Case 27.1 – Abdominal Aortic Aneurysm (AAA)

In thin patients:

• pulsation may be visible on inspection
• pulsatile, expansile swelling in the midline of the abdomen, usually extending towards the left-hand side
• bruit on auscultation in association with origin stenoses of the branches of the abdominal aorta (coeliac axis, superior mesenteric, renal arteries)
• There is an association between AAA and aneurysms elsewhere, so the examiner should specifically exclude the presence of femoral and popliteal aneurysms
• The surface marking of the aortic bifurcation is at the level of the umbilicus, so any pulsation felt below this level is likely to denote the presence of iliac aneurysmal disease.

However, it is important to appreciate that clinical examination alone, even when performed by an experienced vascular surgeon, may be unreliable for confirming the presence or absence of aneurysmal disease and for estimating the size of the aorta.

An AAA may present in the following ways:

• Asymptomatic (30%). The AAA may be detected incidentally on routine physical examination, or most commonly, abdominal ultrasound scan conducted for another reason.
• Symptomatic (20%). AAA may cause pain in the central abdomen, back, loin, iliac fossa or groin. Thrombus within the aneurysm sac may be a source of emboli to the lower limbs. Less commonly, the aneurysm may undergo thrombotic occlusion. AAA may also become inflamed and then compress surrounding structures such as the duodenum, ureter and the inferior vena cava.
• Rupture (50%). AAA may rupture, usually into the retroperitoneum, but sometimes into the peritoneal cavity or rarely into surrounding structures Eg duodenum.

True aneurysms:

All three layers of the arterial wall enclose a true aneurysm

False aneurysms:

If the wall of an artery is pierced, the resulting haematoma sometimes remains in continuity with the lumen via the puncture site. A pulsatile swelling then forms, the wall of which consists of compacted thrombus and surrounding connective tissue. Small aneurysms (2-3 cm in diameter) often thrombose spontaneously. Larger aneurysms tend to expand, especially if the patient is on aspirin, heparin or warfarin, and compress surrounding tissues. The most common site is the groin after common femoral artery instrumentation, and this may cause femoral vein compression and deep venous thrombosis (DVT).

Atherosclerosis:

There is continuing controversy over whether aneurysmal disease is just another manifestation of atherosclerosis. However, many believe it to be a separate condition-medial degenerative disease. Nevertheless, there is no doubt that aneurysmal disease shares the same risk factors as atheromatous occlusive disease (although hypertension appears a more important factor) and that aneurysmal and occlusive arterial disease often coexist. In addition, there is a strong familial element in aneurysmal but not in occlusive disease. Furthermore, there are patients, some of whom have never smoked, who exhibit widespread aneurysmal dilatation (arterial ectasia or arteriomegaly) without any evidence of peripheral, cerebral or coronary occlusive disease.

Inflammation:

In some patients, atherosclerosis, whether associated with aneurysmal dilatation or not, can lead to an intense periadventitial inflammatory and fibrotic response. The reasons are unclear, but clinical problems can occur in consequence.

Dissection:

Weakness of the aortic wall may result in an intimomedial tear and allow blood to track under pressure through and/or out with the various layers of the wall. Such a dissecting aneurysm usually affects the thoraco-abdominal aorta. Rupture may occur outwards (usually fatal) or inwards into the aortic lumen with the subsequent formation of a large saccular aneurysm in the weakened section. Causes of the defect include:

• atherosclerosis, usually with hypertension
• Marfan's syndrome in which there is a structural defect in the biochemical nature of the media.

Infection:

The arterial wall is normally highly resistant to bacterial and other infections. However, certain organisms (Salmonella and Treponema pallidum) have a particular ability to infect, and thus to weaken, the aortic wall, leading to the formation of a mycotic aneurysm and its rupture.

Criteria	Treatment
Symptomatic aneurysms regardless of size	Urgent surgery
Asymptomatic aneurysms of diameter < 5.5 cm	Surveillance if increasing by < 1 cm/year; Elective surgery if increasing by > 1 cm/year
Asymptomatic aneurysms of diameter > 5.5 cm	Elective surgery

The UK Small Aneurysm Trial and the similar US-based ADAM trials have shown that the risks of open surgery generally outweigh the risks of rupture until an asymptomatic AAA has reached 5.5 cm in antero-posterior maximum diameter.

Once a small AAA has been detected, the best way of following up the affected patient is by repeated ultrasound scans at 3-6-monthly intervals and best medical therapy (smoking cessation, control BP, aspirin or other anti-platelet agent, lipid lowering therapy), which affords the same benefits as it does in patients with occlusive disease (which often coexists).

Ultrasound is only accurate to about 0.5 cm and tends to underestimate AAA size. Thus, most surgeons will arrange for a CT scan to be performed when the AAA reaches 5.0 cm, along with other tests designed to assess fitness for surgery. Once the AAA reaches 5.5 cm and assuming the clinical assessment and investigations indicate that the patient is fit for surgery, the surgeon will normally begin discussions with the patient with a view to operative repair (open or endovascular).

Indications for elective repair:

The decision to operate involves weighing the known risk of leaving the AAA in place against that of operation. The first depends upon:

• size
• presence of symptoms
• age and physiological state

The risk of operation depends primarily upon cardiorespiratory status. Anaesthetists and cardiologists can help the surgeon assess this, and also life expectancy, more precisely. There is no advantage to be gained in repairing a small aneurysm at low risk of rupture in an elderly person with severe myocardial disease whose cardiac prognosis is poor.

The reported annual risk of rupture varies quite widely but is probably in the region of:

• 6cm: 5-10%
• 7cm: >20%

Balancing the risks of surgery against those of rupture can be difficult in smaller aneurysms. The UK Small Aneurysm Trial found that for stable AAAs of 4-5 cm diameter, surveillance was safer than surgery, as the rupture risk was about 1% per annum. This does not apply to saccular or mycotic aneurysms, rapidly expanding or symptomatic aneurysms and perhaps equivalent-sized AAAs in small females. Such patients should all be treated surgically.

The 30-day major morbidity and mortality for open AAA repair is approximately 10% for elective asymptomatic AAA, 20% for emergency symptomatic AAA and over 50% for ruptured AAA.

Popliteal aneurysms:

These are present in 10 - 20% of patients with AAA and their presence must be sought, if necessary with ultrasound, in all such patients. Around 50% are bilateral. If a patient presents with a popliteal aneurysm, there is a 50% chance that he or she also has an AAA, which again must be sought.

The main complications of popliteal aneurysm are distal embolization and acute thrombosis; the latter is associated with limb loss in up to 50% of cases because the calf vessels are often chronically occluded, which makes surgical bypass difficult.