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
| Diagnosis | Key Features | Investigation |
|---|---|---|
| Renal colic | Colicky loin-to-groin pain, haematuria | CT KUB, urinalysis |
| Acute MI | Chest/epigastric pain, ECG changes, troponin | ECG, troponin |
| Acute pancreatitis | Epigastric pain radiating to back, raised amylase/lipase | Amylase, CT |
| Mesenteric ischaemia | Severe abdominal pain disproportionate to examination | CT angiography |
| Musculoskeletal back pain | Positional, reproducible, no mass | Clinical assessment |
| Aortic dissection | Tearing pain, BP differential, intimal flap | CT 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
| Diameter | Action |
|---|---|
| <3 cm | Normal — 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
| Feature | EVAR | Open 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 durability | Inferior (endoleak risk) | Superior |
| Anatomical suitability | ~60-70% | All |