). Normal distribution of variables was analysed with the Kolmogorov-Smirnov test. Normally distributed continuous variables are presented as mean ± standard deviation, whereas continuous variables without normal distribution are presented as median + range. Kaplan–Meier analysis was used for evaluation of survival. We analysed the survival both of the entire group and of those patients who survived the initial perioperative period (i.e. all patients except those who died within the first 90 postoperative days).
RESULTS
Preoperative presentation and diagnosis
During the study period, a total of 39 patients (24 men, 62%) were identified with infection of the descending aorta, including both the native aorta (group A) and the prosthesis (group B). The median time from initial surgery to reoperation for graft infection in group B was 205 days (range: 0–11 680 days). Of these, 3 patients presented with an early graft infection (<4 weeks after the initial surgery), and 17 patients had late prosthetic graft infections. In group B, 12 patients had their first intervention in our clinic. We did not observe a major trend of the incidence of cases over time (Supplementary Material, Fig. S1).
The preoperative characteristics of our patients are shown in Table 1. Preoperatively, 3 patients (2 in group A and 1 in group B) received steroid therapy, and 3 patients in group A and no patients in group B received other immunosuppressive drugs.
Preoperative data
| Entire cohort (n = 39) | Group A (native) (n = 19) | Group B (prosthetic) (n = 20) | |
|---|---|---|---|
| Demographic data | |||
| Age (years) | 57 ± 14 | 59 ± 15 | 55 ± 14 |
| Male (n, %) | 24 (62) | 10 (53) | 14 (70) |
| Weight (kg) | 77 ± 20 | 72 ± 19 | 81 ± 20 |
| Height (cm) | 174 ± 12 | 169 ± 9 | 179 ± 12 |
| BMI (kg/m2) | 25 ± 5 | 25 ± 6 | 25 ± 5 |
| Medical history (n, %) | |||
| Diabetes | 5 (13) | 5 (26) | 0 (0) |
| Hyperlipidaemia | 5 (13) | 2 (11) | 3 (15) |
| Arterial hypertension | 26 (67) | 12 (63) | 14 (70) |
| Coronary artery disease | 7 (18) | 4 (21) | 3 (15) |
| COPD | 2 (5) | 2 (11) | 0 (0) |
| Kidney disease | 6 (15) | 3 (16) | 3 (15) |
| Dialysis | 1 (3) | 0 (0) | 1 (5) |
| Stroke | 4 (10) | 2 (11) | 2 (10) |
| Risk factors for graft infection (n, %) | |||
| Immunodeficient | 3 (8) | 3 (16) | 0 (0) |
| Steroid therapy | 3 (8) | 2 (11) | 1 (5) |
| Infection at another site | 18 (46) | 8 (42) | 10 (50) |
| Clinical presentation (n, %) | |||
| Fever | 11 (28) | 2 (11) | 9 (45) |
| Abdominal/back pain | 19 (49) | 12 (63) | 7 (35) |
| Bleedinga | 17 (44) | 6 (32) | 11 (55) |
| Asymptomatic | 4 (10) | 3 (16) | 1 (5) |
| Diagnostic imaging (n, %) | |||
| CT scan | 38 (97) | 18 (95) | 20 (100) |
| PET/CT scan | 7 (18) | 0 (0) | 7 (35) |
| MRI | 3 (8) | 3 (16) | 0 (0) |
| Bronchoscopy | 3 (8) | 0 (0) | 3 (15) |
| Laboratory tests | |||
| Leucocytes (1.000/μl) | 12 ± 6 | 11 ± 4 | 12 ± 7 |
| CRP (mg/l) | 101 (2–337) | 115 (6–311) | 91 (2–337) |
| Entire cohort (n = 39) | Group A (native) (n = 19) | Group B (prosthetic) (n = 20) | |
|---|---|---|---|
| Demographic data | |||
| Age (years) | 57 ± 14 | 59 ± 15 | 55 ± 14 |
| Male (n, %) | 24 (62) | 10 (53) | 14 (70) |
| Weight (kg) | 77 ± 20 | 72 ± 19 | 81 ± 20 |
| Height (cm) | 174 ± 12 | 169 ± 9 | 179 ± 12 |
| BMI (kg/m2) | 25 ± 5 | 25 ± 6 | 25 ± 5 |
| Medical history (n, %) | |||
| Diabetes | 5 (13) | 5 (26) | 0 (0) |
| Hyperlipidaemia | 5 (13) | 2 (11) | 3 (15) |
| Arterial hypertension | 26 (67) | 12 (63) | 14 (70) |
| Coronary artery disease | 7 (18) | 4 (21) | 3 (15) |
| COPD | 2 (5) | 2 (11) | 0 (0) |
| Kidney disease | 6 (15) | 3 (16) | 3 (15) |
| Dialysis | 1 (3) | 0 (0) | 1 (5) |
| Stroke | 4 (10) | 2 (11) | 2 (10) |
| Risk factors for graft infection (n, %) | |||
| Immunodeficient | 3 (8) | 3 (16) | 0 (0) |
| Steroid therapy | 3 (8) | 2 (11) | 1 (5) |
| Infection at another site | 18 (46) | 8 (42) | 10 (50) |
| Clinical presentation (n, %) | |||
| Fever | 11 (28) | 2 (11) | 9 (45) |
| Abdominal/back pain | 19 (49) | 12 (63) | 7 (35) |
| Bleedinga | 17 (44) | 6 (32) | 11 (55) |
| Asymptomatic | 4 (10) | 3 (16) | 1 (5) |
| Diagnostic imaging (n, %) | |||
| CT scan | 38 (97) | 18 (95) | 20 (100) |
| PET/CT scan | 7 (18) | 0 (0) | 7 (35) |
| MRI | 3 (8) | 3 (16) | 0 (0) |
| Bronchoscopy | 3 (8) | 0 (0) | 3 (15) |
| Laboratory tests | |||
| Leucocytes (1.000/μl) | 12 ± 6 | 11 ± 4 | 12 ± 7 |
| CRP (mg/l) | 101 (2–337) | 115 (6–311) | 91 (2–337) |
The variable bleeding includes haemoptysis (n = 3), aortobronchial fistula (n = 4), aorto-oesophageal fistula (n = 6) and haemothorax (n = 4).
BMI: body mass index; COPD: chronic obstructive pulmonary disease; CRP: C-reactive protein; CT: computed tomography; MRI: magnetic resonance imaging; PET/CT: positron emission tomography/computed tomography.
Preoperative data
| Entire cohort (n = 39) | Group A (native) (n = 19) | Group B (prosthetic) (n = 20) | |
|---|---|---|---|
| Demographic data | |||
| Age (years) | 57 ± 14 | 59 ± 15 | 55 ± 14 |
| Male (n, %) | 24 (62) | 10 (53) | 14 (70) |
| Weight (kg) | 77 ± 20 | 72 ± 19 | 81 ± 20 |
| Height (cm) | 174 ± 12 | 169 ± 9 | 179 ± 12 |
| BMI (kg/m2) | 25 ± 5 | 25 ± 6 | 25 ± 5 |
| Medical history (n, %) | |||
| Diabetes | 5 (13) | 5 (26) | 0 (0) |
| Hyperlipidaemia | 5 (13) | 2 (11) | 3 (15) |
| Arterial hypertension | 26 (67) | 12 (63) | 14 (70) |
| Coronary artery disease | 7 (18) | 4 (21) | 3 (15) |
| COPD | 2 (5) | 2 (11) | 0 (0) |
| Kidney disease | 6 (15) | 3 (16) | 3 (15) |
| Dialysis | 1 (3) | 0 (0) | 1 (5) |
| Stroke | 4 (10) | 2 (11) | 2 (10) |
| Risk factors for graft infection (n, %) | |||
| Immunodeficient | 3 (8) | 3 (16) | 0 (0) |
| Steroid therapy | 3 (8) | 2 (11) | 1 (5) |
| Infection at another site | 18 (46) | 8 (42) | 10 (50) |
| Clinical presentation (n, %) | |||
| Fever | 11 (28) | 2 (11) | 9 (45) |
| Abdominal/back pain | 19 (49) | 12 (63) | 7 (35) |
| Bleedinga | 17 (44) | 6 (32) | 11 (55) |
| Asymptomatic | 4 (10) | 3 (16) | 1 (5) |
| Diagnostic imaging (n, %) | |||
| CT scan | 38 (97) | 18 (95) | 20 (100) |
| PET/CT scan | 7 (18) | 0 (0) | 7 (35) |
| MRI | 3 (8) | 3 (16) | 0 (0) |
| Bronchoscopy | 3 (8) | 0 (0) | 3 (15) |
| Laboratory tests | |||
| Leucocytes (1.000/μl) | 12 ± 6 | 11 ± 4 | 12 ± 7 |
| CRP (mg/l) | 101 (2–337) | 115 (6–311) | 91 (2–337) |
| Entire cohort (n = 39) | Group A (native) (n = 19) | Group B (prosthetic) (n = 20) | |
|---|---|---|---|
| Demographic data | |||
| Age (years) | 57 ± 14 | 59 ± 15 | 55 ± 14 |
| Male (n, %) | 24 (62) | 10 (53) | 14 (70) |
| Weight (kg) | 77 ± 20 | 72 ± 19 | 81 ± 20 |
| Height (cm) | 174 ± 12 | 169 ± 9 | 179 ± 12 |
| BMI (kg/m2) | 25 ± 5 | 25 ± 6 | 25 ± 5 |
| Medical history (n, %) | |||
| Diabetes | 5 (13) | 5 (26) | 0 (0) |
| Hyperlipidaemia | 5 (13) | 2 (11) | 3 (15) |
| Arterial hypertension | 26 (67) | 12 (63) | 14 (70) |
| Coronary artery disease | 7 (18) | 4 (21) | 3 (15) |
| COPD | 2 (5) | 2 (11) | 0 (0) |
| Kidney disease | 6 (15) | 3 (16) | 3 (15) |
| Dialysis | 1 (3) | 0 (0) | 1 (5) |
| Stroke | 4 (10) | 2 (11) | 2 (10) |
| Risk factors for graft infection (n, %) | |||
| Immunodeficient | 3 (8) | 3 (16) | 0 (0) |
| Steroid therapy | 3 (8) | 2 (11) | 1 (5) |
| Infection at another site | 18 (46) | 8 (42) | 10 (50) |
| Clinical presentation (n, %) | |||
| Fever | 11 (28) | 2 (11) | 9 (45) |
| Abdominal/back pain | 19 (49) | 12 (63) | 7 (35) |
| Bleedinga | 17 (44) | 6 (32) | 11 (55) |
| Asymptomatic | 4 (10) | 3 (16) | 1 (5) |
| Diagnostic imaging (n, %) | |||
| CT scan | 38 (97) | 18 (95) | 20 (100) |
| PET/CT scan | 7 (18) | 0 (0) | 7 (35) |
| MRI | 3 (8) | 3 (16) | 0 (0) |
| Bronchoscopy | 3 (8) | 0 (0) | 3 (15) |
| Laboratory tests | |||
| Leucocytes (1.000/μl) | 12 ± 6 | 11 ± 4 | 12 ± 7 |
| CRP (mg/l) | 101 (2–337) | 115 (6–311) | 91 (2–337) |
The variable bleeding includes haemoptysis (n = 3), aortobronchial fistula (n = 4), aorto-oesophageal fistula (n = 6) and haemothorax (n = 4).
BMI: body mass index; COPD: chronic obstructive pulmonary disease; CRP: C-reactive protein; CT: computed tomography; MRI: magnetic resonance imaging; PET/CT: positron emission tomography/computed tomography.
Of our patients, 18 (8 in group A and 10 in group B) presented with infections at other sites, including cholecystitis, gastroenteritis, diverticulitis, pneumonia and endocarditis.
The most common symptoms at the time of presentation included fever, thoracic or abdominal pain and active bleeding. Only 4 patients (3 in group A and 1 in group B) were asymptomatic.
The patients had elevated inflammatory parameters: the average leucocyte count was 12 ± 6/1.000/µl and the C-reactive protein level was 101 (2–337) mg/l. Preoperative imaging modalities included a computed tomography scan of all patients except 1. Positron emission tomography/computed tomography was performed primarily in patients with prosthetic graft infections (group B). Bronchoscopy or upper gastroscopy was performed in 3 patients in group B because of concern for a fistula (Table 1).
The majority of patients received a cryopreserved homograft [n = 23 (59%)]. A silver-coated prosthesis and a Dacron graft were used in 10% and 18%, respectively. A xenogenic pericardium tube was used in 5 patients (25%) for the in situ aortic repair.
Early perioperative outcome
The intraoperative outcomes are shown in Table 2. Of our patients, 11 (8 in group A and 3 in group B) underwent emergency interventions because of an unstable clinical condition, bleeding or rupture. In group B, we used TEVAR to stabilize 3 patients and to prevent further rupture. The majority of patients in both groups received large quantities of blood products during the operation.
Intraoperative data
| Entire cohort (n = 39) | Group A (native) (n = 19) | Group B (prosthetic) (n = 20) | |
|---|---|---|---|
| Status of operation (n, %) | |||
| Elective | 23 (59) | 9 (47%) | 14 (70%) |
| Urgent | 5 (13) | 2 (11%) | 3 (15%) |
| Emergency | 11 (28) | 8 (42%) | 3 (15%) |
| Extent of operation (n, %) | |||
| Descending aortic replacement | 21 (54) | 9 (47) | 12 (60) |
| Thoraco-abdominal aortic replacement | 16 (41) | 9 (47) | 7 (35) |
| Other | 2 (5) | 1 (5) | 1 (5) |
| Type of implanted graft (n, %) | |||
| Dacron graft | 7 (18) | 5 (26) | 2 (10) |
| Cryopreserved aortic homograft | 23 (59) | 11 (58) | 12 (60) |
| Silver graft prosthesis | 4 (10) | 3 (16) | 1 (5) |
| Xenogenic pericardium | 5 (13) | 0 (0) | 5 (25) |
| Intraoperative data | |||
| Operating time (min) | 330 ± 134 | 299 ± 124 | 361 ± 140 |
| ‘Stent first’ approach (n, %) | 3 (77) | 0 (0) | 3 (15) |
| PBC, units | 17 (2–57) | 13 ± 10 | 20 ± 15 |
| FFP, units | 14 (0–63) | 13 ± 12 | 14 ± 15 |
| Platelets, units | 3 (0–11) | 3 ± 2 | 4 ± 3 |
| Entire cohort (n = 39) | Group A (native) (n = 19) | Group B (prosthetic) (n = 20) | |
|---|---|---|---|
| Status of operation (n, %) | |||
| Elective | 23 (59) | 9 (47%) | 14 (70%) |
| Urgent | 5 (13) | 2 (11%) | 3 (15%) |
| Emergency | 11 (28) | 8 (42%) | 3 (15%) |
| Extent of operation (n, %) | |||
| Descending aortic replacement | 21 (54) | 9 (47) | 12 (60) |
| Thoraco-abdominal aortic replacement | 16 (41) | 9 (47) | 7 (35) |
| Other | 2 (5) | 1 (5) | 1 (5) |
| Type of implanted graft (n, %) | |||
| Dacron graft | 7 (18) | 5 (26) | 2 (10) |
| Cryopreserved aortic homograft | 23 (59) | 11 (58) | 12 (60) |
| Silver graft prosthesis | 4 (10) | 3 (16) | 1 (5) |
| Xenogenic pericardium | 5 (13) | 0 (0) | 5 (25) |
| Intraoperative data | |||
| Operating time (min) | 330 ± 134 | 299 ± 124 | 361 ± 140 |
| ‘Stent first’ approach (n, %) | 3 (77) | 0 (0) | 3 (15) |
| PBC, units | 17 (2–57) | 13 ± 10 | 20 ± 15 |
| FFP, units | 14 (0–63) | 13 ± 12 | 14 ± 15 |
| Platelets, units | 3 (0–11) | 3 ± 2 | 4 ± 3 |
FFP: fresh frozen plasma; PBC: packed blood cells.
Intraoperative data
| Entire cohort (n = 39) | Group A (native) (n = 19) | Group B (prosthetic) (n = 20) | |
|---|---|---|---|
| Status of operation (n, %) | |||
| Elective | 23 (59) | 9 (47%) | 14 (70%) |
| Urgent | 5 (13) | 2 (11%) | 3 (15%) |
| Emergency | 11 (28) | 8 (42%) | 3 (15%) |
| Extent of operation (n, %) | |||
| Descending aortic replacement | 21 (54) | 9 (47) | 12 (60) |
| Thoraco-abdominal aortic replacement | 16 (41) | 9 (47) | 7 (35) |
| Other | 2 (5) | 1 (5) | 1 (5) |
| Type of implanted graft (n, %) | |||
| Dacron graft | 7 (18) | 5 (26) | 2 (10) |
| Cryopreserved aortic homograft | 23 (59) | 11 (58) | 12 (60) |
| Silver graft prosthesis | 4 (10) | 3 (16) | 1 (5) |
| Xenogenic pericardium | 5 (13) | 0 (0) | 5 (25) |
| Intraoperative data | |||
| Operating time (min) | 330 ± 134 | 299 ± 124 | 361 ± 140 |
| ‘Stent first’ approach (n, %) | 3 (77) | 0 (0) | 3 (15) |
| PBC, units | 17 (2–57) | 13 ± 10 | 20 ± 15 |
| FFP, units | 14 (0–63) | 13 ± 12 | 14 ± 15 |
| Platelets, units | 3 (0–11) | 3 ± 2 | 4 ± 3 |
| Entire cohort (n = 39) | Group A (native) (n = 19) | Group B (prosthetic) (n = 20) | |
|---|---|---|---|
| Status of operation (n, %) | |||
| Elective | 23 (59) | 9 (47%) | 14 (70%) |
| Urgent | 5 (13) | 2 (11%) | 3 (15%) |
| Emergency | 11 (28) | 8 (42%) | 3 (15%) |
| Extent of operation (n, %) | |||
| Descending aortic replacement | 21 (54) | 9 (47) | 12 (60) |
| Thoraco-abdominal aortic replacement | 16 (41) | 9 (47) | 7 (35) |
| Other | 2 (5) | 1 (5) | 1 (5) |
| Type of implanted graft (n, %) | |||
| Dacron graft | 7 (18) | 5 (26) | 2 (10) |
| Cryopreserved aortic homograft | 23 (59) | 11 (58) | 12 (60) |
| Silver graft prosthesis | 4 (10) | 3 (16) | 1 (5) |
| Xenogenic pericardium | 5 (13) | 0 (0) | 5 (25) |
| Intraoperative data | |||
| Operating time (min) | 330 ± 134 | 299 ± 124 | 361 ± 140 |
| ‘Stent first’ approach (n, %) | 3 (77) | 0 (0) | 3 (15) |
| PBC, units | 17 (2–57) | 13 ± 10 | 20 ± 15 |
| FFP, units | 14 (0–63) | 13 ± 12 | 14 ± 15 |
| Platelets, units | 3 (0–11) | 3 ± 2 | 4 ± 3 |
FFP: fresh frozen plasma; PBC: packed blood cells.
The early postoperative outcomes are shown in Table 3. Early complications included the following: (i) bleeding that required a rethoracotomy during the same hospital stay occurred in 10 patients; (ii) respiratory failure leading to prolonged ventilation (more than 72 h) was necessary in 14 patients in group A (53%) compared to 4 patients in group B (20%); (iii) 12 patients required tracheostomy; neurological complications occurred in 2 patients.
Postoperative data
| Entire cohort (n = 39) | Group A (native) (n = 19) | Group B (prosthetic) (n = 20) | |
|---|---|---|---|
| Early postoperative results | |||
| ICU stay (days) | 11 (0–96) | 9 ± 12 | 13 ± 22 |
| Rethoracotomy (n, %) | 10 (26) | 3 (16) | 7 (35) |
| Ventilation time (h) | 141 (0–1332) | 186 ± 309 | 99 ± 181 |
| Prolonged ventilation >72 h (n, %) | 14 (36) | 10 (53) | 4 (20) |
| Tracheostomy (n, %) | 12 (31) | 4 (21) | 8 (40) |
| Acute kidney injury (n, %) | 9 (23) | 6 (32) | 3 (15) |
| New dialysis (n, %) | 7 (18) | 4 (21) | 3 (15) |
| Neurological injury (n, %) | 2 (5) | 1 (5) | 1 (5) |
| 30-Day mortality (n, %) | 15 (38) | 8 (42) | 7 (35) |
| 90-Day mortality (n, %) | 18 (46) | 9 (47) | 9 (45) |
| Entire cohort (n = 39) | Group A (native) (n = 19) | Group B (prosthetic) (n = 20) | |
|---|---|---|---|
| Early postoperative results | |||
| ICU stay (days) | 11 (0–96) | 9 ± 12 | 13 ± 22 |
| Rethoracotomy (n, %) | 10 (26) | 3 (16) | 7 (35) |
| Ventilation time (h) | 141 (0–1332) | 186 ± 309 | 99 ± 181 |
| Prolonged ventilation >72 h (n, %) | 14 (36) | 10 (53) | 4 (20) |
| Tracheostomy (n, %) | 12 (31) | 4 (21) | 8 (40) |
| Acute kidney injury (n, %) | 9 (23) | 6 (32) | 3 (15) |
| New dialysis (n, %) | 7 (18) | 4 (21) | 3 (15) |
| Neurological injury (n, %) | 2 (5) | 1 (5) | 1 (5) |
| 30-Day mortality (n, %) | 15 (38) | 8 (42) | 7 (35) |
| 90-Day mortality (n, %) | 18 (46) | 9 (47) | 9 (45) |
ICU: intensive care unit.
Postoperative data
| Entire cohort (n = 39) | Group A (native) (n = 19) | Group B (prosthetic) (n = 20) | |
|---|---|---|---|
| Early postoperative results | |||
| ICU stay (days) | 11 (0–96) | 9 ± 12 | 13 ± 22 |
| Rethoracotomy (n, %) | 10 (26) | 3 (16) | 7 (35) |
| Ventilation time (h) | 141 (0–1332) | 186 ± 309 | 99 ± 181 |
| Prolonged ventilation >72 h (n, %) | 14 (36) | 10 (53) | 4 (20) |
| Tracheostomy (n, %) | 12 (31) | 4 (21) | 8 (40) |
| Acute kidney injury (n, %) | 9 (23) | 6 (32) | 3 (15) |
| New dialysis (n, %) | 7 (18) | 4 (21) | 3 (15) |
| Neurological injury (n, %) | 2 (5) | 1 (5) | 1 (5) |
| 30-Day mortality (n, %) | 15 (38) | 8 (42) | 7 (35) |
| 90-Day mortality (n, %) | 18 (46) | 9 (47) | 9 (45) |
| Entire cohort (n = 39) | Group A (native) (n = 19) | Group B (prosthetic) (n = 20) | |
|---|---|---|---|
| Early postoperative results | |||
| ICU stay (days) | 11 (0–96) | 9 ± 12 | 13 ± 22 |
| Rethoracotomy (n, %) | 10 (26) | 3 (16) | 7 (35) |
| Ventilation time (h) | 141 (0–1332) | 186 ± 309 | 99 ± 181 |
| Prolonged ventilation >72 h (n, %) | 14 (36) | 10 (53) | 4 (20) |
| Tracheostomy (n, %) | 12 (31) | 4 (21) | 8 (40) |
| Acute kidney injury (n, %) | 9 (23) | 6 (32) | 3 (15) |
| New dialysis (n, %) | 7 (18) | 4 (21) | 3 (15) |
| Neurological injury (n, %) | 2 (5) | 1 (5) | 1 (5) |
| 30-Day mortality (n, %) | 15 (38) | 8 (42) | 7 (35) |
| 90-Day mortality (n, %) | 18 (46) | 9 (47) | 9 (45) |
ICU: intensive care unit.
The overall 30-day mortality was 38%, with 42% in group A and 35% in group B. The overall 90-day mortality was 46%, with 47% in group A and 45% in group B. The mortality was higher in emergency cases (30 days: 56%; 90 days: 63%) compared to elective cases (30 days: 26%; 90 days: 35%).
The 90-day mortality was extremely high in patients with an aorto-oesophageal fistula (4 patients in group A and 2 in group B with 90-day mortality of 100% in both groups). Patients with an aortobronchial fistula (1 patient in group A and 3 patients in group B) had slightly better outcomes (90-day mortality, 50%).
Causes of death were haemorrhagic (n = 7) and septic shock with multiorgan failure (n = 10). One patient died of a massive stroke with metabolic circulatory failure.
Preoperative blood cultures and/or cultures of intraoperative specimens of the aneurysmal content, the arterial wall or the previous prosthesis revealed bacterial growth in 18 patients. It could be explained as being due to aggressive antibiotic treatment. The identified microbial pathogens are shown in Table 4. Pathogens could be identified in approximately half of all patients (46%). The most commonly identified pathogens were bacteria of the skin, including Staphylococcus aureus in 6 patients (15%) and Staphylococcus epidermidis in 4 patients (10%).
Pathogens
| Entire cohort (n = 39) | Group A (native) (n = 19) | Group B (prosthetic) (n = 20) | |
|---|---|---|---|
| Skin (n, %) | |||
| Staphylococcus aureus | 6 (15) | 5 (26) | 1 (5) |
| Staphylococcus epidermidis | 4 (10) | 1 (5) | 3 (15) |
| Staphylococcus haemolyticus | 0 (0) | 0 (0) | 1 (5) |
| Staphylococcus warneri | 1 (3) | 1 (5) | 0 (0) |
| Oral (n, %) | |||
| Gemella haemolysans | 1 (3) | 0 (0) | 1 (5) |
| Streptococcus anginosus | 1 (3) | 0 (0) | 1 (5) |
| Streptococcus constellatus | 1 (3) | 0 (0) | 1 (5) |
| Gastrointestinal tract (n, %) | |||
| Enterococcus faecalis | 2 (5) | 0 (0) | 2 (10) |
| Escherichia coli | 1 (3) | 0 (0) | 1 (5) |
| Enterobacter chloacae | 1 (3) | 0 (0) | 1 (5) |
| Streptococcus agalactiae | 1 (3) | 1 (5) | 0 (0) |
| Other (n, %) | |||
| Candida albicans | 2 (5) | 0 (0) | 2 (10) |
| Pseudomonas aeruginosa | 1 (3) | 1 (5) | 0 (0) |
| No pathogen identified: | |||
| Unknown | 21 (54) | 10 (53) | 11 (55) |
| Entire cohort (n = 39) | Group A (native) (n = 19) | Group B (prosthetic) (n = 20) | |
|---|---|---|---|
| Skin (n, %) | |||
| Staphylococcus aureus | 6 (15) | 5 (26) | 1 (5) |
| Staphylococcus epidermidis | 4 (10) | 1 (5) | 3 (15) |
| Staphylococcus haemolyticus | 0 (0) | 0 (0) | 1 (5) |
| Staphylococcus warneri | 1 (3) | 1 (5) | 0 (0) |
| Oral (n, %) | |||
| Gemella haemolysans | 1 (3) | 0 (0) | 1 (5) |
| Streptococcus anginosus | 1 (3) | 0 (0) | 1 (5) |
| Streptococcus constellatus | 1 (3) | 0 (0) | 1 (5) |
| Gastrointestinal tract (n, %) | |||
| Enterococcus faecalis | 2 (5) | 0 (0) | 2 (10) |
| Escherichia coli | 1 (3) | 0 (0) | 1 (5) |
| Enterobacter chloacae | 1 (3) | 0 (0) | 1 (5) |
| Streptococcus agalactiae | 1 (3) | 1 (5) | 0 (0) |
| Other (n, %) | |||
| Candida albicans | 2 (5) | 0 (0) | 2 (10) |
| Pseudomonas aeruginosa | 1 (3) | 1 (5) | 0 (0) |
| No pathogen identified: | |||
| Unknown | 21 (54) | 10 (53) | 11 (55) |
Pathogens
| Entire cohort (n = 39) | Group A (native) (n = 19) | Group B (prosthetic) (n = 20) | |
|---|---|---|---|
| Skin (n, %) | |||
| Staphylococcus aureus | 6 (15) | 5 (26) | 1 (5) |
| Staphylococcus epidermidis | 4 (10) | 1 (5) | 3 (15) |
| Staphylococcus haemolyticus | 0 (0) | 0 (0) | 1 (5) |
| Staphylococcus warneri | 1 (3) | 1 (5) | 0 (0) |
| Oral (n, %) | |||
| Gemella haemolysans | 1 (3) | 0 (0) | 1 (5) |
| Streptococcus anginosus | 1 (3) | 0 (0) | 1 (5) |
| Streptococcus constellatus | 1 (3) | 0 (0) | 1 (5) |
| Gastrointestinal tract (n, %) | |||
| Enterococcus faecalis | 2 (5) | 0 (0) | 2 (10) |
| Escherichia coli | 1 (3) | 0 (0) | 1 (5) |
| Enterobacter chloacae | 1 (3) | 0 (0) | 1 (5) |
| Streptococcus agalactiae | 1 (3) | 1 (5) | 0 (0) |
| Other (n, %) | |||
| Candida albicans | 2 (5) | 0 (0) | 2 (10) |
| Pseudomonas aeruginosa | 1 (3) | 1 (5) | 0 (0) |
| No pathogen identified: | |||
| Unknown | 21 (54) | 10 (53) | 11 (55) |
| Entire cohort (n = 39) | Group A (native) (n = 19) | Group B (prosthetic) (n = 20) | |
|---|---|---|---|
| Skin (n, %) | |||
| Staphylococcus aureus | 6 (15) | 5 (26) | 1 (5) |
| Staphylococcus epidermidis | 4 (10) | 1 (5) | 3 (15) |
| Staphylococcus haemolyticus | 0 (0) | 0 (0) | 1 (5) |
| Staphylococcus warneri | 1 (3) | 1 (5) | 0 (0) |
| Oral (n, %) | |||
| Gemella haemolysans | 1 (3) | 0 (0) | 1 (5) |
| Streptococcus anginosus | 1 (3) | 0 (0) | 1 (5) |
| Streptococcus constellatus | 1 (3) | 0 (0) | 1 (5) |
| Gastrointestinal tract (n, %) | |||
| Enterococcus faecalis | 2 (5) | 0 (0) | 2 (10) |
| Escherichia coli | 1 (3) | 0 (0) | 1 (5) |
| Enterobacter chloacae | 1 (3) | 0 (0) | 1 (5) |
| Streptococcus agalactiae | 1 (3) | 1 (5) | 0 (0) |
| Other (n, %) | |||
| Candida albicans | 2 (5) | 0 (0) | 2 (10) |
| Pseudomonas aeruginosa | 1 (3) | 1 (5) | 0 (0) |
| No pathogen identified: | |||
| Unknown | 21 (54) | 10 (53) | 11 (55) |
Late outcomes
The median follow-up time of patients who survived the initial perioperative period was 3.9 (range: 0.4–12.6) years. The Kaplan–Meier survival curves are shown in Fig. 4A and B. Survival of the entire group (including both patients with native and those with prosthetic graft infections) was 44 ± 8%, 39 ± 8% and 39 ± 8% at 1, 2 and 3 years after surgery (Fig. 4A). Survival of patients who survived the initial perioperative period was 81 ± 9%, 71 ± 10% and 71 ± 10% at 1, 2 and 5 years after surgery. With regards to freedom from recurrent infection, 1 patient underwent re-replacement of the previously repaired descending prosthetic aorta due to persistent infection on postoperative day 45. Of note, the survival curves are shown according to the indexed pathology (native and prosthetic graft infection) in Supplementary Material, Fig. S2.
Survival after native and prosthetic aortic infection. (A) Kaplan–Meier survival curve for all patients who had surgery for infection of the native descending aorta or prosthetic graft infection of the descending aorta. (B) The survival curve of all patients who survived the initial perioperative period (‘hospital survivors’) after surgery for infection of the native or prosthetic descending aorta. Survival was truncated when ≤10% of the original population was still alive. Time origin on x-axis denotes day of surgery.
DISCUSSION
Aortic infection remains a challenging problem. It used to be a deadly disease with high morbidity and mortality, which often exceeded 50% and could be as high as 100% for untreated cases [18–20]. The results of this study confirm the high mortality (30-day mortality of 38%, 90-day mortality of 46%) reported by other groups [2, 6, 21]. However, patients who survive the initial perioperative period have an acceptable long-term prognosis. Presenting signs and symptoms are often non-specific. The typical symptoms, which include fever, pain and a pulsatile mass, were observed in only a few patients. The anatomical location of the infection in the thoracic aorta makes it difficult to examine physically [1, 22].
The standard treatment for aortic infection involves resection of the infected aorta with extensive debridement of all infected tissues and reconstruction of the aortic flow with several methods and materials.
The best method for revascularization is still controversial [21]. Sandmann et al. prefer an in situ aortic replacement using a rifampin-soaked, gel-impregnated Dacron prosthesis. Other surgeons, as we frequently do, use cryopreserved arterial homografts. Another option is to use a silver-coated polyester graft [23]. We have also used self-made bovine pericardial tube grafts in some patients. Thus far, none of these materials seems to be significantly superior to others.
Endovascular aortic repair has opened a new arena in the management of aortic disease including infection. Kan et al. [13] reviewed the literature and analysed the data of 48 patients who underwent endovascular treatment of mycotic aneurysms. The 30-day mortality after endovascular treatment of sepsis and bleeding was 10.4% and the 1-year survival was 39%. The mortality rate of 10.4% is lower than that in the present study; however, the survival rate of 39% reported by Kan and colleagues is comparable to the long-term outcomes reported in our study. One has to also keep in mind that the survival rates in our study include patients with both mycotic and graft infections, which implies that endovascular repair for a mycotic aneurysm may not be superior to open surgery.
Moulakakis et al. [24] published a literature review on graft infection after TEVAR, analysing 55 patients treated with preservation of the endovascular graft and 41, with excision. This review showed that preservation of an endograft with antibiotic therapy alone was not a durable and safe option and that the better outcome was observed in patients who underwent endograft excision. Evidence-based results for the endovascular treatment of infected aortas are lacking. We performed endovascular management only in emergency cases such as bleeding or a fistula to stabilize the patients and as a bridge to open surgery. We think that this ‘stent first’ approach is useful in emergency settings but should not be seen as a stand-alone procedure, because the infection is only temporarily controlled and is still present.
In our study, the most commonly identified pathogens were bacteria of the skin, including S.aureus in 6 patients (15%) and S.epidermidis in 4 patients (10%).
Interestingly, we did not find any Salmonella infections in our cohort. Therefore, we cannot confirm or corroborate this issue. In addition to non-Salmonella infection, Hsu et al. [25] also found advanced age to be a risk factor for operative mortality. Some authors determined sepsis as a leading cause for early death for a surgically infected thoracic aorta [5].
We identified a variety of different organisms in blood cultures and specimens. However, given the small sample size of our group, we were not able to perform a statistically reliable risk factor analysis.
Oderich et al. [22] defined 5 risk factors that were associated with operative mortality: extensive periaortic infection, female sex, S.aureus infection, aneurysm rupture and suprarenal location. Due to the small sample size of the present study, we did not perform a multivariate logistic risk factor analysis to identify risk factors. However, we agree that aortic rupture must be a significant risk factor for early death. In these cases, the ‘stent first’ approach should be considered. In this study, we used this approach in only 3 cases. Therefore, future experience will show the usefulness of this approach.
We analysed the outcome of patients who have surgery for mycotic aortic infection and patients who have prosthetic graft infections. One could have expected that patients with prosthetic graft infections would have a higher risk, but we did not find a major difference in outcome in the 2 groups. The short- and long-term outcomes are extremely limited in both patient groups. Therefore, we conclude that both conditions are extremely lethal. Either native or prosthetic graft infection of the descending aorta should warrant the same aggressive surgical approach, aiming at complete excision of the infected aorta and/or the prosthetic graft if applicable.
Our survival analysis showed extremely poor outcomes, as reflected by the survival rates of 44% at 1 year and 39% at 3 years. However, the majority of deaths occurred during the initial perioperative period. Therefore, we also analysed the survival of ‘hospital survivors’, i.e. those patients who survived the initial perioperative period. We observed a more favourable outcome with this group, with survival rates of 81% at 1 year and 71% at 3 years. This result demonstrates that those patients who survive the initial perioperative period have an acceptable long-term prognosis.
Limitations
The number of patients in our retrospective study is low, which is attributed to the extremely low incidence of aortic infection. However, in light of the rare incidence of infection of the native or prosthetic aorta, we think that assembling 39 patients represents a serious contribution to this topic. Furthermore, the patients in this study were treated over a period of almost 20 years. Therefore, time might be regarded as a potential bias.
CONCLUSIONS
The results of this study confirm that infections of the native or prosthetic thoracic aorta are associated with both high morbidity and mortality. However, patients who survive the initial perioperative period have an acceptable long-term prognosis. In emergency situations, TEVAR implantation may help to stabilize critically ill patients and serve as a bridge to open repair.
SUPPLEMENTARY MATERIAL
Supplementary material is available at EJCTS online.
Funding
This study was funded by departmental grants.
Conflict of interest: none declared.
Author contributions
Saad Rustum: Data curation; Investigation; Methodology; Validation; Writing—original draft. Erik Beckmann: Conceptualization; Formal analysis; Investigation; Methodology; Supervision; Validation; Visualization; Writing—original draft. Andreas Martens: Conceptualization; Investigation; Methodology; Supervision. Heike Krueger: Data curation; Formal analysis; Investigation; Software. Morsi Arar: Data curation; Investigation; Methodology; Software. Tim Kaufeld: Data curation; Formal analysis; Investigation; Methodology. Axel Haverich: Conceptualization; Project administration; Resources; Supervision. Malakh Shrestha: Conceptualization; Project administration; Resources; Supervision.
Reviewer information
European Journal of Cardio-Thoracic Surgery thanks Mario Giovanni Gerardo D'Oria, Gabriele Piffaretti, Santi Trimarch and the other anonymous reviewers for their contribution to the peer review process of this article.
Presented at the 34th Annual Meeting of the European Association for Cardio-Thoracic Surgery, Barcelona, Spain, 8–10 October 2020.
REFERENCES
ABBREVIATION
Author notes
The first two authors contributed equally to this study.
