Abdominal aortic aneurysm

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A plate from Gray's anatomy with yellow lines depicting the most common infrarenal location of the AAA.

Abdominal aortic aneurysm (AAA) is a term, which is used to describe a localized dilatation of the abdominal aorta, that exceeds the normal diameter by more than 50%. 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.

[edit] History

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.^[1] 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.^[2]

[edit] Epidemiology

AAA is uncommon in individuals of African, African American, Asian and Hispanic heritage. The frequency rate 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.^[3] In the US, the incidence of AAA is 2-4% in the adult population. ^[4]. Rupture of the AAA occurs in 1-3% of men aged 65 or more, the mortality is 70-95%^[5].

[edit] Etiology

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.^[6] 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.^[4]

• 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.^[3]

• 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.^[4]

• Other causes: Other causes of the development of AAA include: infection, trauma, arteritis, cystic medial necrosis (m. Erdheim) and connective tissue disorders (e.g. Marfan syndrome, Ehlers-Danlos syndrome).^[3]

[edit] Pathophysiology

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.^[3] 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. ^[4] Other pathophysiological cause for development of the AAA is inflammation.

[edit] Manifestations and Diagnosis

AAAs are commonly divided according to their size and symptomatology. The 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). If the outer diameter exceeds 5 cm, the aneurysm is considered to be large. Small aneurysms under 5 cm don't have such a big tendency to rupture and are usually treated conservatively.^[3][5] 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.^[7] 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.^[4]

The diagnosis consists of 2 steps - screening and assessment of severity. 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. Skilled physicians can also suspect the presence of the AAA from abdominal palpation. Ultrasonography provides the initial assessment of the size and extent of the aneurysm. The subsequent examinations include CT, MRI and special modes thereof, like CT/MR angiography. Although non-invasive imaging methods now prevail in the diagnostics of AAA, angiography remains the diagnostic standard for AAA, and can be ordered to assess the degree of renal / visceral involvement, or in case of renal abnormality.

[edit] Rupture

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.^[7] The bleeding can be retroperitoneal or intraperitoneal, or the rupture can create an aortocaval or aortointestinal fistula.^[3]. Flank ecchymosis is a sign of retroperitoneal hemorrhage, and is also called the Grey-Turner sign.^[4]

[edit] Treatment

There are currently three modes of treatment available for the AAA: conservative, open aneurysm repair (OR), and endovascular aneurysm repair (EVAR).

• Conservative treatment is indicated in patients with small asymptomatic aneurysms and in high-risk patients. The two mainstays of the conservative treatment are smoking cessation and blood pressure control.
• Open repair (operation) is indicated in young patients as an elective procedure, or in growing or large, symptomatic or ruptured aneurysms.
• Endovascular repair is indicated in older, high-risk patients or patients unfit for open repair. However, according to the latest studies, the EVAR procedure doesn't offer any overall survival benefit.^[8]

[edit] References

1. ^ Livesay JJ et al. Milestones in Treatment of Aortic Aneurysm. Tex Heart Inst J 2005; 32: 130–134. PMCID 1163455
2. ^ Famous Patients, Famous Operations, 2002 - Part 3: The Case of the Scientist with a Pulsating Mass from Medscape Surgery
3. ^ ^{a b c d e f} Treska V. et al.:Aneuryzma břišní aorty, Prague, 1999, ISBN 80-7169-724-9
4. ^ ^{a b c d e f} eMedicine med/3443
5. ^ ^{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
6. ^ Clifton, MA: Familial abdominal aortic aneurysms. Br. J. Surg., 64, 1977, p. 765-766
7. ^ ^{a b} O'Connor RE: Aneurysm, Abdominal, on emedicine, accessed June 23rd, 2006.
8. ^ 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