on 14-Feb-2021 (Sun)

Although Takayasu arteritis and giant cell arteritis are the most common rheumatologic causes of aortitis, the other systemic diseases, such as rheumatoid arthritis, systemic lupus erythematosus, Behçet disease, and Cogan syndrome, may also be associated with aortitis

Pyogenic aortitis secondary to Salmonella species and Staph- ylococcus aureus infection is the commonest form of infectious aortitis, whereas the large-vessel vasculitides, such as Ta- kayasu arteritis (TA) and giant cell arteritis (GCA), are the common types of noninfectious aortitis.

In patients with a clinical suspicion of aortitis, an emergent evaluation of the entire aorta with an appropriate imaging technique is critical for the diagnosis and appropriate man- agement. The major goals of imaging of these patients include evaluation of the aortic wall changes, luminal changes, and disease extent

The common computed tomography (CT) find- ings of aortitis include irregular aortic wall thickening with associated periaortic fat stranding. CT is less sensitive in as- sessing periaortic inflammation and disease activity. The other disadvantages of CT include radiation exposure and administration of iodinated contrast.

Both aortic wall as well as lumen can be evaluated with MRA, and accurate characterizations of the vessel wall with dedicated MRI protocols such as “edema-weighted” se- quences have been used. 5 In addition, disease activity, extent of the aneurysms, and arterial stenoses can be assessed with MRA

Among all, S. pneumoniae and Enterococcus are com- monly involved in thoracic aortitis, whereas Salmonella infection is most prevalent in abdominal aortitis

Abdominal pain, chest/back pain, fever, and chills are the most frequent clin- ical findings. Patients with aneurysms are more symptomatic than those without aneurysms

Imaging findings of infectious aortitis include aortic wall thickening with or without contrast enhancement, periaortic soft tissue mass, fluid collections, fat stranding, rapidly progressing saccular aneurysms, and air within the aortic wall 2,8 (Fig. 1)

Advanced age, delay in diagno- sis, thoracic location, immunosuppression, gram-negative bacilli infection, and complicated cases show worse progno- sis.

Without appropriate treatment, natural progression of infectious aortitis is rapid with the develop- ment of mycotic aneurysms and subsequent rupture. In some patients, aortic rupture may occur without the formation of aneurysm.

Infectious aortitis is almost always fatal if left un- treated; however, the combination of appropriate medical and surgical therapy may lead to a survival rate of 75%-100% before aneurysm formation

Pyogenic Aortitis Salmonella species, Clostridium, S. pneumoniae, and Staphylo- coccus are the common bacterial pathogens associated with infectious aortitis; among them, Salmonella is the commonest bacterium that usually affects the native aorta. 10

Sudden de- velopment of fever and abdominal/chest pain in an elderly patient who has positive blood cultures for Salmonella should arise the suspicion of aortitis and should be evaluated accord- ingly.

Prevalence and etiology Mycotic aneurysms reflect fewer than 1% of aortic aneurysms that are surgically repaired, are more common in men, and are more likely to rupture than non-infected aneurysms (2-5)

Mycotic aneurysms are more likely to occur in the aorta than other arteries (6-8)

Previously, MAs were associated with endocarditis, β -hemolytic group A streptococci, pneumococci, and Haemophilus influenza (8,9). Since the introduction of more targeted antibiotic regimens, MAs are more commonly associated with intravascular intervention and intravenous drug abuse, and Staphylococcus and Salmonella (6,9)

Syphilitic aortitis is rare but may cause aortic wall thickening and aneurysmal dilatation, and is typically limited to the ascending and thoracic aorta (10).

MAs are thought to arise due to degeneration of the arterial wall (8). MAs tend to more rapidly progress compared with non-infected aneurysms: the acute inflammation in response to pathogenic infection resulting in neutrophilic infiltration of the arterial wall (4,11,12) leads to the activation of collagenolytic and elastolytic enzymes and concomitant breakdown and saccular dilation (13-15). This process leads to the characteristic saccular appearance of MAs.

Typically, infection initiates in a nidus such as in an ulcerated atherosclerotic plaque or in the vasa vasorum (12). The vasa vasorum is thought to be key in the pathogenesis of MA formation; due to its small lumen size and slower flow, it is more susceptible to bacterial colonization (19,20). The vasa vasorum is more pronounced in larger arteries, which may explain why the aorta is the most common site of MA formation

In the setting of pre-existing endocarditis, prior invasive procedures, intravenous drug use or immunocompromise should increase suspicion (8,24)

Certain features may distinguish MA from non-infected aneurysms, including serial imaging which may reveal rapid progression typical of infected aneurysms. Other characteristic features include contrast-enhancement and a saccular outpouching configuration, whereas non-infected atherosclerotic aneurysms tend to be fusiform (28). Saccular configuration may also suggest imminent rupture, alerting the need for further urgent diagnostic workup. Other features include irregularity of the arterial wall and peri-aortic gas, edema, mass or stranding (28)

Due to its elusive presentation, MA is often difficult to treat because of delayed diagnosis. Rapid diagnosis and treatment is key, as aortic MA is associated with 15–50% mortality (7-9,24)

Antibiotics are tailored based on culture sensitivity when available. When cultures are not available, consultation with one’s infectious disease specialists is suggested, as there are regional differences in antibiotic resistance. No consensus exists regarding the duration of antibiotic course, with some advocating for life-long suppressive antibiotics while others suggest at minimum a 6–8-week post-operative course (30)

Aortic MAs usually necessitate surgical repair, with two possible available approaches including extraanatomic bypass (EAB) and in situ graft placement. By tradition, EAB has been used for infrarenal aneurysms and in situ graft placement for thoracic or suprarenal aneurysms. While EAB avoids graft placement within an infected field, it may lead to aortic stump disruption, amputation, and reinfection (2,3,21,31). Several graft materials are available for in situ graft placement, such as silver-coated grafts, cryopreserved arterial allografts, rifampicin-impregnated grafts, and autogenous vein grafts (2,32-34)

A large multicenter retrospective series of endovascular repair of 130 aortic MAs in 123 patients reported 91% 1-month survival and 75% 1-year survival at 1 year; only 6 were converted to open repair (39). Open surgery remains the gold standard intervention (40), though endovascular treatment can be considered as a temporizing measure particularly for critically ill patients (41).

Nonaneurysmal infectious aortitis Infectious aortitis most commonly presents as a MA, though there are case reports of nonaneurysmal infection (42). Nonaneurysmal infectious aortitis is more difficult to diagnose on imaging than MA, given the lack of aortic dilation, but even so may be complicated by rupture (43,44). A more recent case report described achieving an elusive diagnosis of infectious nonaneurysmal infectious aortitis by using broad-range polymerase chain reaction and DNA sequencing, which allowed for identification of the microbial species despite negative blood cultures (45)

The incidence of graft infection after aortic aneurysm repair is low, below 0.5%, and is equally likely with open or endovascular repair, despite the finding that open repair was more likely to be complicated perioperative septicemia, pneumonia, and surgical site infection (46). Infections within the first 3 post-operative months are considered early and those after 3 months are considered late.

For patients who present with infection within 3 months of repair, contamination during endograft placement is considered the likely source (47). Aortoenteric and aortobronchial fistulas are a common cause of infection and portend a poorer prognosis (Figure 1) (48). Culprit organisms include Staphylococcus, Streptococcus and Propionibacterium species, Enterobacter cloacae, Escherichia coli, Pseudomonas aeruginosa, and Listeria monocytogenes (47,49)

In one study, graft infection was more common after thoracic endovascular aneurysm repairs (EVAR) (5%) compared to aortic aneurysm repairs (0.3%) (49), though another study showed no significant difference in rates (47). Emergent repairs are more likely to be complicated by graft infection than elective procedures (47)

Diagnosis Clinically, patients present with constitutional symptoms including pain, fever and chills, which may prompt suspicion for postoperative infection (49,50). Aortic graft infections occurring more than 3 months after repair are initially evaluated with CT or MRI, which may reveal ectopic gas, peri-graft inflammation and fluid, thickening of adjacent bowel, and pseudoaneurysm formation at the graft anastomosis (51). Imaging may reveal contained rupture or abscess formation (49). Imaging is problematic in the first 3 months following repair, as peri-graft fluid and inflammation may be normally present. Radionuclide scanning, particularly with white blood cell labeling, may helpful to diagnose early vascular graft infection (51,52)

Henryk Jerzy Chmielewski, ps. Papcio Chmiel (ur. 7 czerwca 1923 w Warszawie^[1], zm. 22 stycznia 2021 tamże^[2][3]) – polski grafik, rysownik i publicysta, autor serii komiksowej „Tytus, Romek i A’Tomek”, powstaniec warszawski. Kawaler Orderu Orła Białego^[4].

You will read the word “static” a lot in Java tutorials or books. So it is better to form a clear understanding of this word as soon as possible. In English, the word static means something that doesn‘t change or move. From that perspective, it is a misnomer in Java. Java has a different word for something that doesn’t change: final. I will talk more about “final” later

You will read the word “static” a lot in Java tutorials or books. So it is better to form a clear understanding of this word as soon as possible. In English, the word static means something that doesn‘t change or move. From that perspective, it is a misnomer in Java. Java has a different word for something that doesn’t change: final. I will talk more about “final” later

Each instance of that class is then the cookie and each field will be imprinted on the cookie - except the fields defined as static. In that sense, a static member is kind of a tag stuck to a cookie cutter. It doesn’t apply to the instances. It stays only with the class