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Abdominal aortic aneurism

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.
Management

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
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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