Introduction
Infection of the aorta is rare but potentially very dangerous[1]. Under normal circumstances the aorta is very resistant to infections. Following
some afflictions, such as atherosclerotic ulcers, trauma, or cystic necrosis of the
tunica media, an infection can pass to the aorta from blood or surrounding tissues.
Other risk factors for infection of the aorta include diabetes mellitus, vascular
malformations, and any invasive catheterization[2]
[3]. Infection of the large arteries is always a serious and life-threatening disease,
especially in the case of aortic infection. Infection of the thoracic aorta in patients
with syphilis, which was relatively common in the past, has practically disappeared.
However, it has been replaced by other types of infections, especially of the abdominal
aorta, which are variable from the etiopathogenetic point of view. Whether typical
mycotic aneurysm (caused by septic embolism), infectious pseudoaneurysms, infected
preexisting aneurysms, or infectious aortitis, all these cases are always serious
and require acute therapy. However, the discussions on the method of therapy of these
emergency conditions [whether concerning the type of reconstruction (in situ/extra-anatomic),
the type of the graft used, or duration of antibiotic therapy] continue. Use of endovascular
methods of therapy remains controversial as well. The authors present their 5-year
experience with therapy of various types of infections of the abdominal aorta. They
discuss methods of diagnosis and therapy.
Methods
Data were collected from medical records. In the 5-year period between January 2008
and December 2012, in the Surgical Clinic of the University Hospital in Pilsen (tertiary
referral hospital for a large geographic area), we treated 17 patients with acute
infection of the abdominal aorta. These included patients with acute infectious perforated
aortitis, acute infectious symptomatic or rupturing aneurysm of the abdominal aorta,
or acute symptomatic pseudoaneurysm of the abdominal aorta ([Fig. 1]). These cases were always acute, not elective, surgeries with a positive culture
finding. They included 9 males and 8 females. The mean age was 73 years (range 58-90).
The most common pathogens were Salmonella (7), Staphylococcus aureus (2), Klebsiella pneumoniae (1), Listeria monocytogenes (1), and Candida albicans (1). Two cases included mixed bacteria and no infectious agent was cultured in three
cases ([Fig. 2]). In these 3 cases we were convinced of an infectious etiology based on further
information (medical history, clinical course, macroscopic appearance, laboratory
tests). The infectious microorganisms were obtained from a smear from the aortic wall
tissue or intraluminal thrombus; blood culture was the source of the result in 6 cases.
Figure 1. Demographics of patient group by diagnosis. The group included patients with acute
infectious perforated aortitis, acute infectious symptomatic or rupturing aneurysm
of the abdominal aorta, or acute symptomatic pseudoaneurysm of the abdominal aorta.
Figure 2. Demographics of patient group by infectious organism. Two cases included mixed bacteria
and no infectious agent was cultured in three cases.
In 14 cases (82.6%) we decided on an open surgical solution, i.e., resection of the
affected abdominal aorta, extensive debridement, and vascular reconstruction. In all
14 cases we decided on in situ reconstruction. Twelve cases were treated using silver-impregnated
prostheses. An antibiotic (ATB; rifampicin)-impregnated graft was used in one case,
and fresh aortic allograft in one case.
In one case (5.9%) we decided on an endovascular solution, i.e., insertion of a bifurcation
stent graft and prolonged antibiotic therapy.
In two cases (11.8%) we decided on a conservative procedure as both patients refused
any surgical therapy. Detailed information on the group of patients is included in
[Table 1].
Table 1.
Details of Patient Group
|
No.
|
Sex
|
Age
|
Pathogen
|
Imagine finding
|
ATB
|
Therapy
|
Hospital outcome
|
Late
outcome
|
|
1
|
1F
|
88
|
Staphyloccocus aureus
|
Subrenal aorta pseudoaneurysm
|
Ceftriaxon
|
Resection, ABI bypass (silvergraft)
|
Ok, discharged 17th day
|
Alive 2 years after surgery
|
|
2
|
M
|
62
|
Salmonella enters
|
Symptom. aortitis
|
Ciprofloxacin, Ampicilin
|
Resection, ABI bypass (allograft)
|
Ok, discharged 15th day
|
Alive 4 years after surgery
|
|
3
|
M
|
62
|
Salmonella enteritidis
|
AAA rupture
|
Ceftriaxon
|
Resection, AA graft (silvergraft)
|
OK, dischargerd 51st day
|
Alive 1 year after surgery
|
|
4
|
M
|
64
|
Salmonella enteritidis
|
Perforated aortitis
|
Ampicilin, Ciprofloxacin
|
Resection, AA graft (silovergraft)
|
OK, discharged 8th day
|
Alive 5 years after surgery
|
|
5
|
F
|
89
|
Salmonella enteritidis
|
Perforated aortitis
|
Ciprofloxacin
|
Resection, AA graft (ATB graft)
|
OK, discharged 24th day
|
Died 2 months after surgery
|
|
6
|
F
|
89
|
Stahyloccocus aureus
|
AAA rupture
|
0
|
Conservative
|
Died 4 th day, refuse surgery
|
|
|
7
|
F
|
90
|
Mixed
|
Perforated aortitis
|
Vancomycin
|
EVAR
|
OK, discharged 16th day
|
Alive 1 year after EVAR
|
|
8
|
F
|
89
|
Klebsiela pneumonie
|
Subrenal aorta pseudoaneurysm
|
Amoxicilin
|
Conservative
|
OK, discharged 14th day
|
Alive 2 years after diagnostic
|
|
9
|
M
|
84
|
Unknown
|
Symptomatic AAA
|
Ciprofloxacin, Ampicilin
|
Resection, AA graft (silvergraft)
|
OK, discharged 8th day
|
Unknown
|
|
10
|
M
|
78
|
Salmonella enteritidis
|
AAA rupture
|
Ciprofloxacin
|
Resection, ABF bypass (silvergraft)
|
OK, discharged 20th day
|
Alive 4 years after surgery
|
|
11
|
F
|
69
|
Mixed
|
Aorto-duodenal fistula
|
PNC, Genta, Metronidazol
|
Resection, ABF bypass (silvergraft)
|
OK, discharged 26th day (limb lost)
|
Alive 2 years after surgery
|
|
12
|
M
|
63
|
Listeria monocytogenes
|
Perforated aortitis
|
Gentamycin, Ampicilin
|
Resection, AA graft (silvergraft)
|
OK, discharged 18th day
|
Alive 2 years after surgery
|
|
13
|
M
|
62
|
Salmonella enteritidis
|
Perforated aortitis
|
Ciprofloxacin, Cefotaxim
|
Resection, AA graft (silvergraft)
|
OK, discharged 8th day
|
Unknown
|
|
14
|
F
|
59
|
Salmonella species
|
Perforated aortitis
|
Ciprofloxacin
|
Resection, AA graft (silvergraft)
|
OK, discharged 14th day
|
Alive 3 years after surgery
|
|
15
|
F
|
58
|
Candida albicans
|
Symptomatic AAA
|
Cefazolin
|
Resection, AA graft (silvergraft)
|
OK, discharged 12th day
|
Alive 3 years after surgery
|
|
16
|
M
|
65
|
Unknown
|
Aortoduodenal fistula
|
Vancomycin
|
Resection, ABF bypass (silvergraft)
|
OK, discharged 31st day
|
Alive 6 months after surgery
|
|
17
|
M
|
71
|
Unknown
|
Perforated aortitis
|
Vancomycin
|
Resection, AA graft (silvergraft)
|
OK, discharged 28th day
|
Unknown
|
PNC + penicili.
Results
Morbidity in our group of patients was 47.2% (8 patients). This most commonly included
transient respiratory failure (associated with comorbidities of the patients and duration
of surgery), renal failure, and wound infection. In one case we had to perform a reoperation
on a patient on the 15th postoperative day to evacuate a postoperative hematoma.
The 30-day mortality was 5.9% (1 patient). This was a female patient with rupture
of the abdominal aortic aneurysm (AAA) who refused surgery. She died on the 4th day
following admission to hospital. The hospitalization mortality was 11.8% (2 patients).
One patient, following resection of perforated aortitis, died on the 42nd postoperative
day due to multiorgan failure.
During follow-up (average 3.5 years), we had no case of infection or thrombosis in
the vascular prosthesis (one patient was lost to follow-up).
Discussion
Aortic ruptures in patients with syphilis were described as early as the 16th century.
In the 19th century, Kochr and Rokitanski described case reports of rupturing infectious
aortic aneurysms[11]. In 1885, William Osler gave a lecture for the Royal College of Physicians in London
in which he described a mycotic aneurysm “caused most probably by an alleged fungal infection[11].”
Since that time, a number of types of infectious aortitides have been described. In
the preantibiotic era they were caused mostly by streptococcus during infectious endocarditis.
A significant reduction of this etiopathogenetic agent occurred following the advent
of antibiotic therapy. However, other mechanisms of infectious aortitides and other
infectious agents have emerged. Under normal circumstances, the aorta is well resistant
against infection (tunica intima is a barrier). Infectious aortitis often has roots
in existing aortic pathology, including atherosclerosis and ulceration. Also, immunocompromised
individuals (chronic disease or medication) are vulnerable; the infection can spread
from bacteremia (e.g., following salmonella gastroenteritis, pneumococcal bronchopneumonia)
or by direct extension from the surrounding organs (pancreas, intervertebral disc).
The risk factors for aortic infection include any catheterization procedures (infection,
injury of tunica intima)[2]
[3]. Post-traumatic lesions may also be involved. It is not clear why there is a significant
epidemiological difference between the European and Asian population. Incidence of
aortic infection in the European—but also American—population ranges between 1 and
2%[4]
[5]
[6], while in the Asian population it is around 13%[6]. The typical age for infection of the aorta is > 50 years, but cases have been described
in the literature in all age groups, including newborns[3]
[4].
Most authors report that more than one third of pathogens are represented by Salmonella, and the other microorganisms include Staphylococcus, Pneumococcus, Escherichia coli, Streptococcus
[1]
[7], and, more rarely, Candida, Aspergillus, and Listeria monocytogenes. The aneurysms caused by Gram-negative bacteria have a much higher risk of expansion
and rupture compared to Gram-positive infections[8]. The results of cultivation of pathogens in our group correspond to the literature
data, with a dominance of Salmonella. In three cases we failed to cultivate a pathogen, which is also in compliance with
the literature data[9]. Preoperatively initiated antibiotic therapy may be the reason. It has to be emphasized
that, based on the literature, approximately 30% of AAAs are colonized mostly by less
virulent strains[10], and these aneurysms cannot be classified as mycotic or infectious. Therefore, a
positive microbiological finding from the AAA sac does not necessarily mean an infectious
etiopathogenesis of the aneurysm.
Nomenclature for infections of the aorta is problematic. Most authors use the term
mycotic aneurysm for all infectious aneurysms. In clinical practice it is a fully
sufficient name that describes infectious etiology. From the didactical point of view,
we should differentiate between various etiopathogenetic mechanisms, which are well
described in the Rutherford classification of infections of the aorta[11]. In our group of patients, we recorded all types from the four categories of this
classification (mycotic aneurysm, microbial aortitis, infected preexisting aneurysm,
infectious pseudoaneurysm).
In some cases the single categories are mixed. An infected pseudoaneurysm occurs commonly
in the case of aortic perforation on the basis of infected atherosclerotic plaque.
Therefore, is it a perforated aortitis or infected pseudoaneurysm? These discussions
have absolutely no bearing on the diagnosis and therapy.
The symptoms depend on the type of infection. In the case of aortic perforation, the
typical signs are the same as in the rupture of a common aneurysm. In nonbleeding
lesions, the course can be transiently asymptomatic; however, more often, there can
be seen fever, abdominal and back discomfort, tiredness, exhaustion, and signs of
sepsis. Four patients in our group reported severe gastroenteritis in the recent 4
weeks, out of which two had a positive cultivation for Salmonella during their gastroenteritis. Both patients with primary aortic-duodenal fistula
had signs of bleeding into the upper gastrointestinal tract.
Following careful medical history and physical examination, standard imaging methods
are most beneficial for diagnosis. We preferred mostly CT (computer tomography); rarely,
we used MRI or the hybrid methods [positron emission tomography with CT (PET CT),
or single-photon emission CT (SPECT)]. A typical picture of aortitis or mycotic aneurysm
is a thickened margin of hyperdense tissue around the aortic wall, and there is often
a suspicion of leakage from the aneurysm. Bubbles of gas indicate an advanced finding
and practically an abscess in the retroperitoneum or the presence of a fistula between
the aorta and gastrointestinal tract (mostly duodenum) ([Fig. 3]). In infected aneurysms, a rapid increase of diameter may occur up to the point
of rupture.
Figure 3. A typical CT scan of aortitis or mycotic aneurysm.
Bizarre eccentric shapes of the AAA may be seen ([Fig. 4]). If a perforation of the nondilated aorta occurs (mostly on the basis of rupture
at the site of the infected atherosclerotic plaque), a pseudoaneurysm often develops
and no massive extravascular leakage usually occurs ([Fig. 5]).
Figure 4. Characteristics of the of the AAA.
Figure 5. A pseudoaneurysm.
Patients with infectious aortitis should be immediately indicated for the relevant
therapy. Preoperative preparation should include only the necessary steps and must
not cause unnecessary delay of surgery. In our group of patients, we mostly decided
on surgery (open repair), which is still a gold standard of therapy. Open questions
remain regarding options for reconstruction. However, in recent years, most authors
prefer anatomic (in situ) reconstruction using grafts which are more resistant to
inflammation[12]
[13]. We also used in situ reconstruction in all cases. In extra-anatomical reconstructions,
there is poorer long-term patency, and the main disadvantage is the risk of failure
of the suture line of the aortic stump, so-called “stump blowout syndrome,” which
is practically always fatal. Silver-impregnated prostheses are popular and were used
extensively in our series. In one case we used a prosthesis saturated with antibiotic
and in one case a fresh aortic allograft. Use of fresh or cryopreserved aortic allografts
is beneficial as it is associated with minimum risk of reinfection. However, it has
disadvantages, including the necessary immunosupression; also, the logistics of obtaining
the allograft in acute conditions are not easy. We have not used reconstruction with
superficial femoral veins, which is mentioned in the literature[14]. A certain disadvantage associated with this method is the extension of time of
surgery, and the veins cannot always be used in acute conditions. Always, when we
expected an infectious etiology, we initiated therapy with broad-spectrum bactericidal
antibiotics administered preoperatively; later, we adjusted this therapy based on
the results of microbiological cultivation. In our opinion, the antibiotic therapy
should never be shorter than 2 months, and a control CT and examination of inflammatory
markers should be performed before its discontinuation.
Endovascular therapy is still a bit controversial in this field, even though there
is considerable literature data justifying this method[15]
[16]
[17]
[18]
[19]
[20]. Some studies report successful therapy of mycotic AAA with a retroperitoneal abscess
using a stent graft and percutaneous drainage[15]
[21]. We used stent grafts once in our group of patients in acute symptomatic aortitis
with a good result. A study with long-term results is missing in this field. Endografting
can be considered as a possible method of solution for infectious aneurysms or aortitides.
In some cases, it may serve as a bridge, i.e., bridging of the acute phase before
later resection.
Most authors agree that simple conservative therapy with antibiotics is absolutely
insufficient, with mortality almost 100%[22]. In our group of patients, we used conservative therapy in two cases, and a patient's
refusal regarding an invasive solution was always accepted. One female patient died
due to rupture of the mycotic AAA; another female patient is undergoing successful
conservative treatment of infectious pseudoaneurysm. The follow-up period in this
female patient is now 2 years, and she has no complications.
Morbidity of patients with an aortic infection is often related to a number of comorbidities
occurring in elderly patients and depends also on the severity, or the surgical or
endovascular procedure. Respiratory failure, renal failure, or multiorgan failure
is most common. Wound infection occurs more commonly compared to routine vascular
reconstruction. The most serious complication is the infection of the graft. We had
no such case in our group of patients (the mean follow-up period is 3 years).
Patients with mycotic aneurysms or acute aortitides always have a high risk of death.
There are five known independent factors associated with high mortality: extensive
periaortic infection, female gender, Staphylococcus aureus as an infectious agent, aortic rupture, and suprarenal location[23]. These patients should be referred to cardiovascular centers which have greater
experience with aortic therapy. One can legitimately expect an increase of “aortic
infections” with regard to increase of immunocompromised individuals (chronic diseases,
HIV, chronic medication, post-transplantation state). The required surgical procedures
are always demanding and require excellent interdisciplinary cooperation and a thoughtful
approach to the patient.
