Abdominal aortic aneurysm
Abdominal aortic aneurysm
Classification & external resources
|| I71.3, I71.4
|| 441.3, 441.4
|| med/3443 emerg/27 radio/1
Abdominal aortic aneurysm, also written as AAA and often pronounced 'triple-A', is a localized dilatation of the abdominal aorta, that exceeds the normal diameter by more than 50%. The normal diameter of the infrarenal aorta is 2 cm. It is caused by a degenerative process of the aortic wall, however the exact etiology remains unknown. It is most commonly located infrarenally (90%), other possible locations are suprarenal and pararenal. The aneurysm can extend to include one or both of the iliac arteries. An aortic aneurysm may also occur in the thorax.
The first historical records about AAA are from Ancient Rome, more precisely from the 2nd century AD, when Greek surgeon Antyllus tried to treat the AAA with proximal and distal ligature, central incision and evacuation 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. Albert Einstein was operated on by Rudolf Nissen with use of this technique in 1949, and survived five years after the operation.
AAA is uncommon in individuals of African, African American, Asian, and Hispanic heritage. The frequency varies strongly between males and females. The peak incidence is among males around 70 years of age, the prevalence among males over 60 years totals 2-6%. The frequency is much higher in smokers than in non-smokers (8:1). Other risk factors include hypertension and male sex. In the US, 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, the mortality is 70-95%.
The exact causes of the degenerative process remain unclear. There are, however, some theories and risk factors defined.
- Genetic influences: The influence of genetic factors is highly probable. The high familial prevalence rate is most notable in male individuals. There are many theories 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, some experimental works favored the theory of X-linked mutation, which would explain the lower incidence in heterozygous females. Other theories of genetic etiology were also formulated.
- Hemodynamic influences: Abdominal aortic aneurysm is a focal degenerative process with predilection for the subrenal aorta. The histological structure and mechanical characteristics of subrenal aorta differ from those of the thoracic aorta. The diameter decreases from the root to the bifurcation, and the wall of the abdominal aorta also contains a lesser proportion of elastin. The mechanical tension in 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.
- Atherosclerosis: The AAA was long considered to be caused by atherosclerosis, because the walls of the AAA are frequently affected heavily. However, this theory cannot be used to explain the initial defect and the development of occlusion, which is observed in the process.
The most striking histopathological changes of aneurysmatic aorta are seen in tunica media and intima. These include accumulation of lipids in foam cells, extracellular free cholesterol crystals, calcifications, ulcerations and ruptures of the layers and thrombosis. There is an adventitial inflammatory infiltrate.
However, the degradation of tunica media by means of proteolytic process seems to be the basic pathophysiologic mechanism of the AAA development. Some researchers report increased expression and activity of matrix metalloproteinases in individuals with AAA. This leads to elimination of elastine from the media, rendering the aortic wall more susceptible to the influence of the blood pressure.  Other pathophysiological cause for development of the AAA is inflammation.
A clinical practice guideline by the U.S. Preventive Services Task Force (USPSTF) 'recommends one-time screening for abdominal aortic aneurysm (AAA) by ultrasonography in men age 65 to 75 years who have ever smoked'. This is a grade B recommendation. An re-analysis of the meta-analysis estimated a number needed to screen of approximately 850 patients.
In the USA, effective January 1, 2007, provisions of the SAAAVE Act (Screening Abdominal Aortic Aneurysm Very Efficiently) now provide a free, one-time, ultrasound AAA screening benefit for those qualified seniors. Men who have smoked at least 100 cigarettes during their life, and men and women with a family history of AAA qualify for the one-time ultrasound screening.
Enrollees must visit their healthcare professional for their Welcome to Medicare physical within six months of enrollment in order to qualify for the free screening.
The Welcome to Medicare Physical Exam must be completed within the first six months of Medicare eligibility, but there is no published time limit thereafter for completion of the AAA screening. Providers who perform the physical and order the AAA screening need to document the AAA risk factors.
The largest of the randomized controlled trials on which this guideline was based studied a screening program that consisted of:
- Screening men ages 65-74 years (not restricted to ever smokers). 'Men in whom abdominal aortic aneurysms (> or =3 cm in diameter) were detected were followed-up... Patients with an aortic diameter of 3·0–4·4 cm were rescanned at yearly intervals, whereas those with an aortic diameter of 4·5–5·4 cm were rescanned at 3-monthly intervals ... Surgery was considered on specific criteria (diameter > or =5.5 cm, expansion > or =1 cm per year, symptoms)'.
This trial reported significant short ( number needed to screen after 4 years of approximately 590 to prevent nonfatal ruptured AAA plus AAA-related deaths) and long term ( number needed to screen after 7 years of approximately 280 to prevent nonfatal ruptured AAA plus AAA-related deaths) benefit and cost effectiveness. Subsequent randomized controlled trials also found benefit:
Manifestations and Diagnosis
AAAs are commonly divided according to their size and symptomatology. An aneurysm is usually considered to be present if the measured outer aortic diameter is over 3 cm (normal diameter of aorta is around 2 cm). The natural history is of increasing diameter over time, followed eventually by the development of symptoms (usually rupture). If the outer diameter exceeds 5 cm, the aneurysm is considered to be large. For aneurysms under 5 cm, the risk of rupture is low, so that the risks of surgery usually outweigh the risk of rupture. Aneurysms less than 5cm are therefore usually kept under surveillance until such time as they become large enough to warrant repair, or develop symptoms.
The vast majority of aneurysms are asymptomatic. The risk of rupture is high in a symptomatic aneurysm, which is therefore considered an indication for surgery. Possible symptoms include low back pain, flank pain, abdominal pain, groin pain or pulsating abdominal mass. The complications include rupture, peripheral embolisation, acute aortic occlusion, aortocaval or aortoduodenal fistulae. On physical examination, a palpable abdominal mass can be noted. Bruits can be present in case of renal or visceral arterial stenosis.
As most of the AAAs are asymptomatic, their presence is usually revealed during an abdominal examination for another reason - the most common being abdominal ultrasonography. A physician may also detect the presence of an AAA by abdominal palpation. Ultrasonography provides the initial assessment of the size and extent of the aneurysm, and is the usual modality for surveillance. Preoperative examinations include CT, MRI and special modes thereof, like CT/MR angiography. Angiography may be useful also, as an additional method of measurement for the planning of endoluminal repair. Note that an aneurysmal aorta may appear normal on angiogram, due to thrombus within the sac.
The clinical manifestation of ruptured AAA can include low back, flank, abdominal or groin pain, but the bleeding usually leads to a hypovolemic shock with hypotension, tachycardia, cyanosis, and altered mental status. The mortality of AAA rupture is 75-90%, with 65% of patients dying before they arrive at hospital. The bleeding can be retroperitoneal or intraperitoneal, or the rupture can create an aortocaval or aortointestinal fistula.. Flank ecchymosis is a sign of retroperitoneal hemorrhage, and is also called the Grey-Turner sign.
Ruptured AAA is a clinical diagnosis: the presence of the triad of abdominal pain, shock and pulsatile abdominal mass makes the diagnosis; no further investigations are required for diagnostic purposes, and imaging should be avoided unless specifically requested by a vascular surgeon.
The treatment options for asymptomatic AAA are immediate repair, surveillance with a view to eventual repair, and conservative.
There are currently two modes of repair available for an AAA: open aneurysm repair (OR), and endovascular aneurysm repair (EVAR).
- Conservative treatment is indicated in patients where repair carries a high risk of mortality and also in patients where repair is unlikely to improve life expectancy. The two mainstays of the conservative treatment are smoking cessation and blood pressure control.
- Surveillance is indicated in small aneurysms, where the risk of repair exceeds the risk of rupture. As an AAA grows in diameter the risk of rupture increases. Although some controversy exists around the world, most vascular surgeons would not consider repair until the aneurysm reached a diameter of 5cm. 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 comorbitities that increase operative risk or decrease life expectancy.
- Open repair (operation) is indicated in young patients as an elective procedure, or in growing or large, symptomatic or ruptured aneurysms. Open repair has been the mainstay of intervention from the 1950's until recently.
- Endovascular repair first became practical in the 1990's 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 AAA's, depending on the morphology of the aneurysm. The main advantage over open repair is that the peri-operative period has less impact on the patient (less time in intensive care, less time in hospital overall, 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 doesn't offer any overall survival benefit. Regarding unruptured aneurysms, EVAR is associated with lower operative mortality than open repair but unknown long-term mortality
Stanford University is conducting a study to gather information on AAA risk factors and to determine whether an exercise
program reduces the rate of AAA enlargement.
- ^ Livesay JJ et al. Milestones in Treatment of Aortic Aneurysm. Tex Heart Inst J 2005; 32: 130–134. PMCID 1163455
- ^ Famous Patients, Famous Operations, 2002 - Part 3: The Case of the Scientist with a Pulsating Mass from Medscape Surgery
- ^ a b c d e f Treska V. et al.:Aneuryzma břišní aorty, Prague, 1999, ISBN 80-7169-724-9
- ^ a b c d e f med/3443 at eMedicine
- ^ a b Lindholt JS, Juul S, Fasting H, Henneberg EW. Screening for abdominal aortic aneurysms: single centre randomised controlled trial. BMJ 2005; 330: 750. PMCID: 555873
- ^ Clifton, MA: Familial abdominal aortic aneurysms. Br. J. Surg., 64, 1977, p. 765-766
- ^ U.S. Preventive Services Task Force (2005). "Screening for abdominal aortic aneurysm: recommendation statement". Ann. Intern. Med. 142 (3): 198-202. PMID 15684208.
- ^ Fleming C, Whitlock EP, Beil TL, Lederle FA (2005). "Screening for abdominal aortic aneurysm: a best-evidence systematic review for the U.S. Preventive Services Task Force". Ann. Intern. Med. 142 (3): 203-11. PMID 15684209.ACP Journal Club
- ^ Cinà CS, Devereaux PJ (2005). "Review: population-based screening for abdominal aortic aneurysm reduces cause-specific mortality in older men". ACP J. Club 143 (1): 11. PMID 15989299.
- ^ Society for Vascular Surgery
- ^ a b Ashton HA, Buxton MJ, Day NE, et al (2002). "The Multicentre Aneurysm Screening Study (MASS) into the effect of abdominal aortic aneurysm screening on mortality in men: a randomised controlled trial". Lancet 360 (9345): 1531-9. PMID 12443589. ACP Journal Club
- ^ Cina CS (2003). "Screening for abdominal aortic aneurysm reduced death from AAA in older men". ACP J. Club 138 (3): 66. PMID 12725621.
- ^ Kim LG, P Scott RA, Ashton HA, Thompson SG (2007). "A sustained mortality benefit from screening for abdominal aortic aneurysm". Ann. Intern. Med. 146 (10): 699-706. PMID 17502630.
- ^ Multicentre Aneurysm Screening Study Group (2002). "Multicentre aneurysm screening study (MASS): cost effectiveness analysis of screening for abdominal aortic aneurysms based on four year results from randomized controlled trial". BMJ 325 (7373): 1135. PMID 12433761. ACP Journal Club
- ^ Lindholt JS, Juul S, Fasting H, Henneberg EW (2005). "Screening for abdominal aortic aneurysms: single centre randomised controlled trial". BMJ 330 (7494): 750. doi:10.1136/bmj.38369.620162.82. PMID 15757960. ACP Journal Club
- ^ Ashton HA, Gao L, Kim LG, Druce PS, Thompson SG, Scott RA (2007). "Fifteen-year follow-up of a randomized clinical trial of ultrasonographic screening for abdominal aortic aneurysms". The British journal of surgery 94 (6): 696-701. doi:10.1002/bjs.5780. PMID 17514666.
- ^ a b O'Connor RE: Aneurysm, Abdominal, on emedicine, accessed June 23, 2006.
- ^ Rutherford RB. Randomized EVAR Trials and Advent of Level I Evidence: A Paradigm Shift in Management of Large Abdominal Aortic Aneurysms? Semin Vasc Surg 2006; 19:69-74. PMID 16782510
- ^ Lederle FA, Kane RL, MacDonald R, Wilt TJ (2007). "Systematic review: repair of unruptured abdominal aortic aneurysm". Ann. Intern. Med. 146 (10): 735-41. PMID 17502634.
|Circulatory system pathology (I, 390-459)|
|Hypertension||Hypertensive heart disease - Hypertensive nephropathy - Secondary hypertension (Renovascular hypertension)|
|Ischaemic heart disease||Angina pectoris (Prinzmetal's angina) - Myocardial infarction - Dressler's syndrome|
|Pulmonary circulation||Pulmonary embolism - Cor pulmonale|
|Pericardium||Pericarditis - Pericardial effusion - Cardiac tamponade|
|Endocardium/heart valves||Endocarditis - mitral valves (regurgitation, prolapse, stenosis) - aortic valves (stenosis, insufficiency) - pulmonary valves (stenosis, insufficiency) - tricuspid valves (stenosis, insufficiency)|
|Myocardium||Myocarditis - Cardiomyopathy (Dilated cardiomyopathy, Hypertrophic cardiomyopathy, Loeffler endocarditis, Restrictive cardiomyopathy) - Arrhythmogenic right ventricular dysplasia|
|Electrical conduction system|
of the heart
|Heart block: AV block (First degree, Second degree, Third degree) - Bundle branch block (Left, Right) - Bifascicular block - Trifascicular block|
Pre-excitation syndrome (Wolff-Parkinson-White, Lown-Ganong-Levine) - Long QT syndrome - Adams-Stokes syndrome - Cardiac arrest - Sudden cardiac death
Arrhythmia: Paroxysmal tachycardia (Supraventricular, AV nodal reentrant, Ventricular) - Atrial flutter - Atrial fibrillation - Ventricular fibrillation - Premature contraction (Atrial, Ventricular) - Ectopic pacemaker - Sick sinus syndrome
|Other heart conditions||Heart failure - Cardiovascular disease - Cardiomegaly - Ventricular hypertrophy (Left, Right)|
|Cerebrovascular diseases||Intracranial hemorrhage/cerebral hemorrhage: Extra-axial hemorrhage (Epidural hemorrhage, Subdural hemorrhage, Subarachnoid hemorrhage)|
Intra-axial hematoma (Intraventricular hemorrhages, Intraparenchymal hemorrhage) - Anterior spinal artery syndrome - Binswanger's disease - Moyamoya disease
|Atherosclerosis (Renal artery stenosis) - Aortic dissection/Aortic aneurysm (Abdominal aortic aneurysm) - Aneurysm - Raynaud's phenomenon/Raynaud's disease - Buerger's disease - Vasculitis/Arteritis (Aortitis) - Intermittent claudication - Arteriovenous fistula - Hereditary hemorrhagic telangiectasia - Spider angioma|
|Veins, lymphatic vessels|
and lymph nodes
|Thrombosis/Phlebitis/Thrombophlebitis (Deep vein thrombosis, May-Thurner syndrome, Portal vein thrombosis, Venous thrombosis, Budd-Chiari syndrome, Renal vein thrombosis, Paget-Schroetter disease) - Varicose veins / Portacaval anastomosis (Hemorrhoid, Esophageal varices, Varicocele, Gastric varices, Caput medusae) - Superior vena cava syndrome - Lymph (Lymphadenitis, Lymphedema, Lymphangitis)|
|Other||Hypotension (Orthostatic hypotension)|
|See also congenital (Q20-Q28, 745-747) |