Abdominal Aortic Aneurysm
An abdominal aortic aneurysm (AAA) is defined as a dilatation of the abdominal aorta greater than 3cm.
In the UK, around 1 in 70 men over 65yrs have an AAA and over 3,000 deaths occur each year from a ruptured AAA.
In this article, we shall look at the clinical features, investigations and management of abdominal aortic aneurysms.
The aetiology of abdominal aortic aneurysm is largely unknown. Possible causes include trauma, infection, connective tissue disease (e.g. Marfan’s disease), or inflammatory disease (e.g. Takayasu’s aortitis).
Risk factors* for AAA include smoking, hypertension, hyperlipidaemia, family history, male gender, and increasing age
*Diabetes mellitus is not a risk factor for AAA.
Many abdominal aortic aneurysms are asymptomatic and are simply detected on incidental finding. In the UK, the national abdominal aortic aneurysm screening programme (NAAASP) performs an abdominal USS for all men in their 65th year.
A symptomatic AAA can present with:
- Abdominal pain
- Back or loin pain
- Distal embolisation producing limb ischaemia
On examination, a pulsatile mass can be felt in the abdomen (above the umbilical level). Rarely, signs of retroperitoneal haemorrhage (Grey-Turn’s sign or Cullen’s sign) may be evident.
A patient with a ruptured AAA may present with pain (abdominal, back, or loin), and a degree of shock or syncope.
The main differential diagnosis is renal colic, with several patients’ scans for renal colic often being found to have an AAA.
In addition, diverticulitis, inflammatory bowel disease, irritable bowel syndrome, GI haemorrhage, appendicitis, ovarian torsion or ovarian rupture, or splenic infarctions may be possible differentials.
In the routine outpatient setting, any suspected AAA should be initially investigated by an ultrasound scan (USS); an AXR is not indicated as it will only rarely show an AAA if there is significant calcification of the arterial wall.
Once an USS has confirmed this diagnosis, a follow-up CT scan with contrast is warranted when at threshold diameter for 5.5cm. This provides more anatomical details in order to determine suitability for endovascular procedures.
Any AAA less than 5.5cm can be monitored via Duplex USS:
- 0-4.4 cm: yearly ultrasound
- 5-5.4 cm: 3-monthly ultrasound
A patient with a small (3cm-5.5cm) AAA has a 3% per year risk of cardiovascular mortality, hence cardiovascular risk factors should be reduced as appropriate:
- Smoking cessation (reduces rate of expansion and risk of rupture)
- Improve blood pressure control
- Commence statin and aspirin
- Weight loss and increased exercise
Note: In the UK, any AAA >6cm requires notification to the DVLA and disqualifies from driving until repaired.
Surgery should be considered for an AAA >5.5cm in diameter, AAA expanding at >1cm/year, or a symptomatic AAA in a patient who is otherwise fit. In unfit patients the AAA may be left until 6cm prior to repair, due to the significant risk of mortality due to elective repair compared to the risk of mortality if not repaired.
The main treatment options are open repair or endovascular repair
- Open repair involves a midline laparotomy or long transverse incision, exposing the aorta, and clamping the aorta proximally and the iliac arteries distally. This segment is then removed and replaced with a prosthetic graft.
- Endovascular repair involves introducing a graft via the femoral arteries and fixing the stent across the aneurysm.
Both open repair and endovascular repair have similar long term outcomes. Endovascular repair does have an improved short term outcome in terms of decreasing hospital stay and 30 day mortality, yet has a higher rate of reintervention and aneurysm rupture. After 2 years the mortality for both procedures is the same, therefore in young fit patients an open repair may be more appropriate.
An important complication for EVAR aneurysmal repair is endovascular leak, whereby an incomplete seal forms around the aneurysm resulting in blood leaking around the graft.
Endoleaks are often asymptomatic hence regular surveillance (usually via CT angiography) is needed. If left untreated, the aneurysm can expand and subsequently rupture. As such, any aneurysm expansion following EVAR warrants investigation for endoleak.
Endoleaks can be classified by the underlying mechanism causing the leak:
|Type 1||A leak occurs at the graft ends due to an inadequate seal, most common following thoracic aneurysm repairs; 1a = proximal, 1b = distal, 1c = iliac occlude|
|Type 2||Sac filling occurs from a branch vessel, most common in AAA repairs (also termed retroleak). Most resolve spontaneously and require no treatment. 2a = single vessel, 2b = two or more vessels|
|Type 3||A leak occurs through a defect in the graft fabric. 3a = separation of sections of the graft, 3b = hole in the graft.|
|Type 4||A leak occurs through the graft fabric due to the graft porosity, often occurs intraoperative and resolves with cessation of anticoagulants|
|Type 5||Continued expansion of the aneurysm sac without any demonstrable leak on imaging (also termed endotension)|
The main complication of AAA is rupture, as discussed below
Other less common complications include:
- Retroperitoneal leak
- Aortoduodenal fistula
The risk of AAA rupture increases exponentially with the diameter of the aneurysm, the risk is also increased by smoking, hypertension, and being female.
An AAA rupture can present with abdominal pain, back pain, syncope, or vomiting. On examination they will typically be haemodynamically compromised, with a pulsatile abdominal mass and tenderness.
- Around 50% patients present with the ‘classic triad’ of ruptured AAA (flank or back pain, hypotension, and a pulsatile abdominal mass).
20% of AAA ruptures will rupture anteriorly into the peritoneal cavity (which are associated with a very poor prognosis), whilst 80% rupture posteriorly into the retroperitoneal space
Managing a Suspected AAA Rupture
Any suspected AAA rupture warrants immediate high flow O2, IV access (2x large bore cannulae), and bloods taken (FBC, U&Es, clotting, and crossmatch (minimum 6U)).
- Treat any shock initially with fluids and O negative blood, keeping the BP≤100mmHg (a term called ‘permissive hypotension’, preventing excessive blood loss)
If the patient is unstable, they will require immediate transfer to theatre for open surgical repair. If the patient is stable, they will require a CT angiogram to determine whether the aneurysm is suitable for endovascular repair.
The patient should be transferred to the local vascular unit, with the vascular registrar, consultant, anaesthetist, theatre, and blood transfusion lab informed.