Abdominal aortic aneurism


    • A permanent pathological dilation of the aorta with a diameter >1.5 times the expected PA diameter of that segment, given the patient's gender and body size

      • This is approximately 3 cm in most people

    • More than 90% of aneurysms originate below the renal arteries

Risk Factors

    • Strong

      • Cigarette smoking

      • Hereditary/family history

      • Increased age

      • Male sex (prevalence)

      • Female sex (rupture)

      • Congenital/connective tissue disorders

    • Weak

      • Hyperlipidaemia

      • COPD

      • Atherosclerosis (i.e., CAD, peripheral arterial occlusive disease)

      • HTN

      • Increased height

      • Central obesity

      • Non-diabetic

Differential diagnosis


    • A Cochrane review (2007) found that, between the age of 65 and 79 years, 5% to 10% of men have AAA. [8]

    • The general prevalence of 2.9 cm to 4.9 cm AAAs range from 1.3% for men aged 45 to 54 years, to 12.5% for men 75 to 84 years of age (0% and 5.2% for women, respectively). [3]

    • The prevalence of aneurysms among men increases by about 6% per decade. [7]

    • In 2004 AAA was the 14th leading cause of death for the 60- to 85-year-old age group in the US, and there were 13,753 deaths from aortic aneurysm and dissection combined in 2004. [9] [10]

    • Prevalence among men is 4 to 6 times higher than in women. [1] [11]


    • The aetiology is multi-factorial

    • Traditionally, arterial aneurysms were thought to arise from atherosclerotic disease, and certainly intimal atherosclerosis reliably accompanies AAA. [12]

    • More recent data suggest that altered tissue metalloproteinases may diminish the integrity of the arterial wall. [4]

    • The underlying pathophysiology remains constant with aortic elastic medial degeneration and mild cystic medial necrosis resulting in aortic dilation and aneurysm formation.

Clinical features

    • Palpable pulsatile abdominal mass

      • Has been shown to be sensitive only in thin patients and those with AAA >5 cm (sensitivity and specificity of 68% and 75%, respectively)

    • Abdominal, back, or groin pain

      • However, patients are usually asymptomatic and their aneurysm is detected incidentally

    • Hypotension

      • Patients with ruptured aneurysm present with the triad of abdominal and/or back pain, pulsatile abdominal mass and hypotension.


    • The pathogenesis is complex and multi-factorial

    • Histologically there is:

      • obliteration of collagen and elastin in the media and adventitia

      • smooth muscle cell loss with resulting tapering of the medial wall

      • infiltration of lymphocytes and macrophages

      • neovascularisation. [12]

    • There are 4 mechanisms applicable and relevant to development: [13]

      • Proteolytic degradation of aortic wall connective tissue

        • matrix metalloproteinases (MMPs) and other proteases are derived from macrophages and aortic smooth muscle cells and secreted into the extracellular matrix.

        • Disproportionate proteolytic enzyme activity in the aortic wall may promote deterioration of structural matrix proteins (e.g., elastin and collagen). [3]

        • Increased expression of collagenases MMP-1 and -13 and elastases MMP-2, -9, and -12 have been demonstrated in human AAAs. [14] [15] [16] [17]

      • Inflammation and immune responses

        • An extensive transmural infiltration by macrophages and lymphocytes is present on aneurysm histology

        • These cells may release a cascade of cytokines that subsequently activate many proteases. [12]

        • Additionally, deposition of IgG into the aortic wall supports the hypothesis that AAA formation may be an autoimmune response.

        • There is currently interest in the role of reactive oxygen species and antioxidants in AAA formation. [14] [18] [19] [20] [21]

      • Biomechanical wall stress

        • Elastin levels and the elastin-collagen ratio decrease progressively distal down the aorta.

        • Diminished elastin is associated with aortic dilation and collagen degradation predisposes to rupture. [11] [14] [22] [23]

      • Molecular genetics

        • There is familial clustering, a common HLA subtype, and several altered gene expressions and polymorphisms linked, suggesting a genetic role in pathogenesis. [14] [24] [25]

    • Additionally, data support increased MMP-9 expression and activity, disordered flow and an increase in wall tension, and relative tissue hypoxia in the distal aorta (i.e., infra-renal).


    • abdominal ultrasound

      • aortic dilation of >1.5 times the expected anterior-posterior diameter of that segment, given the patient's sex and body size

      • this is approximately 3 cm in most individuals

    • ESR/CRP

      • Raised in inflammatory AAA

    • FBC

      • leukocytosis, anaemia in infective AAA

    • Blood cultures

      • Positive in infective AAA

    • CT

      • Aortic dilation of >1.5 times the expected anterior-posterior diameter of that segment, given the patient's sex and body size

      • May demonstrate signs of impending rupture

        • blood within the thrombus (crescent sign)

        • low thrombus-to-lumen ratio

        • retroperitoneal haematoma

        • discontinuity of the aortic wall

        • extravasation of contrast into the peritoneal cavity

      • Also useful in diagnosing aortic aneurysms close to the origins of, or proximal to, the renal arteries. [4] [52] [53]

    • MRI/magnetic resonance angiography (MRA)

      • if a patient has an iodinated contrast allergy.

    • Contrast aortography

      • Adjunctive modality for preoperative planning.


a) conservative

    • Patients presenting with a ruptured aneurysm require emergent repair, and for patients with symptomatic aortic aneurysms, repair is indicated regardless of diameter. [4]

    • For AAA detected as an incidental finding, repair is deferred until the theoretical risk of rupture exceeds the estimated risk of operative mortality.

    • Generally, repair is indicated in patients with large asymptomatic AAA (e.g., with a diameter exceeding 5.5 cm in men or 5.0 cm in women in the US)

b) medical

    • Treatment of coexisting cardiac disease

    • Hypotensive resuscitation

      • Aggressive fluid replacement may exacerbate bleeding

        • Dilutional and hypothermic coagulopathy

        • Secondary clot disruption from increased blood flow, increased perfusion pressure, and decreased blood viscosity

      • Infusing more than 3.5 litres of fluid preoperatively may increase the relative risk of death. [106]

      • A target systolic BP of 50 to 70 mmHg and withholding fluids is advocated preoperatively

c) surgical

    • Open repair

      • Retroperitoneal (RP) or transperitoneal incision

      • A prosthetic graft is sutured from normal proximal aorta to normal distal aorta

    • Endovascular repair (EVAR)

      • Involves the transfemoral endoluminal delivery of a covered stent graft into the aorta

      • Thus seals off the aneurysm wall from systemic pressures, preventing rupture, and allowing for sac shrinkage


    • Ruptured AAA

      • Overall mortality is about 90%; [4]

      • Mortality in those that reach the operating suite is 50%. [47]

    • The natural course involves slow and steady growth with ultimate progression to rupture

    • Given the morbidity and mortality associated with surgical intervention, repair is typically deferred until the theoretical risk of rupture exceeds the estimated risk of operative mortality

    • The majority of patients undergoing open repair remain without significant graft-related complications during the remainder of their lives (0.4% to 2.3% incidence of late graft-related complications). [1] [143]

    • Five-year survival rates after intact aneurysm repair average 60% to 75%

    • Those undergoing endovascular repair are more likely to have a delayed complication and require re-intervention