Ішек қантамырларының кеңеюі: себептері, диагностикасы және қауіп факторлары

AAAs occur most commonly in men, those over 50 and those with a family history of the disease. Genetic conditions with an increased risk include Marfan syndrome and Ehlers–Danlos syndrome. In the United Kingdom and Sweden, screening all men over 65 is recommended. Once an aneurysm is found, further ultrasounds are typically done on a regular basis. There does not appear to be a difference in longer term outcomes between the two. Repeat procedures are more common with EVAR. AAAs affect 2 8% of males over the age of 65. In those with an aneurysm less than 5.5 cm, the risk of rupture in the next year is below 1%. In the United States AAAs resulted in between 10,000 and 18,000 deaths in 2009.

The vast majority of aneurysms are asymptomatic. However, as the abdominal aorta expands and/or ruptures, the aneurysm may become painful and lead to pulsating sensations in the abdomen or pain in the chest, lower back, legs, or scrotum.

The complications include rupture, peripheral embolization, acute aortic occlusion, and aortocaval (between the aorta and inferior vena cava) or aortoduodenal (between the aorta and the duodenum) fistulae. On physical examination, a palpable and pulsatile abdominal mass can be noted. Bruits can be present in case of renal or visceral arterial stenosis. The bleeding can be retroperitoneal or into the abdominal cavity. Rupture can also create a connection between the aorta and intestine or inferior vena cava. Flank ecchymosis (appearance of a bruise) is a sign of retroperitoneal bleeding and is also called Grey Turner's sign.

The exact causes of the degenerative process remain unclear. There are, however, some hypotheses and well defined risk factors. Tobacco smoking: More than 90% of people who develop an AAA have smoked at some point in their lives. Alcohol and hypertension: The inflammation caused by prolonged use of alcohol and hypertensive effects from abdominal edema which leads to hemorrhoids, esophageal varices, and other conditions, is also considered a long term cause of AAA. Genetic influences: The influence of genetic factors is high. AAA is four to six times more common in male siblings of known patients, with a risk of 20–30%. The high familial prevalence rate is most notable in male individuals. There are many hypotheses about the exact genetic disorder that could cause higher incidence of AAA among male members of the affected families. Some presumed that the influence of alpha 1 antitrypsin deficiency could be crucial, while other experimental works favored the hypothesis of X linked mutation, which would explain the lower incidence in heterozygous females. Other hypotheses of genetic causes have also been formulated. Atherosclerosis: The AAA was long considered to be caused by atherosclerosis, because the walls of the AAA frequently carry an atherosclerotic burden. However, this hypothesis cannot explain the initial defect and the development of occlusion, which is observed in the process. Other causes of the development of AAA include: infection, trauma, arteritis, and cystic medial necrosis. There is also a reduced amount of vasa vasorum in the abdominal aorta (compared to the thoracic aorta); consequently, the tunica media must rely mostly on diffusion for nutrition, which makes it more susceptible to damage. Hemodynamics affect the development of AAA, which has a predilection for the infrarenal aorta. The histological structure and mechanical characteristics of the infrarenal aorta differ from those of the thoracic aorta. The diameter decreases from the root to the aortic bifurcation, and the wall of the infrarenal aorta also contains a lesser proportion of elastin. The mechanical tension in the abdominal aortic wall is therefore higher than in the thoracic aortic wall. The elasticity and distensibility also decline with age, which can result in gradual dilatation of the segment. Higher intraluminal pressure in patients with arterial hypertension markedly contributes to the progression of the pathological process.

An abdominal aortic aneurysm is usually diagnosed by physical exam, abdominal ultrasound, or CT scan. Plain abdominal radiographs may show the outline of an aneurysm when its walls are calcified. However, the outline will be visible by X ray in less than half of all aneurysms. Ultrasonography is used to screen for aneurysms and to determine their size if present. Additionally, free peritoneal fluid can be detected. It is noninvasive and sensitive, but the presence of bowel gas or obesity may limit its usefulness. CT scan has nearly 100% sensitivity for an aneurysm and is also useful in preoperative planning, detailing the anatomy and possibility for endovascular repair. In the case of suspected rupture, it can also reliably detect retroperitoneal fluid. Alternative less often used methods for visualization of an aneurysm include MRI and angiography. An aneurysm ruptures if the mechanical stress (tension per area) exceeds the local wall strength; consequently, peak wall stress (PWS), mean wall stress (MWS), and peak wall rupture risk (PWRR) have been found to be more reliable parameters than diameter to assess AAA rupture risk. Medical software allows computing these rupture risk indices from standard clinical CT data and provides a patient specific AAA rupture risk diagnosis. This type of biomechanical approach has been shown to accurately predict the location of AAA rupture.

Aortic aneurysm rupture may be mistaken for the pain of kidney stones, or muscle related back pain. Among this group who does not smoke, screening may be selective. In the United Kingdom the NHS AAA Screening Programme invites men in England for screening during the year they turn 65. Men over 65 can contact the programme to arrange to be screened. In Sweden one time screening is recommended in all males over 65 years of age. Australia has no guideline on screening. Repeat ultrasounds should be carried out in those who have an aortic size greater than 3.0 cm.

The treatment options for asymptomatic AAA are conservative management, surveillance with a view to eventual repair, and immediate repair. Two modes of repair are available for an AAA: open aneurysm repair, and endovascular aneurysm repair (EVAR). An intervention is often recommended if the aneurysm grows more than 1 cm per year or it is bigger than 5.5 cm. Repair is also indicated for symptomatic aneurysms. Ten years after open AAA repair, the overall survival rate was 59%. Mycotic abdominal aorta aneurysm (MAAA) is a rare and life threatening condition. Because of its rarity, there is a lack of adequately powered studies and consensus on its treatment and follow up. A management protocol on the management of mycotic abdominal aortic aneurysm was recently published in the Annals of Vascular Surgery by Premnath et al.

Conservative management is indicated in people where repair carries a high risk of mortality and in patients where repair is unlikely to improve life expectancy. The mainstay of the conservative treatment is smoking cessation. Surveillance is indicated in small asymptomatic aneurysms (less than 5.5 cm) where the risk of repair exceeds the risk of rupture.

No medical therapy has been found to be effective at decreasing the growth rate or rupture rate of asymptomatic AAAs.

The threshold for repair varies slightly from individual to individual, depending on the balance of risks and benefits when considering repair versus ongoing surveillance. The size of an individual's native aorta may influence this, along with the presence of comorbidities that increase operative risk or decrease life expectancy. Evidence, however, does not usually support repair if the size is less than 5.5 cm. In patients unfit for open repair, EVAR plus conservative management was associated with no benefit, more complications, subsequent procedures and higher costs compared to conservative management alone. Endovascular treatment for paraanastomotic aneurysms after aortobiiliac reconstruction is also a possibility. A 2017 Cochrane review found tentative evidence of no difference in outcomes between endovascular and open repair of ruptured AAA in the first month.

In those with aortic rupture of the AAA, treatment is immediate surgical repair. There appear to be benefits to allowing permissive hypotension and limiting the use of intravenous fluids during transport to the operating room.

AAA Size (cm) Growth rate (cm/yr) Annual rupture risk (%) 3.0–3.9 0.39 0 4.0–4.9 0.36 0.5–5 5.0–5.9 0.43 3–15 6.0–6.9 0.64 10–20 >=7.0 20–50
Although the current standard of determining rupture risk is based on maximum diameter, it is known that smaller AAAs that fall below this threshold (diameter<5.5 cm) may also rupture, and larger AAAs (diameter>5.5 cm) may remain stable. In one report, it was shown that 10–24% of ruptured AAAs were less than 5 cm in diameter. Vorp et al. later deduced from the findings of Darling et al. that if the maximum diameter criterion were followed for the 473 subjects, only 7% (34/473) of cases would have died from rupture prior to surgical intervention as the diameter was less than 5 cm, with 25% (116/473) of cases possibly undergoing unnecessary surgery since these AAAs may never have ruptured. It is also known that wall stress alone does not completely govern failure as an AAA will usually rupture when the wall stress exceeds the wall strength. In light of this, rupture assessment may be more accurate if both the patient specific wall stress is coupled together with patient specific wall strength. A noninvasive method of determining patient dependent wall strength was recently reported, with more traditional approaches to strength determination via tensile testing performed by other researchers in the field. Some of the more recently proposed AAA rupture risk assessment methods include: AAA wall stress; AAA expansion rate; degree of asymmetry; a rupture potential index (RPI); a finite element analysis rupture index (FEARI); biomechanical factors coupled with computer analysis; growth of ILT; geometrical parameters of the AAA; and also a method of determining AAA growth and rupture based on mathematical models. The postoperative mortality for an already ruptured AAA has slowly decreased over several decades but remains higher than 40%. However, if the AAA is surgically repaired before rupture, the postoperative mortality rate is substantially lower, approximately 1 6%.

The occurrence of AAA varies by ethnicity. In the United Kingdom, the rate of AAA in Caucasian men older than 65 years is about 4.7%, while in Asian men it is 0.45%. It is also less common in individuals of African, and Hispanic heritage. In the U. S., the incidence of AAA is 2–4% in the adult population. Rupture of the AAA occurs in 1–3% of men aged 65 or more, for whom the mortality rate is 70–95%.

The first historical records about AAA are from Ancient Rome in the 2nd century AD, when Greek surgeon Antyllus tried to treat the AAA with proximal and distal ligature, central incision and removal of thrombotic material from the aneurysm. However, attempts to treat the AAA surgically were unsuccessful until 1923. In that year, Rudolph Matas (who also proposed the concept of endoaneurysmorrhaphy), performed the first successful aortic ligation on a human. Other methods that were successful in treating the AAA included wrapping the aorta with polyethene cellophane, which induced fibrosis and restricted the growth of the aneurysm. Endovascular aneurysm repair was first performed in the late 1980s and has been widely adopted in the subsequent decades. Endovascular repair was first used for treating a ruptured aneurysm in Nottingham in 1994.

There have been many calls for alternative approaches to rupture risk assessment over the past number of years, with many believing that a biomechanics based approach may be more suitable than the current diameter approach. Numerical modeling is a valuable tool to researchers allowing approximate wall stresses to be calculated, thus revealing the rupture potential of a particular aneurysm. Experimental models are required to validate these numerical results and provide a further insight into the biomechanical behavior of the AAA. In vivo, AAAs exhibit a varying range of material strengths from localised weak hypoxic regions to much stronger regions and areas of calcifications. Finding ways to predict future AAA growth is seen as a research priority. Another related line of research is utilizing mathematical decision modeling (e. g., Markov decision processes) to determine improved treatment policies. Initial results suggest that a more dynamic policy could provide benefits, although such claims have not been clinically verified. A study recently showed that aneurysms can be accurately predicted as to whether they are stable (lacking repair or intervention), requiring repair, or at risk of rupture from scans years prior to any event based on a machine learning based classification tool.

Experimental models can now be manufactured using a novel technique involving the injection moulding lost wax manufacturing process to create patient specific anatomically correct AAA replicas. Work has also focused on developing more realistic material analogues to those in vivo, and recently a novel range of silicone rubbers was created allowing the varying material properties of the AAA to be more accurately represented. These rubber models can also be used in a variety of experimental situations, from stress analysis using the photoelastic method New endovascular devices are being developed that are able to treat more complex and tortuous anatomies.

An animal study showed that removing a single protein prevents early damage in blood vessels from triggering a later stage, complications. By eliminating the gene for a signaling protein called cyclophilin A (CypA) from a strain of mice, researchers were able to provide complete protection against abdominal aortic aneurysm. Other recent research identified Granzyme B (GZMB) (a protein degrading enzyme) to be a potential target in the treatment of abdominal aortic aneurysms. Elimination of this enzyme in mice models both slowed the progression of aneurysms and improved survival.

The mechanisms that lead to AAA development are still not completely understood at a cellular and molecular level. In order to better understand the pathophysiology of AAA, it is often necessary to use experimental animal models. It is often questioned how well do these models translate to human disease. Even though there is no animal model that exactly represents the human condition, all the existing ones focus on one different pathophysiological aspect of the disease. Combining the results from different animal models with clinical research can provide a better overview of the AAA pathophysiology. The most common animal models are rodents (mice and rats), although for certain studies, such as testing preclinical devices or surgical procedures, large animal models (pig, sheep) are more frequently used. The rodent models of AAA can be classified according to different aspects. There are dissecting models vs non dissecting models and genetically determined models vs chemically induced models. The most commonly used models are the angiotensin II infusion into ApoE knockout mice (dissecting model, chemically induced), the calcium chloride model (non dissecting, chemically induced) and the elastase model (non dissecting, chemically induced model). A recent study has shown that β Aminopropionitrile plus elastase application to abdominal aorta causes more severe aneurysm in mice as compared to elastase alone.