Abdominal aortic aneurysm
Abnormal dilation of the abdominal aorta.
Abdominal aortic aneurysms (AAA) are present in 2% of men aged 60–84 years and are an important cause of death, 6000 per annum in United Kingdom.
Increases with age, rare under 50 years.
M > F (10–20:1)
Becoming more common in the developed world.
Risk factors are as for atherosclerosis, including smoking, hypercholesterolaemia, age, sex, diabetes. Hypertension in particular plays an important role in the enlargement and rupture. Patients with abdominal aortic aneurysms commonly have associated coronary artery disease, cerebrovascular disease and more extensive peripheral vascular disease.
The arterial wall becomes thinned and is replaced with fibrous tissue and stretches to form a dilated saccular or fusiform aneurysm. The majority (95%) are infrarenal, i.e. arise below the renal arteries, but they may extend down to the iliacs or there may be multiple separate aneurysms, e.g. femoral and popliteal. Suprarenal aneurysms may also involve the thoracic aorta.
As the aneurysms slowly enlarge at an average of 0.5 cm per year, they cause local pressure problems and have an increased risk of rupture. They may dissect and cut off blood supply to tissue (e.g. kidneys) or rupture with resulting haemorrhage.
Altered flow patterns predispose to thrombus formation, which may embolise to distal arteries or cause occlusion at the site of the aneurysm.
Abdominal aortic aneurysms may be found incidentally as a central expansile mass on examination or as calcification on an X-ray. A tender mass suggests a high risk of rupture.
Patients may present with a dull, aching chronic or intermittent epigastric or back pain due to expansion. Rupture causes a tearing epigastric pain that radiates through to the back or referred sciatic or loin to groin pain. Rupture through all three layers of the wall causes profound shock. Occasionally a small leak ‘herald bleed’ may cause a shorter, less severe episode of pain some days or weeks before rupture occurs.
Fistula formation into the bowel causes catastrophic fresh rectal bleeding.
Thirty per cent of aneurysms will eventually rupture. More than half of aneurysms over 6 cm will rupture within 2 years – thromboembolism.
CT with contrast and ultrasound scans will demonstrate the position and wall thickness of the aneurysm. Angiography or 3-D MRI reconstruction may be used to define the anatomy prior to deciding on surgical man-agement.
Ruptured abdominal aortic aneurysm is a surgical emergency.
Careful resuscitation is required, maximal systolic blood pressure should be 80–90 mmHg to maintain renal and cerebral perfusion without exacerbating the leakage. O negative blood may be required until blood is crossmatched, as blood loss can be massive.
Surgery at a specialist centre gives the best outcome, but patients may not be fit for transfer.
The aneurysm is cross-clamped, partially excised and replaced with a Dacron graft. If the aneurysm is too low, or when the iliac and femoral arteries are either aneurysmal or too diseased with atherosclerosis, a ‘trouser’ bifurcation graft is used to anastomose to the iliac or femoral arteries.
Asymptomatic small aneurysms should be managed conservatively with aggressive management of hypertension and other risk factors for atherosclerosis and yearly ultrasound scans to monitor progress.
Abdominal aortic aneurysms over 5 cm should be treated electively. Whilst surgical techniques remain the standard treatment, increasingly endovascular stenting techniques are being used that can be performed under local anaesthetic.
Mortality rate in elective surgery is 5% or less. In ruptured abdominal aortic aneurysms only 20% survive,
even if patients survive to surgery mortality is 50%. Suprarenal aneurysms have a much poorer prognosis with a high risk of renal impairment. Many patients have concomitant ischaemic heart disease or cerebrovascular disease, which affects outcome.
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