Abdominal Aortic Aneurysm

An abdominal aortic aneurysm (AAA) is a permanent focal dilation of the abdominal aorta to at least 3.0 cm in anteroposterior diameter, or more than 50% greater than the expected normal diameter at that level. Normal infrarenal aortic diameter is about 2.0 cm in men and 1.8 cm in women.

About 85% of AAAs are infrarenal. The remainder are juxtarenal, pararenal or suprarenal, which matters because the proximal seal zone determines whether standard endovascular repair is feasible.

The core pathology is medial degeneration with loss of elastin and smooth muscle, chronic transmural inflammation, and excess matrix metalloproteinase activity (MMP-2 and MMP-9).

Wall tension rises with diameter (Laplace), so growth accelerates as the aneurysm enlarges. Mean growth is about 2 to 3 mm per year, faster in smokers and in larger aneurysms.

Risk factors :

• Smoking is the dominant modifiable factor, with duration of exposure mattering more than intensity.
• Male sex (prevalence about 4 to 8 times higher) and age over 65.
• Family history in a first degree relative (about a 2 to 4 fold risk).
• Hypertension, coexisting atherosclerotic disease and chronic obstructive pulmonary disease.

Diabetes is paradoxically associated with lower prevalence and slower growth. Women develop AAAs later, but rupture at smaller diameters and have higher rupture mortality.

Annual rupture risk by diameter is approximately: under 4.0 cm below 0.5%; 4.0 to 5.0 cm 0.5 to 5%; 5.0 to 6.0 cm 3 to 15%; 6.0 to 7.0 cm 10 to 20%; above 7.0 cm 20 to 50%.

Overall mortality from rupture is 80 to 90% once pre-hospital deaths are included. Elective repair carries 1 to 2% mortality for endovascular repair and 3 to 5% for open repair.

Inflammatory, mycotic (infected) and anastomotic aneurysms are distinct subtypes.

Inflammatory AAA shows a thickened, fibrotic wall with periaortic adhesions to the duodenum, ureters and inferior vena cava, and is associated with raised ESR and IgG4-related disease.

Most AAAs are asymptomatic and discovered incidentally on imaging or by screening.

A pulsatile, expansile epigastric or periumbilical mass is detected clinically in only a minority, and sensitivity falls sharply for aneurysms under 5 cm and in obese patients. Palpation is not a screening method.

Symptomatic non-ruptured aneurysm presents with new or recent abdominal, flank or back pain, which signals expansion or impending rupture and is an indication for urgent assessment. Other presentations include:

• Distal embolisation (blue toe syndrome) from mural thrombus

• Aneurysm thrombosis causing acute bilateral limb ischaemia

• Compression of the duodenum (early satiety, vomiting), ureter (hydronephrosis) or IVC

• Aortocaval fistula with high output heart failure, a machinery bruit and sudden leg oedema

• Primary aortoenteric fistula with herald haematemesis or melaena

Ruptured AAA classically presents with the triad of abdominal or back pain, hypotension and a pulsatile mass, but all three are present in fewer than half.

Pain may radiate to the groin, flank or thigh. Retroperitoneal rupture can be temporarily contained, giving the patient a window for transfer.

Intraperitoneal rupture produces profound shock. Misdiagnosis as renal colic, diverticulitis or musculoskeletal pain occurs in up to 30%, so any older male with abdominal or back pain and syncope or shock has a ruptured AAA until imaging shows otherwise.

Grey Turner or Cullen signs are late findings.

• Ultrasound is the screening and surveillance test. Measurement is outer wall to outer wall (or inner to inner, but it must be consistent within a programme) in the anteroposterior plane, perpendicular to the vessel axis.
• Population screening with a single ultrasound at age 65 in men reduces aneurysm related mortality by about 40 to 50%. Targeted screening is also reasonable for women aged 65 to 75 who have smoked, and for first degree relatives.
• CT angiography is the definitive test for planning. It defines the proximal neck (length, diameter, angulation, thrombus and calcification), the iliac access vessels, the renal and visceral arteries, accessory renal arteries and any associated iliac aneurysms.
• Suitability for endovascular repair generally requires an infrarenal neck of at least 10 to 15 mm, neck angulation below 60 degrees (ideally below 45), neck diameter under about 32 mm, and iliac access diameter of at least 7 mm.
• In suspected rupture in an unstable patient, do not delay for CT. Bedside ultrasound confirms the aneurysm and free fluid and takes minutes.
• If the patient is stable enough, CT angiography shows retroperitoneal haematoma, contrast extravasation, the draped aorta sign and the hyperattenuating crescent sign (high attenuation in mural thrombus, indicating impending rupture).
• Baseline blood tests before intervention: full blood count, renal function, coagulation, group and crossmatch (at least 6 units for suspected rupture), ECG, and cardiac and pulmonary risk assessment. Contrast load requires attention to renal function.

Risk factor modification (all patients). Stop smoking (varenicline 0.5 mg daily for 3 days, 0.5 mg twice daily for 4 days, then 1 mg twice daily for 12 weeks, or nicotine replacement). Start a high intensity statin (atorvastatin 40 to 80 mg nightly). Control blood pressure to under 140/90 mmHg.

Prescribe low dose aspirin 75 to 100 mg daily if there is coexisting atherosclerotic disease. Beta blockers do not reliably slow growth. Doxycycline and other MMP inhibitors have not shown benefit.

Surveillance by diameter (ultrasound).

• 3.0 to 3.9 cm: every 3 years
• 4.0 to 4.4 cm: every 12 months
• 4.5 to 5.4 cm: every 3 months
• Move to vascular surgical referral at 5.5 cm in men (5.0 cm in women), or earlier if growth is rapid

Indications for elective repair. Diameter 5.5 cm or more in men, 5.0 cm or more in women; growth over 1 cm in a year or over 0.5 cm in 6 months; symptomatic aneurysm; saccular morphology; mycotic or inflammatory aneurysm with complications; and associated embolisation.

Choice of repair. Endovascular aneurysm repair (EVAR) has lower 30-day mortality (about 0.5 to 1.5% against 3 to 5% for open repair) and shorter recovery.

The survival advantage of EVAR disappears by 2 to 3 years. There is a lifelong need for surveillance and reintervention (about 15 to 20% at 5 years).

Open repair is preferred in younger fit patients with a long life expectancy, hostile neck anatomy, connective tissue disease or infection. Fenestrated or branched endografts treat juxtarenal and pararenal aneurysms in fit patients.

Open repair essentials. Midline or retroperitoneal approach, proximal and distal control, heparin 100 IU/kg before clamping, aortic clamp, tube or bifurcated graft sewn in with the aneurysm sac closed over it. Clamp time above 30 to 40 minutes increases renal injury, especially with suprarenal clamping.

EVAR surveillance. CT angiography or duplex ultrasound at 30 days, then at 12 months, then annually (duplex for stable patients).

Endoleaks: type I (attachment site leak) and type III (component disjunction) need prompt repair. Type II (retrograde flow from lumbar or inferior mesenteric branches) is observed unless the sac grows more than 5 mm. Type IV (graft porosity) is self-limiting. Type V (endotension) means sac growth with no visible leak.

Ruptured AAA. Activate the major haemorrhage protocol. Use permissive hypotension with a target systolic pressure around 70 to 90 mmHg (maintaining consciousness), avoid large crystalloid volumes, and give blood products in 1:1:1 ratio. Give tranexamic acid 1 g IV over 10 minutes, then 1 g over 8 hours. Keep the patient warm.

Transfer directly to the operating theatre. Ideally induce anaesthesia with the patient prepped and draped and the surgeon scrubbed, because loss of abdominal tone at induction can precipitate catastrophic haemorrhage.

Endovascular repair for suitable anatomy has lower perioperative mortality than open repair. Resuscitative endovascular balloon occlusion of the aorta (REBOA) is an option for control in selected centres. Overall in hospital mortality after rupture repair is 30 to 40%.

Complications. Colonic ischaemia (1 to 2% elective, up to 20% after rupture; a left colon at risk if the inferior mesenteric artery is ligated), spinal cord ischaemia (rare), acute kidney injury, limb ischaemia, graft infection, aortoenteric fistula, and abdominal compartment syndrome after rupture repair, which requires bladder pressure monitoring.