Arterial emergencies and aortic disease
Abdominal aortic aneurysm and rupture
Overview and approach
AAA surveillance/repair depends on size, growth, symptoms and patient risk; rupture is catastrophic.
- Definition: an artery enlarged to more than 1.5 times its expected diameter; for the infrarenal aorta the accepted threshold is 3.0 cm1.
- Epidemiology: about 4-7% of men and 1-2% of women over 65 years. Risk factors: age, male sex, smoking, family history, atherosclerosis, hypertension, hypercholesterolaemia, other aneurysm. First-degree relatives have up to 20% lifetime risk1.
- Natural history: ongoing expansion, about 2-3 mm/year when under 5.5 cm and faster when larger. Annual rupture risk by diameter: 3.0-3.9 cm about 0%; 4.0-4.9 cm about 1%; 5.0-5.9 cm 1-10%; 6.0-6.9 cm 10-22%; 7 cm or more 30-50%1.
- Screening: no formal Australian screening program; ultrasound screening of men 65 years and over reduces aneurysm-related mortality in trials (including a Western Australian one), and is most cost-effective in smokers or those with a family history1,2.
- Why it forms: the media weakens when matrix breakdown outpaces repair. Macrophages in atherosclerotic plaque release matrix metalloproteinases that digest elastin and collagen, and lower levels of their natural inhibitors add to the damage. A thickened intima also starves the inner media of oxygen, leading to smooth muscle loss and scarring5.
- More than 90% of AAAs over 4 cm are atherosclerotic, and most sit below the renal arteries4. Atheroma is not the whole story: nearly all older men have abdominal aortic atherosclerosis, yet fewer than 5% develop an AAA5.
- The sac usually holds layered, poorly organised mural thrombus, which can embolise distally or block branch ostia (renal, mesenteric)4,5. Iliac aneurysms often coexist5.
Less common AAA types worth knowing5.
| Type | Key features | Why it matters |
|---|---|---|
| Inflammatory (5-10%) | Younger patients, back pain, raised CRP, dense fibrosis around the aorta into the retroperitoneum | Some are IgG4-related disease, which responds to steroids |
| Mycotic | Organisms seed the wall (e.g. from endocarditis or nearby infection) | Suppuration destroys the media, so it grows fast and ruptures early |
| Connective tissue disorder | Marfan, Loeys-Dietz, vascular Ehlers-Danlos | Weak wall, can rupture at a smaller size |
Assessment and clinical features
Assess known aneurysm, abdominal/back pain, syncope and shock; a palpable mass is not always present.
- Asymptomatic AAA is usually found incidentally on imaging or by targeted screening.
- Symptomatic or rupture: abdominal, back or flank pain, tenderness over the aneurysm, syncope, hypotension, a pulsatile mass; distal embolisation can cause blue toe or acute limb ischaemia1.
- Retroperitoneal rupture may transiently tamponade and give a window for life-saving intervention; intraperitoneal rupture is usually rapidly fatal1.
- Examining for AAA: feel for a pulsatile mass that is also expansile (pushes your fingers apart, not just up); an intact aneurysm is usually non-tender. A clear gap between the top of the mass and the costal margin suggests it starts below the renal arteries. Check for iliac and popliteal aneurysms and all distal pulses; a popliteal aneurysm makes an AAA more likely4,6.
- Ruptured AAA picture: usually a smoker with vascular disease elsewhere. Central abdominal pain going through to the back, sometimes to the groin along the genitofemoral nerve. Collapse may come before the pain. Pale, sweaty, restless, tachycardic, with cold peripheries6.
- Early hypotension can slow the bleeding and give a false sense of recovery6. Free blood, obesity, guarding and hypotension can all make a leaking aneurysm impalpable6.
- Cullen's sign (periumbilical bruising) and Grey Turner's sign (flank bruising) are late signs of a rupture that has been leaking for days6.
- Other complications: distal embolism from thrombus or atheroma, branch occlusion (leg, kidney, gut, spinal cord), and pressure effects such as ureteric compression or vertebral erosion5.
Differentials and investigations
Ultrasound for stable assessment; urgent CT angiography in suitable stable patients, with immediate vascular involvement for rupture concern.
- Differentials for pain with a known or suspected AAA: renal colic, aortic dissection, mesenteric ischaemia, perforated viscus, pancreatitis, GI bleed, musculoskeletal back pain. Diagnosis in a shocked patient with a known AAA should not wait for imaging.
- Ultrasound: modality of choice for detection, screening and surveillance. Measure the maximum transverse diameter perpendicular to flow1.
- CT angiography: investigation of choice to plan repair (morphology, neck, access vessels). Limits: iodinated contrast (renal impairment) and radiation1.
- Plain X-ray may show a calcified aortic rim, but about a quarter of AAAs are not calcified, so a normal film does not exclude one4.
- Angiography pitfall: mural thrombus narrows the lumen, so a luminal study (catheter angiography) can underestimate the true diameter. Measure size on ultrasound or CT4.
- Surveillance intervals (RACGP/ESVS-style, local protocols vary): 3.0-3.9 cm every 24 months; 4.0-4.5 cm every 12 months; 4.6-5.0 cm every 6 months; over 5.0 cm every 3 months1. Newer SVS (RESCAN-based) intervals are longer (for example 3.0-3.9 cm every 3 years), and ANZSVS had not endorsed a guideline when RACGP published3.
Management and follow-up
Vascular-directed surveillance/elective repair; suspected rupture follows emergency resuscitation and surgical pathways.
- Small AAA: surveillance plus cardiovascular risk management: smoking cessation, statin, antiplatelet and antihypertensive therapy. No proven drug to slow growth. No evidence that exercise or travel causes rupture1.
- Indications for repair: male over 5.5 cm; female over 5.0 cm; growth over 1.0 cm/year; symptomatic AAA (pain, tenderness, distal embolisation). Trials show no survival benefit from repairing 4.0-5.5 cm aneurysms1. Saccular aneurysms are often treated earlier3.
- EVAR vs open: operative mortality lower with EVAR (trials: EVAR-1 2.3% vs 6.0%; DREAM 1.2% vs 4.6%; OVER 0.5% vs 3.0%). EVAR needs suitable neck and access anatomy, can be done under local or regional anaesthetic, shorter stay, but needs lifelong (usually yearly) surveillance and more reinterventions, mostly for endoleak (type-based; endoleak is flow outside the graft but within the sac)1.
- Open repair: durable; ICU 1-2 days, hospital stay about 5-7 days; complications include cardiac (about 5%), pulmonary, renal, bowel ischaemia, graft infection, aorto-enteric fistula1.
- Ruptured AAA: immediate transfer to a vascular centre, activate massive transfusion, hypotensive resuscitation (avoid over-resuscitation). Overall mortality 80-90%; open repair mortality 30-40%; EVAR may improve survival1.
Red flags and clinical pearls
Painful aneurysm or shock with concerning pain needs urgent escalation. Do not use a single elective size threshold for every patient.
- Known AAA plus abdominal/back pain, syncope or tenderness = urgent vascular surgeon assessment1.
- Hypotensive resuscitation, not aggressive fluids, while en route to theatre1.
- Size alone is a crude surrogate of rupture risk; women rupture at smaller diameters, hence the lower 5.0 cm threshold1,3.
- New pain in a known aneurysm often heralds rupture and is an emergency, even if the patient looks well4.
- An AAA is a marker of widespread atherosclerosis. Coronary and cerebrovascular disease are common and strongly shape long-term prognosis, so treat cardiovascular risk aggressively4,5.
- Viva: thresholds for repair, surveillance intervals, EVAR vs open, what an endoleak is.
References
- RACGP: Aortic aneurysms - screening, surveillance and referral (AFP 2013)
- Medicine Today: Abdominal aortic aneurysms (Cardiology Today 2016)
- RACGP AJGP 2018: AAA screening and surveillance
- Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J, editors. Harrison's Principles of Internal Medicine. 18th ed. New York: McGraw-Hill; 2012. Chapter 248, Diseases of the aorta.
- Kumar V, Abbas AK, Aster JC, editors. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Philadelphia: Elsevier Saunders; 2015. Chapter 11, Blood vessels.
- Burnand KG, Black J, Corbett SA, Thomas WEG, editors. Browse's Introduction to the Symptoms and Signs of Surgical Disease. 5th ed. Boca Raton: CRC Press; 2015. Chapter 15, The abdomen.
Last updated from Sen’s notes on 22 October 2026.