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Abdominal Aortic Aneurysm
Abdominal Aortic Aneurysm

Introduction

Abdominal aortic aneurysm, also known as AAA (often pronounced 'triple-A'), is a dilation 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 cause remains unknown. The aneurysm is typically located below the kidneys (infrarenally; 90%). Other possible locations are above or at the level of the kidneys (suprarenal and pararenal). The aneurysm can extend to include one or both of the iliac arteries. This type of aneurysm may also occur in the thorax. Typically, the ages which are most affected by AAA are between the ages of 65 and 75 and more prevalent in men and smokers. There is evidence to support screening in individuals with these risk factors. The majority of abdominal aortic aneurysms do not cause symptoms. Symptomatic and large aneurysms (>5 cm in diameter) are considered for repair. The most important complication of an abdominal aortic aneurysm is rupture. Ruptures are typically fatal.

Causes

The exact causes remain unclear, however, some theories and risk factors are defined below:

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 a higher incidence of AAA among male members of the affected families. Primarily, the etiology is assumed to be genetic. There are two commonw theories supporting this. One cause is thought the be an alpha 1-antitrypsin deficiency. Other experimental works favored the theory of X-linked mutation, which would explain the lower incidence in heterozygous females.

Hemodynamic influences: Abdominal aortic aneurysm is a specific degenerative process which targets 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 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 dilation of the segment. Higher intraluminal pressure in patients with arterial hypertension markedly contributes to the progression of the pathological process.

Atherosclerosis: 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.

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).

Screening

A clinical practice guideline by the U.S. Preventive Services Task Force "recommends one-time screening for abdominal aortic aneurysm (AAA) by ultrasonography in men age 65 to 75 years who have ever smoked". In the U.S., 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 enrolment 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.

Symptoms and Treatment

Symptoms 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 up to 90%. 65-75% of patients die before they arrive at hospital and up to 90% die before they reach the operating room.

The treatment options include immediate repair, surveillance, or conservative management. There are currently two methods of repair for AAA, open aneurysm repair and endovascular aneurysm repair. Conservative treatment involves smoking cessation and blood pressure control. Recent studies have shown possible protective effects with therapy using angiotensin converting enzyme inhibitors or statins.

Surveillance is more typical of smaller aneurysms because the risk of repair exceeds the risk of rupture. Typically the decision for surgery is based upon the individual's native aorta typically is versus its current size.

Open repair is typically an elective surgery for younger individuals. Open repair has been the standard procedure for intervention since the 1950's.

Endovascular repair became a practical alternative to the OR in the 1990s. Although this procedure is a practical alternative, it's current role has not been clearly defined yet. Generally it is reserved for older patients or who at a high risk. Endovascular repair has several advantages over open repair, such as; peri-operative mortality, less time in intensive care, less time in hospital overall and earlier return to normal activity. However the disadvantages of endovascular repair include a requirement for more frequent ongoing hospital reviews, and a higher chance of further procedures being required.

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