AAA occurs when there is dilation of the abdominal aorta such that the diameter is >3cm. The normal infrarenal aorta size (after 50 years old) is 1.5cm in females.
🏘 Epidemiology
AAA is present in 1 in 70 men >65 years of age. It kills about 3000 every year due to rupture of the AAA.
Pathophysiology
Let’s recap our aorta anatomy quickly:
It is an elastic artery as it has a thick tunica media layer that has many elastic fibres. It also has an internal elastic lamina + endothelium within the intima layer. While the outer layer is made up of the adventitia and an external elastic lamina. So as we can see, the elasticity of the aorta is vital for its function and structural integrity.
It occurs primarily due to dysfunction of elastic proteins, thus leading to dilation of all layers of the arterial wall. The failure of these proteins may be due to congenital or acquired diseases/factors.
AAA is initiated by a loss of the tuna intima elastin fibres and the subsequent layers follow.
The process is accelerated as we get increased proteolytic activity and lymphocyte infiltration.
⚠️ Risk factors
As the aetiology is unknown it us difficult to pinpoint risk factors. However, some are:
- Connective tissue disorders
- Ehlers Danlos type 1
- Marfan’s
- Syphilis
- Atherosclerosis
- Takayasu’s aortitis
- Previous trauma
Other risk factors include:
- Smoking
- Hyperlipidaemia
- Hypertension and existing CV disease
- Family history
- Male gender
- Increasing age
Supposedly diabetes mellitus is protective, but this is not well understood.
😷 Presentation
Most AAAs are asymptomatic and are an incidental finding.
Patients who are symptomatic present with:
- Abdominal pain
- Back/loin pain - this gives clinicians the differential diagnosis for renal colic as back pain is present sometimes without any other symptoms.
- Limb ischaemia due to distal embolisation, can also be end-organ ischaemia. Trashing occurs when we get multiple, small distal emboli (leaving a non-blanching rash).
- Aortaenteric fistula
On examination:
⭐️ Non-tender, laterally expansile mass above the umbilical level.
- Severe central abdominal radiating to back/loin pain
- Signs of shock
- Syncope
🔍 Investigations
👀 Screening
Screening for AAA entails a single abdominal USS for males aged 65 years old.
The outcome of this scan will determine further screening options:
Aorta width | Interpretation | Action |
< 3 cm | Normal - No further action | |
3 - 4.4 cm | Small aneurysm | Rescan every 12 months |
4.5 - 5.4 cm | Medium aneurysm | Rescan every 3 months |
>= 5.5cm | Large aneurysm | Refer within 2 weeks to vascular surgery for probable intervention.
Only found in 1 per 1,000 screened patients |
🧰 Management
Criteria for elective surgery:
- Anyone with an AAA >5.5.cm should be considered for surgery
- AAA expanding at >1cm annually
- Symptomatic AAA
Surgery may be performed via open repair or with endovascular repair, both have similar outcomes long term.
- Open repair - midline laparotomy/long transverse incision to expose the aorta. The aorta is clamped proximally and the iliac arteries are clamped distally. The segment with the aneurysm is then removed and a graft is inserted to replace it.
- Endovascular repair - a graft is introduced by the femoral arteries and placed across the aneurysm.
🚨 Complications
- Endovascular leak - an incomplete seal is formed with the graft and so blood leaks around it. They are asymptomatic and usually found on follow up. EV leaks warrant regular surveillance, as if they are left untreated the aneurysm will continue to expand and rupture. We can classify the leaks from type 1 - type 5:
Classification | Description |
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. 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) |
- Retroperitoneal leak
- Embolisation
- Aortoduodenal fistula
😷 Presentation
⭐️ Severe central abdominal radiating to the back/loin pain
⭐️ Signs of shock (hypotension, tachycardia)
⭐️ Syncope
⭐️ Pulsatile abdominal mass
20% of ruptures are anteriorly into the peritoneal cavity (has worse prognosis) while 80% are into the retroperitoneal space.
🧰 Management
It is a surgical emergency and so we need to give:
- High flow oxygen
- 2 x large bore IV cannulae for IV access
- Urgent bloods (FBCs, U&Es, clotting, crossmatching of at least 6 units)
→ If the patient is haemodynamically unstable - they need to be transferred to theatre immediately for open repair.
→ If the patient is haemodynamically stable - a CT angiogram should be taken to determine if they are suitable for endovascular repair as opposed to open. However, open repairs have better long-term outcomes.