Get Abdominal Aortic Aneurysm essential facts below. View Videos or join the Abdominal Aortic Aneurysm discussion. Add Abdominal Aortic Aneurysm to your Like2do.com topic list for future reference or share this resource on social media.
Abdominal Aortic Aneurysm
Abdominal aortic aneurysm
CT reconstruction image of an abdominal aortic aneurysm (white arrows)
Abdominal aortic aneurysm (AAA or triple A) is a localized enlargement of the abdominal aorta such that the diameter is greater than 3 cm or more than 50% larger than normal diameter. They usually cause no symptoms except when ruptured. Occasionally, abdominal, back, or leg pain may occur. Large aneurysms can sometimes be felt by pushing on the abdomen. Rupture may result in pain in the abdomen or back, low blood pressure, or loss of consciousness, and often results in death.
Not smoking is the single best way to prevent the disease. Other methods of prevention include treating high blood pressure, treating high blood cholesterol and not being overweight. Surgery is usually recommended when an AAA's diameter grows to >5.5 cm in males and >5.0 cm in females. Other reasons for repair include the presence of symptoms and a rapid increase in size (more than one centimeter per year). Repair may be either by open surgery or endovascular aneurysm repair (EVAR). As compared to open surgery, EVAR has a lower risk of death in the short term and a shorter hospital stay, but may not always be an option. There does not appear to be a difference in longer term outcomes between the two. With EVAR there is a higher need for repeat procedures.
AAAs affect between 2 and 8% of males over the age of 65. Rates among women are one-fourth as high. In those with an aneurysm less than 5.5 cm the risk of rupture in the next year is less than 1%. Among those with an aneurysm between 5.5 and 7 cm, the risk is about 10%, while for those with an aneurysm greater than 7 cm the risk is about 33%.Mortality if ruptured is 85% to 90%. During 2013, aortic aneurysms resulted in 168,200 deaths, up from 100,000 in 1990. In the United States AAAs resulted in between 10,000 and 18,000 deaths in 2009.
Signs and symptoms
Abdominal aortic aneurysm location
The vast majority of aneurysms are asymptomatic. However, as abdominal aortic aneurysms expand, they may become painful and lead to pulsating sensations in the abdomen or pain in the chest, lower back, or scrotum. The risk of rupture is high in a symptomatic aneurysm, which is therefore considered an indication for surgery. 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 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-linkedmutation, which would explain the lower incidence in heterozygous females. Other hypotheses of genetic causes have also been formulated.Connective tissue disorders, such as Marfan syndrome and Ehlers-Danlos syndrome, have also been strongly associated with AAA. Both relapsing polychondritis and pseudoxanthoma elasticum may cause abdominal aortic aneurysm.
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 be used to explain the initial defect and the development of occlusion, which is observed in the process.
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. Suitable hemodynamic conditions may be linked to specific intraluminal thrombus (ILT) patterns along the aortic lumen, which in turn may affect AAA's development.
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, this is the case in less than half of all aneurysms. Ultrasonography is used to screen for aneurysms and to determine the size of any 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 a 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) 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.
Abdominal aortic aneurysms are commonly divided according to their size and symptomatology. An aneurysm is usually defined as an outer aortic diameter over 3 cm (normal diameter of the aorta is around 2 cm), or more than 50% of normal diameter. If the outer diameter exceeds 5.5 cm, the aneurysm is considered to be large.
A ruptured AAA is a clinical diagnosis involving the presence of the triad of abdominal pain, shock, and a pulsatile abdominal mass. If these conditions are present, indicating AAA rupture, no further clinical investigations are needed before surgery.
The suprarenal aorta normally measures about 0.5 cm larger than the infrarenal aorta.
The U.S. Preventive Services Task Force (USPSTF) recommends a single screening abdominal ultrasound for abdominal aortic aneurysm in males age 65 to 75 years who have a history of smoking. It is unclear if screening is useful in women who have smoked and the USPSTF recommend against screening in women who have never smoked.
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. This has been found to decrease the risk of death from AAA by 42% with a number needed to screen of just over 200. Australia has no guideline on screening.
Repeat ultrasounds should be carried out in those who have an aortic size greater than 3.0 cm. In those whose aorta is between 3.0 and 3.9 cm this should be every three years, if between 4.0 and 4.4 cm every two year, and if between 4.5 and 5.4 cm every year.
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.
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. As an AAA grows in diameter, the risk of rupture increases. Surveillance until an aneurysm has reached a diameter of 5.5 cm has not been shown to have a higher risk as compared to early intervention.
No medical therapy has been found to be effective at decreasing the growth rate or rupture rate of asymptomatic AAAs.Blood pressure and lipids should, however, be treated per usual.
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 support repair if the size is between 4 cm and 5.5 cm.
Open repair is indicated in young patients as an elective procedure, or in growing or large, symptomatic or ruptured aneurysms. The aorta must be clamped off during the repair, denying blood to the abdominal organs and sections of the spinal cord; this can cause a range of complications. It is essential to make the critical part of the operation fast, so the incision is typically made large enough to facilitate the fastest repair. Recovery after open AAA surgery takes significant time. The minimums are a few days in intensive care, a week total in the hospital and a few months before full recovery.
Abdominal aortic endoprosthesis, CT scan, original aneurysm marked in blue
Endovascular repair first became practical in the 1990s and although it is now an established alternative to open repair, its role is yet to be clearly defined. It is generally indicated in older, high-risk patients or patients unfit for open repair. However, endovascular repair is feasible for only a proportion of AAAs, depending on the morphology of the aneurysm. The main advantages over open repair are that there is less peri-operative mortality, less time in intensive care, less time in hospital overall and earlier return to normal activity. Disadvantages of endovascular repair include a requirement for more frequent ongoing hospital reviews, and a higher chance of further procedures being required. According to the latest studies, the EVAR procedure does not offer any benefit for overall survival or health-related quality of life compared to open surgery, although aneurysm-related mortality is lower. 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 appears to be benefits to allowing permissive hypotension and limiting the use of intravenous fluids during transport to the operating room.
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. It has also been reported that of 473 non-repaired AAAs examined from autopsy reports, there were 118 cases of rupture, 13% of which were less than 5 cm in diameter. This study also showed that 60% of the AAAs greater than 5 cm (including 54% of those AAAs between 7.1 and 10 cm) never experienced rupture. 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 succumbed to 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.
Alternative methods of rupture assessment have been recently reported. The majority of these approaches involve the numerical analysis of AAAs using the common engineering technique of the finite element method (FEM) to determine the wall stress distributions. Recent reports have shown that these stress distributions have been shown to correlate to the overall geometry of the AAA rather than solely to the maximum diameter. 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 non-invasive 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; presence of intraluminal thrombus (ILT); 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 post-operative 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 post-operative 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. They occur four times more often in men than women.
Rupture of the AAA occurs in 1-3% of men aged 65 or more, the mortality 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 distalligature, 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.
Society and culture
Theoretical physicist Albert Einstein was operated on for an abdominal aortic aneurysm in 1949 by Rudolph Nissen, who wrapped the aorta with polyethene cellophane. Einstein's aneurysm ruptured on April 13, 1955. He declined surgery, saying, "I want to go when I want. It is tasteless to prolong life artificially. I have done my share, it is time to go. I will do it elegantly." He died five days later at age 76.
Ouriel said that the team inserted a Y-shaped tube through an incision in Dole's leg and placed it inside the weakened portion of the aorta. The aneurysm will eventually contract around the stent, which will remain in place for the rest of Dole's life.
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.
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 testing from stress analysis using the photoelastic method to deterimining whether the locations of rupture experimentally correlate with those predicted numerically. New endovascular devices are being developed that are able to treat more complex and tortuous anatomies.
Prevention and treatment
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.
^ abcLeFevre ML (19 August 2014). "Screening for abdominal aortic aneurysm: U.S. Preventive Services Task Force recommendation statement". Annals of Internal Medicine. 161 (4): 281-90. doi:10.7326/m14-1204. PMID24957320.
^ abSvensjö, S; Björck, M; Wanhainen, A (December 2014). "Update on screening for abdominal aortic aneurysm: a topical review". European Journal of Vascular and Endovascular Surgery. 48 (6): 659-67. doi:10.1016/j.ejvs.2014.08.029. PMID25443524.
^Biancari F, Catania A, D'Andrea V (November 2011). "Elective endovascular vs. open repair for abdominal aortic aneurysm in patients aged 80 years and older: systematic review and meta-analysis". European Journal of Vascular and Endovascular Surgery. 42 (5): 571-6. doi:10.1016/j.ejvs.2011.07.011. PMID21820922.
^Paravastu SC, Jayarajasingam R, Cottam R, Palfreyman SJ, Michaels JA, Thomas SM (23 January 2014). "Endovascular repair of abdominal aortic aneurysm". The Cochrane Database of Systematic Reviews. 1: CD004178. doi:10.1002/14651858.CD004178.pub2. PMID24453068.
^Ilyas S, Shaida N, Thakor AS, Winterbottom A, Cousins C (February 2015). "Endovascular aneurysm repair (EVAR) follow-up imaging: the assessment and treatment of common postoperative complications". Clinical radiology. 70 (2): 183-196. doi:10.1016/j.crad.2014.09.010. PMID25443774.
^Doyle BJ, McGloughlin TM, Miller K, Powell JT, Norman PE (2014). "Regions of high wall stress can predict the future location of rupture in abdominal aortic aneurysm". Cardiovasc Intervent Radiol. 37 (3): 815-818. doi:10.1007/s00270-014-0864-7. PMID24554200.
^ abHirsch AT, Haskal ZJ, Hertzer NR, Bakal CW, Creager MA, Halperin JL, Hiratzka LF, Murphy WR, Olin JW, Puschett JB, Rosenfield KA, Sacks D, Stanley JC, Taylor LM, White CJ, White J, White RA, Antman EM, Smith SC, Adams CD, Anderson JL, Faxon DP, Fuster V, Gibbons RJ, Hunt SA, Jacobs AK, Nishimura R, Ornato JP, Page RL, Riegel B (September 2006). "ACC/AHA Guidelines for the Management of Patients with Peripheral Arterial Disease (lower extremity, renal, mesenteric, and abdominal aortic): a collaborative report from the American Associations for Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology, and the ACC/AHA Task Force on Practice Guidelines (writing committee to develop guidelines for the management of patients with peripheral arterial disease)--summary of recommendations". J Vasc Interv Radiol. 17 (9): 1383-97, quiz 1398. doi:10.1097/01.RVI.0000240426.53079.46. PMID16990459.
^Powell JT, Brown LC, Forbes JF, Fowkes FG, Greenhalgh RM, Ruckley CV, Thompson SG (Jun 2007). "Final 12-year follow-up of surgery versus surveillance in the UK Small Aneurysm Trial". Br J Surg. 94 (6): 702-8. doi:10.1002/bjs.5778. PMID17514693.
^Badger, S; Forster, R; Blair, PH; Ellis, P; Kee, F; Harkin, DW (26 May 2017). "Endovascular treatment for ruptured abdominal aortic aneurysm". The Cochrane Database of Systematic Reviews. 5: CD005261. doi:10.1002/14651858.CD005261.pub4. PMID28548204.
^Hamilton H, Constantinou J, Ivancev K (April 2014). "The role of permissive hypotension in the management of ruptured abdominal aortic aneurysms". The Journal of cardiovascular surgery. 55 (2): 151-9. PMID24670823.
^Brewster DC, Cronenwett JL, Hallett JW, Johnston KW, Krupski WC, Matsumura JS (May 2003). "Guidelines for the treatment of abdominal aortic aneurysms. Report of a subcommittee of the Joint Council of the American Association for Vascular Surgery and Society for Vascular Surgery". J. Vasc. Surg. 37 (5): 1106-17. doi:10.1067/mva.2003.363. PMID12756363.
^Darling RC, Messina CR, Brewster DC, Ottinger LW (September 1977). "Autopsy study of unoperated abdominal aortic aneurysms. The case for early resection". Circulation. 56 (3 Suppl): II161-4. PMID884821.
^Vande Geest JP, Wang DH, Wisniewski SR, Makaroun MS, Vorp DA (2006). "Towards A Noninvasive Method for Determination of Patient-Specific Wall Strength Distribution in Abdominal Aortic Aneurysms". Annals of Biomedical Engineering. 34 (7): 1098-1106. doi:10.1007/s10439-006-9132-6. PMID16786395.
^Raghavan ML, Kratzberg J, Castro de Tolosa EM, Hanaoka MM, Walker P, da Silva ES (2006). "Regional distribution of wall thickness and failure properties of human abdominal aortic aneurysm". Journal of Biomechanics. 39 (16): 3010-6. doi:10.1016/j.jbiomech.2005.10.021. PMID16337949.
^Raghavan ML, Webster MW, Vorp DA (1996). "Ex vivo biomechanical behavior of abdominal aortic aneurysm: assessment using a new mathematical model". Annals of Biomedical Engineering. 24 (5): 573-82. doi:10.1007/BF02684226. PMID8886238.
^Fillinger MF, Raghavan ML, Marra SP, Cronenwett JL, Kennedy FE (September 2002). "In vivo analysis of mechanical wall stress and abdominal aortic aneurysm rupture risk". Journal of Vascular Surgery. 36 (3): 589-97. doi:10.1067/mva.2002.125478. PMID12218986.
^Venkatasubramaniam AK, Fagan MJ, Mehta T, Mylankal KJ, Ray B, Kuhan G, Chetter IC, McCollum PT (August 2004). "A comparative study of aortic wall stress using finite element analysis for ruptured and non-ruptured abdominal aortic aneurysms". European Journal of Vascular and Endovascular Surgery. 28 (2): 168-76. doi:10.1016/j.ejvs.2004.03.029. PMID15234698.
^Hirose Y, Takamiya M (February 1998). "Growth curve of ruptured aortic aneurysm". The Journal of Cardiovascular Surgery. 39 (1): 9-13. PMID9537528.
^Wang DH, Makaroun MS, Webster MW, Vorp DA (September 2002). "Effect of intraluminal thrombus on wall stress in patient-specific models of abdominal aortic aneurysm". Journal of Vascular Surgery. 36 (3): 598-604. doi:10.1067/mva.2002.126087. PMID12218961.
^Doyle BJ, Callanan A, Walsh MT, Grace PA, McGloughlin TM (2009). "A finite element analysis rupture index (FEARI) as an additional tool for abdominal aortic aneurysm rupture prediction". Vascular Disease Prevention. 6: 114-121. doi:10.2174/1567270000906010114.
^Stenbaek J, Kalin B, Swedenborg J (November 2000). "Growth of thrombus may be a better predictor of rupture than diameter in patients with abdominal aortic aneurysms". European Journal of Vascular and Endovascular Surgery. 20 (5): 466-9. doi:10.1053/ejvs.2000.1217. PMID11112467.
^Giannoglou G, Giannakoulas G, Soulis J, Chatzizisis Y, Perdikides T, Melas N, Parcharidis G, Louridas G (2006). "Predicting the risk of rupture of abdominal aortic aneurysms by utilizing various geometrical parameters: revisiting the diameter criterion". Angiology. 57 (4): 487-94. doi:10.1177/0003319706290741. PMID17022385.
^Watton PN, Hill NA, Heil M (November 2004). "A mathematical model for the growth of the abdominal aortic aneurysm". Biomechanics and Modeling in Mechanobiology. 3 (2): 98-113. doi:10.1007/s10237-004-0052-9. PMID15452732.
^Vorp DA, Lee PC, Wang DH, Makaroun MS, Nemoto EM, Ogawa S, Webster MW (2001). "Association of intraluminal thrombus in abdominal aortic aneurysm with local hypoxia and wall weakening". Journal of Vascular Surgery. 34 (2): 291-299. doi:10.1067/mva.2001.114813. PMID11496282.
^Speelman L, Bohra A, Bosboom EM, Schurink GW, van de Vosse FN, Makaorun MS, Vorp DA (2007). "Effects of wall calcifications in patient-specific wall stress analyses of abdominal aortic aneurysms". Journal of Biomechanical Engineering. 129 (1): 105-109. doi:10.1115/1.2401189. PMID17227104.
^Doyle BJ, Morris LG, Callanan A, Kelly P, Vorp DA, McGloughlin TM (2008). "3D reconstruction and manufacture of real abdominal aortic aneurysms: From CT scan to silicone model". Journal of Biomechanical Engineering. 130 (3): 034501. doi:10.1115/1.2907765. PMID18532870.