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

• Diverticulitis

• Renal colic

• Irritable bowel syndrome (IBS)

  • Inflammatory bowel disease

• Appendicitis

• Ovarian torsion

  • GI haemorrhage

  • Splanchnic artery aneurysms/acute occlusion

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