Aortic Aneurysm — Causes, Symptoms, Risks & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

An aortic aneurysm is an abnormal, localised pathological dilation of the aorta — the body's largest artery, transporting approximately 5 litres of oxygenated blood per minute from the heart to the systemic circulation — defined as a diameter of 3 cm or more (abdominal aorta) or more than 1.5 times the expected normal diameter. The most common location is the infrarenal abdominal aorta (below the renal arteries) — abdominal aortic aneurysm (AAA), which accounts for approximately 75% of aortic aneurysms. Less commonly, aneurysms affect the thoracic aorta (thoracic aortic aneurysm/TAA — involving the ascending aorta, aortic arch, or descending thoracic aorta), and thoraco-abdominal aneurysms span both regions. AAA affects 1-2% of men aged 65-74 and up to 10% of men over 80 in developed countries; it is 4-6 times less common in women but has higher rupture risk at equivalent sizes. Aortic aneurysm is predominantly a disease of older men with cardiovascular risk factors, and its key danger is silent progression to rupture — typically occurring when the AAA diameter exceeds 5.5 cm (or 5.0 cm in women). Ruptured AAA is one of the most lethal surgical emergencies, with an overall population mortality of 65-85% (including those who die before reaching hospital); even with emergency surgery, operative mortality is 30-50%.

Aortic aneurysm formation results from progressive degradation of elastin and collagen in the aortic media and adventitia — driven by proteolytic enzymes (matrix metalloproteinases/MMPs activated by macrophages), oxidative stress, smooth muscle cell apoptosis, and chronic inflammation — ultimately weakening the aortic wall until the vessel dilates under haemodynamic pressure. The most common underlying pathological process is degenerative (atherosclerotic) aortic disease — the same process causing coronary and peripheral arterial disease — driven by lipid deposition, endothelial dysfunction, and macrophage infiltration. Other aetiology: heritable connective tissue disorders — Marfan syndrome (FBN1 mutation — tall, ectomorphic, lens dislocation — characteristically causes ascending aortic aneurysm with aortic root dilation and risk of aortic dissection type A); Loeys-Dietz syndrome; vascular Ehlers-Danlos syndrome (COL3A1 mutation — high risk of spontaneous arterial rupture); bicuspid aortic valve (associated with aortic root and ascending aortic dilation regardless of valve stenosis severity — present in 50-80% of bicuspid aortic valve patients by middle age); aortic dissection; large-vessel vasculitis (giant cell arteritis, Takayasu arteritis — particularly thoracic aneurysms); and mycotic (infectious) aneurysm — from bacteraemia, particularly Salmonella or Staphylococcus. Major modifiable risk factors for AAA: current or prior cigarette smoking (the strongest modifiable risk factor — 4-8x increased risk, with dose-dependent relationship); hypertension; hyperlipidaemia; and peripheral arterial disease (a strong marker of aneurysm disease). Non-modifiable risk factors: male sex (6:1 ratio vs. women); age over 65; Caucasian ethnicity; and first-degree family history (first-degree relative with AAA increases risk 2-4-fold).

Most aortic aneurysms are asymptomatic — the majority of AAAs are discovered incidentally during abdominal ultrasound or CT performed for another indication, or through the NHS AAA Screening Programme. Symptomatic (unruptured) AAA: pulsatile epigastric or central abdominal mass — palpable in thin patients with large aneurysms; dull, aching back, flank, or lower abdominal discomfort from aortic wall tension or vertebral erosion. New or worsening pain in a patient with a known aneurysm should trigger urgent vascular surgery assessment as it may indicate impending rupture. Thoracic aortic aneurysm symptoms from compression of adjacent mediastinal structures: chest or interscapular back pain (descending thoracic aorta); hoarseness (recurrent laryngeal nerve compression); cough and dyspnoea (tracheobronchial compression); dysphagia (oesophageal compression); and superior vena cava syndrome from right-sided arch involvement. Ruptured AAA is a surgical emergency with the 'classic triad' (present in only 50%): sudden severe tearing or ripping abdominal, flank, or back pain radiating to the groin; haemodynamic shock (hypotension, pallor, tachycardia); and a pulsatile abdominal mass. Contained (retroperitoneal) rupture may present with less severe or intermittent pain before free intraperitoneal haemorrhage and cardiovascular collapse. Any clinical suspicion of rupture requires immediate emergency transfer to a vascular centre without delay.

Abdominal ultrasound is the first-line diagnostic test for AAA screening and surveillance — accurate (sensitivity above 95%), non-invasive, widely available, inexpensive, and involves no radiation; it measures maximum aortic diameter at its widest point in the anteroposterior plane; serial surveillance intervals (annually for 3.0-3.9 cm, every 6 months for 4.0-4.4 cm, every 3 months for 4.5-5.4 cm, and surgery threshold at 5.5 cm for men). AAA is defined as maximum aortic diameter of 3.0 cm or more (normal abdominal aorta measures below 2.0 cm). CT angiography (CTA) with intravenous contrast: provides precise three-dimensional anatomical detail essential for surgical planning — measures aneurysm length, diameter, neck morphology, and relationship to renal arteries and iliac bifurcation; determines EVAR suitability (neck length above 10 mm, diameter 17-32 mm, angulation below 60 degrees); essential before elective repair. MRI/MRA: avoids radiation and iodinated contrast; used when CT is contraindicated (contrast allergy, renal impairment); equivalent accuracy to CTA for anatomy. Transthoracic and transoesophageal echocardiography (TTE/TOE) assess thoracic aortic aneurysms and aortic root dilation. Cardiac MRI and CT angiography for thoracic aortic aneurysms in Marfan syndrome and connective tissue disorders — annual surveillance. Genetic testing (FBN1 for Marfan syndrome; COL3A1 for vascular Ehlers-Danlos; SMAD3, TGFBR1/2 for Loeys-Dietz) for suspected heritable aortic disease. The UK NHS Abdominal Aortic Aneurysm Screening Programme invites all men aged 65 for a single one-off screening abdominal ultrasound.

Treatment is determined by aneurysm size, growth rate, symptoms, and patient fitness for intervention. Conservative management and surveillance: small AAAs (below 5.5 cm in men, below 5.0 cm in women) are managed with surveillance ultrasound — every 3 months for 4.5-5.4 cm, every 6 months for 4.0-4.4 cm, and annually for 3.0-3.9 cm — combined with aggressive risk factor modification: smoking cessation (the most effective intervention for slowing aneurysm growth); blood pressure control targeting below 130/80 mmHg (using ACE inhibitors, ARBs, or beta-blockers); high-intensity statin therapy (atorvastatin 40-80 mg) for cardiovascular risk reduction and possible aneurysm growth attenuation; and exercise restriction from activities markedly elevating blood pressure. Doxycycline (a metalloproteinase inhibitor) has shown modest benefit in reducing growth rate in small trials but is not yet standard practice. Surgical repair — indicated for: AAA diameter 5.5 cm or more in men (5.0 cm in women); symptomatic AAA of any size (back pain, tenderness); rapid expansion above 1 cm in 12 months; and ruptured AAA (emergency). Endovascular Aneurysm Repair (EVAR): a stent-graft is deployed inside the aneurysm sac via femoral artery catheterisation under fluoroscopic guidance, excluding the aneurysm from the systemic circulation — 30-day mortality approximately 1-2% elective versus 30-50% emergency; advantages include reduced blood loss, shorter recovery, lower short-term mortality; disadvantage is need for lifelong CT surveillance for endoleak (persistence of blood flow into aneurysm sac — occurring in 15-30%, requiring reintervention in 10%). Open surgical repair: traditional aortic cross-clamp, aortic resection and Dacron graft interposition — 30-day mortality 2-5% elective; more durable long-term with fewer re-interventions; preferred for complex anatomy, young patients, and connective tissue disorders (Marfan/Loeys-Dietz). Ruptured AAA: emergency EVAR or open repair — outcome depends entirely on speed of diagnosis and time to operative team; 30-day mortality even with surgery is 30-50%.

The primary catastrophic complication of untreated large AAA is rupture, carrying an overall mortality of 65-85% (many patients die before reaching hospital). Risk of rupture increases markedly with size: 1% per year for aneurysms under 4 cm, rising to over 25% per year for aneurysms over 6 cm. Untreated aneurysms also carry risk of thrombosis within the aneurysm sac with peripheral embolisation (clot to the legs), aorto-enteric fistula, and aorto-caval fistula. Elective repair has a far lower mortality (0.5-2%) than emergency repair.

Smoking cessation is the single most important modifiable risk factor — smokers have a 4-8 fold increased risk of AAA. Optimal blood pressure control (ACE inhibitors/ARBs, calcium channel blockers) slows aneurysm growth. Statins reduce cardiovascular risk and may slow AAA progression. Maintain a healthy weight and exercise regularly. Screening: all men aged 65 should undergo AAA ultrasound screening as per UK and US recommendations. Avoid heavy lifting and strenuous Valsalva manoeuvres in patients with known aneurysm. Regular surveillance ultrasound is essential for known small aneurysms.

Call emergency services (999/911) immediately for: sudden severe tearing or ripping pain in the abdomen, back, or flank — especially in anyone with a known aortic aneurysm, male over 65, a smoker, or hypertensive — suspected AAA rupture is a life-threatening emergency; collapse, dizziness, or loss of consciousness alongside abdominal or back pain; severe abdominal pain of sudden onset in any older adult with cardiovascular risk factors — consider ruptured aneurysm even without a known diagnosis. If you have a known aneurysm: attend all surveillance appointments — missing a scan allows undetected growth beyond the surgical threshold; contact your GP or vascular surgery team urgently if you develop new or worsening back pain, abdominal discomfort, or awareness of a pulsatile abdominal mass — even if symptoms are mild. Do not drive yourself to hospital with severe acute pain — call 999.