Definition - 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 Epidemiology - 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]
Aetiology - 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.
Pathophysiology - 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).
Investigations- 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.
Managementa) 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
Prognosis- 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
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