Abdominal aortic aneurysm

Published on 02/04/2015 by admin

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Last modified 22/04/2025

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123 Abdominal aortic aneurysm

Instruction

This patient presented with low-back pain; examine the abdomen.

Salient features

History

• Vague abdominal pain

• History of embolization

• Family history of rupture of abdominal aortic aneurysm

• History of smoking.

Remember: Three-quarters of the patients are asymptomatic.

Examination

• Large expansile pulsation along the course of the abdominal aorta (examination for a pulsatile mass should be done by bimanual palpation of the supraumbilical area)

• Auscultate for bruit over the aneurysm and over the femoral pulses

• ‘Trash’ foot: digital infarcts in patient with easily palpable pulses (suggests either a popiliteal or abdominal aneursysmal source of emboli) (BMJ 2000;320:1193–6)

• Examine all peripheral pulses.

Proceed as follows:

• Tell the examiner that you would like to check the following:

• Urine for sugar
• BP
• Serum lipid panel.

Remember:

• Popliteal artery aneurysms often coexist and, in fact, their presence should prompt the physician to look for an abdominal aortic aneurysm.

• Ninety per cent of atherosclerotic abdominal aortic aneurysms present below the origin of the renal arteries and can involve the aortic bifurcation.

• The infrarenal aorta is normally 2 cm in diameter; when it exceeds 4 cm an aneurysm is said to exist.

• True arterial aneurysms are defined as 50% increase in the normal diameter of the vessel.

• Aneursymal process may affect any medium or large artery.

• The most commonly affected vessels are the aorta and iliac arteries, followed by popiliteal, femoral and carotid vessels.

Diagnosis

This patient has a large pulsatile mass in the epigastrium (lesion) caused by an aneurysm of the abdominal aorta (aetiology). The patient complains of pain over the location of the mass, suggesting inflammation and impending rupture (functional status).

Questions

Is clinical examination sensitive in the detection of abdominal aortic aneurysm?

Sensitivity of abdominal palpation for detection of abdominal aortic aneurysms increases with the diameter of the lesion: 61% for aneurysms 3·0–3·9 cm, 69% for those 4·0–4·9 cm and 82% for those ≥5·0 cm. The palpation sensitivity also depends inversely on the size of the abdominal waistline (Arch Intern Med 2000; 160:833–6).

Which investigations would you do to confirm your diagnosis?

• B mode ultrasonography of the abdomen: a simple, cheap and accurate screening test.

• Large aneurysms require angiography, but angiography may underestimate the size of lumen because of large clots.

• MRI is useful, particularly as it does not require administration of contrast.

• CT (Fig. 123.1).

image image

Fig. 123.1 An infrarenal abdominal aortic aneurysm by CT (A) and in three-dimensional CT reconstruction.

(With permission from Bhangu, Keighley 2007.)

Remember: Plain abdominal radiography shows a calcified aneursymal aortic wall in only half the cases (Fig. 123.2).

image image

Fig. 123.2 Calcification of the abdominal aorta (arrowheads) in plain radiographs. Calcification of the abdominal aorta is usually much easier to see on the lateral view (B).

(With permission from Mettler 2004.)

Advanced-level questions

How would you manage an abdominal aneurysm?

<4.5 cm: follow-up with ultrasonography every 6 months

4.5–5.0 cm: follow-up with ultrasonography every 3 or 6 months

5.0–5.5 cm: surgery or follow-up

>5.5 cm: pooled data suggest there is a high risk of rupture and hence patients should be referred for surgery if there are no confounding factors that increase the risk of surgery.

The UK small aneurysm trial studied 1090 patients with an aortic aneurysm of diameter 4–5 cm and found a 30 day mortality of 5.8%, mean annual risk of rupture for small aneurysms of 1% and no difference in survival between their treatment groups at 2, 4 or 6 years (Lancet 1998;352:1649–55). Smaller aneurysms must be followed up as they enlarge at a rate of about 0.5 cm a year. In selected cases, an endovascular prosthesis is preferred.

What factors predispose to rupture of the abdominal aneurysm?

• Diameter of the aneurysm

• History of smoking

• Diastolic BP

• COAD

• Family history of ruptured aneurysm

• Rate of expansion

• Inflammatory aneurysms.

What is the prognosis of aneurysms >55 mm?

Mortality rate for a patient undergoing elective surgery is <5%, whereas that for a ruptured aneurysm is nearly 90%.

What are the sites of rupture of abdominal aortic aneurysm?

• Anterolateral free rupture in the abdominal cavity:

• Retroperitoneal rupture
• Rupture of retroperitoneal sac
• Rupture into the duodenum
• Rupture into the inferior vena cava.

What are the types of abdominal aortic aneurysm?

• Aneurysms are usually classified into true, false and dissecting aneurysms.

• The Crawford classification defines into four types by anatomic location and extent of involvement:

I: involve all or most of the descending thoracic aorta and the upper abdominal aorta
II: aneurysms involve all or most of the descending thoracic aorta and all or most of the abdominal aorta
III: involve the lower portion of the descending thoracic aorta and most of the abdominal aorta
IV: involve all or most of the abdominal aorta, including the visceral segment.

• Pathological types of abdominal aortic aneurysm include:

• inflammatory: characterized by dense periaortic fibrosis containing abundant lymphoplasmacytic inflammation with many macrophages and often giant cells; cause unclear
• mycotic: lesions that have become infected by the lodging of circulating microorganisms in the wall (particularly in bacteraemia from a primary Salmonella gastroenteritis); suppuration further destroys the media, potentiating rapid dilation and resulting in rupture.

What do you know about the pathogenesis of abdominal aortic aneurysms?

Abdominal aortic aneurysm is linked to the degradation of the elastic media of the atheromatous aorta. An inflammatory cell infiltrate, neovascularization and production and activation of various proteases and cytokines also contribute to its development Although elastin fragmentation and attenuation of the tunica media are the most important characteristics of the wall of an aneurysm, the adventitial tissue, in which collagen is predominant, is responsible for the resistance of the aorta in the absence of elastin in the tunica media. Collagen degradation is currently considered the ultimate cause of rupture.

The elastic and collagen fibres are degraded by proteolytic enzymes, mostly represented by matrix metalloproteinases (MMP) locally activated by either other MMPs or by plasmin generated by plasminogen activators. The role of MMPs and plasmin in the development of abdominal aortic aneurysms has been shown in animal models. The tissue inhibitors of matrix metalloproteinases (TIMP) are also increased in the wall of the aneurysm. The balance between proteases and antiproteases seems to be tilted in the favour of proteolysis (Lancet 2005; 365:1577–89).

What do you understand by endovascular repair?

The technique of endovascular repair was introduced by Parodi in 1991 (Ann Vasc Surg 1991;5:491–9) and consists of the placement of a graft across the aneurysm and the fixation to the normal aortic and iliac wall with stents at both ends. The aortomonoiliac percutaneous approach consists of the insertion of a stent graft, which is a tube of conventional graft fabric containing at least two stents. A successful attachment requires a segment of non-dilated aorta (neck) between the renal arteries and the aneurysm that is at least 1.5 cm in length, and the device insertion requires that lumens of the iliac arteries be at least 7 mm in diameter. The complete exclusion of blood by the endovascular repair lowers the pressure in the aneurysm sac, which causes the graft to shrink. However, ‘an endoleak’ from the top or bottom (type 1) or though the graft defect (type 3) is associated with persistent risk of rupture. In the United Kingdom Endovascular Aneurysm Repair 1 (EVAR 1), a large randomized trial, endovascular repair of large abdominal aortic aneurysm (at least 5.5 cm in diameter on CT) was associated with a significantly lower operative mortality than open surgical repair. However, no differences were seen in total mortality or aneurysm-related mortality in the long term. Endovascular repair was associated with increased rates of graft-related complications and re-interventions and was more costly (N Engl J Med 2010; 362:1863–71). In the United Kingdom Endovascular Aneurysm Repair 2 (EVAR 2) randomized trial involving patients who were ineligible for open repair, endovascular repair of abdominal aortic aneurysm was associated with a significantly lower rate of aneurysm-related mortality than no repair. However, endovascular repair was not associated with a reduction in the rate of death from any cause. The rates of graft-related complications and reinterventions were higher with endovascular repair, and it was more costly (N Engl J Med 2010; 362:1863–71).

In 1951, C Dubost from Paris performed the first successful aortic resection for aneurysm.

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