TextbookCardiologyAbdominal Aortic Aneurysm

Abdominal Aortic Aneurysm

Permanent dilatation of the abdominal aorta to ≥3 cm, most commonly infrarenal. Usually asymptomatic until rupture, which carries ~80% overall mortality. UK NHS screening programme for men at age 65.

Key Facts

Definition: aortic diameter ≥3 cm (normal infrarenal aorta ~2 cm); most commonly infrarenal (95%) Risk factors: smoking (strongest modifiable), male sex, age >65, family history, hypertension, atherosclerosis Usually asymptomatic: detected incidentally or through NHS AAA screening programme NHS AAA screening: ultrasound offered to all men at age 65 in England Elective repair: indicated when diameter ≥5.5 cm (men) or ≥5.0 cm (women), or growth ≥1 cm/year, or symptomatic EVAR (endovascular repair) vs open surgical repair: EVAR has lower perioperative mortality (~1-2% vs ~5%) but higher re-intervention rate Ruptured AAA: triad of sudden abdominal/back pain, hypotension, pulsatile abdominal mass — requires emergency surgery; overall mortality ~80% UK Aneurysm Growth Study and EVAR-1/EVAR-2 trials: guided current thresholds and repair strategies

Overview

Key Facts

Abdominal aortic aneurysm (AAA) is a permanent dilatation of the abdominal aorta to a diameter of ≥3 cm. It most commonly affects the infrarenal aorta. The major risk is rupture, which is often fatal.

Epidemiology

  • Prevalence: ~4-8% of men >65 years; ~1-2% of women >65 years
  • Male:female ratio ~6:1
  • UK NHS screening has reduced AAA-related mortality
  • Declining prevalence due to reduced smoking rates

Aetiology

  • Atherosclerosis: degenerative process; primary risk factor
  • Smoking: strongest modifiable risk factor (odds ratio ~5-6)
  • Hypertension: contributes to wall stress
  • Family history: ~20% have first-degree relative with AAA
  • Connective tissue disorders: Marfan, Ehlers-Danlos (more thoracic)
  • Inflammatory: inflammatory AAA (~5%); periaortic fibrosis
  • Infectious (mycotic): Salmonella, Staphylococcus, TB (rare)

Pathophysiology

  • Degradation of aortic wall: loss of elastin and collagen by matrix metalloproteinases (MMPs)
  • Chronic inflammation and oxidative stress in arterial wall
  • Loss of smooth muscle cells
  • Progressive dilatation → increased wall tension (Laplace's law: wall tension ∝ pressure × radius)
  • Rupture occurs when wall stress exceeds wall strength
  • Risk of rupture increases exponentially with diameter: ~1%/year at 4-5 cm; ~30-40%/year at >8 cm

Clinical Presentation

Unruptured AAA

  • Usually asymptomatic: discovered incidentally or on screening
  • Pulsatile abdominal mass: expansile (hands pushed apart, not just pulsatile)
  • Vague abdominal or back pain (suggests expansion or impending rupture)

Ruptured AAA

  • Classic triad: sudden severe abdominal/back pain, hypotension/shock, pulsatile abdominal mass
  • Often presents with cardiovascular collapse
  • May mimic renal colic, MI, mesenteric ischaemia
  • Retroperitoneal rupture: may be temporarily contained (patient may be transiently stable)
  • Free intraperitoneal rupture: rapid exsanguination, usually fatal before reaching hospital

Red Flags

  • New-onset abdominal/back pain in patient with known AAA
  • Hypotension with pulsatile mass
  • Rapid growth (>1 cm/year)
  • Symptomatic AAA of any size

Differential Diagnosis

DiagnosisKey FeaturesInvestigation
Renal colicColicky loin-to-groin pain, haematuriaCT KUB, urinalysis
Acute MIChest/epigastric pain, ECG changes, troponinECG, troponin
Acute pancreatitisEpigastric pain radiating to back, raised amylase/lipaseAmylase, CT
Mesenteric ischaemiaSevere abdominal pain disproportionate to examinationCT angiography
Musculoskeletal back painPositional, reproducible, no massClinical assessment
Aortic dissectionTearing pain, BP differential, intimal flapCT aortogram

Diagnosis / Investigation

Bedside

  • Abdominal examination: pulsatile, expansile mass above umbilicus
  • Observations: HR, BP, peripheral pulses

Bloods

  • FBC, U&Es, coagulation, crossmatch: essential for ruptured AAA (emergency surgery preparation)
  • Lactate: elevated in ruptured AAA with hypoperfusion
  • Group and save: all AAA patients

Imaging

  • Abdominal ultrasound: first-line for screening and monitoring; highly accurate for diameter measurement
  • CT angiography: gold standard for detailed anatomy, pre-operative planning, and ruptured AAA diagnosis
  • MR angiography: alternative if CT contraindicated

NHS AAA Screening Programme

DiameterAction
<3 cmNormal — no further screening
3.0-4.4 cm (small AAA)Annual USS surveillance
4.5-5.4 cm (medium)3-monthly USS surveillance
≥5.5 cm (large)Refer for surgical assessment

Management

Non-pharmacological

  • Smoking cessation: most important modifiable intervention (slows growth)
  • Cardiovascular risk management: exercise, healthy diet
  • Surveillance USS: as per screening programme intervals

Pharmacological

  • Cardiovascular risk optimisation:
    • Statin (atorvastatin 80mg OD)
    • Antihypertensive therapy (target BP <140/90)
    • Antiplatelet (aspirin 75mg) if concurrent cardiovascular disease
  • No pharmacological therapy has been proven to slow AAA growth (trials of doxycycline, ACEi, statins have been inconclusive)
  • Ruptured AAA: activate massive transfusion protocol, permissive hypotension (SBP ~80-100 mmHg) to reduce further bleeding while maintaining perfusion

Surgical/Interventional

Elective repair indications:

  • Diameter ≥5.5 cm (men) or ≥5.0 cm (women)
  • Growth ≥1 cm/year
  • Symptomatic AAA of any size

Repair options:

  • EVAR (endovascular aneurysm repair): endograft placed via femoral arteries
    • Perioperative mortality: ~1-2%
    • Suitable anatomy required (~60-70% of elective cases)
    • Higher re-intervention rate (~10-20% over 5 years)
    • EVAR-1 trial: lower perioperative mortality vs open repair; no long-term survival advantage
    • EVAR-2 trial: EVAR in patients unfit for open repair; no survival benefit vs conservative management
  • Open surgical repair: aortic replacement with synthetic graft (Dacron)
    • Perioperative mortality: ~5%
    • More durable; lower re-intervention rate
    • Higher perioperative morbidity

Ruptured AAA:

  • Emergency surgery (open or EVAR if anatomy suitable and haemodynamically stable)
  • Mortality: ~40-50% for those reaching hospital alive; ~80% overall

Referral Criteria

  • AAA ≥5.5 cm: vascular surgery referral
  • Rapid growth or symptomatic AAA: urgent referral
  • Ruptured AAA: emergency transfer to vascular centre

Prognosis

  • Elective repair mortality: EVAR ~1-2%; open ~5%
  • Ruptured AAA: ~80% overall mortality (including pre-hospital deaths); ~40-50% for those undergoing emergency surgery
  • 5-year survival post-elective repair: ~65-70% (limited by comorbidities)
  • Small AAA (<5.5 cm): annual rupture risk ~1% for 4-5 cm; surveillance is safe
  • Large AAA (>7 cm): annual rupture risk ~20-40%
  • EVAR: higher re-intervention rate but lower perioperative risk
  • Open repair: more durable long-term repair
  • NHS screening programme: estimated to reduce AAA-related mortality by ~50% in screened men

Other Relevant Information

Annual Rupture Risk by Diameter

Diameter (cm)Annual Rupture Risk
<4<0.5%
4-5~1%
5-6~5-10%
6-7~10-20%
>7~20-40%

EVAR vs Open Repair Comparison

FeatureEVAROpen Repair
Perioperative mortality~1-2%~5%
Hospital stay~3-5 days~7-14 days
Re-intervention rate~10-20% at 5 years~5% at 5 years
Long-term durabilityInferior (endoleak risk)Superior
Anatomical suitability~60-70%All