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a rough guide to abdominal aortic aneurysms
- 1. A rough guide to abdominal aortic aneurysms By Nick Harper
- 2. The abdominal aorta T12 L4 • Normal diameter:16 to 22mm • Aneurysm: ≥50% increase • Rupture: 8000 deaths in total per year in the UK •1.5% of deaths in men between 65 and 85 •(Sakalihasan, N. et al. 2005)
- 3. Prevalence • Men between 3 to 8% • Women between 0.5 to 1.5% (Wilmink, A.B. & Quick, C.R., 1998). For the ≥50 age group (Vardulaki, K.A. et al. 2000)
- 5. What causes AAAs? •genetic predisposition •Marfans •Loyes-Dietz •Ehlers Danlos •Atherosclerosis •haemodynamic strain •thrombus formation •enzymatic degradation •Vasculitis •Syphilis •cystic medial necrosis •trauma The aortic wall: Elastin Lamellae decrease from thoracic to abdominal
- 6. Proteases Adventitia Media Thrombus Elastin Collagen VSMC P P P TIMP Neutrophils 1 2 3 4 MMPs - Matrix Metalloproteinases TIMPs - Tissue inhibitors of MMPs (Allaire, E. et al. 2009).
- 7. Detection
- 8. Imaging Ultrasound initial assessment and follow up Quick, easy, cheap & no radiation. Can measure the size of the aorta to the nearest 3mm Doppler scans allow visualization of blood flow CT if considering a surgical procedure More accurate, high sensitivity and specificity 3D reconstruction CT angiography BUT! cost, time and radiation exposure Aortic Wall Lumen Thrombus
- 9. Open Repair Procedure 1. general anaesthesia. 2. midline incision 3. AAA is identified 4. Proximal control – Clamp the Aorta (preferably below the renal arteries) 5. Distil Control – Clamp the common iliac arteries 6. The aneurysm is opened and any thrombus is removed 7. A graft is anastamosed to either end of the affected section 8. Clamps are removed and blood flow is returned Mortality rates following elective open repair: 4.6% 30 days post-op 6.3% after 4 Years (AAA related mortality only)
- 10. •Bilateral femoral artery access via Seldinger technique •Aortogram •Catheter insertion •Deployment of main body •Insertion and deployment of contralateral limb Endovascular aortic aneurysm repair (EVAR) Deployment Catheter EVAR stent graft Main body Contralateral limb Mortality rates following elective EVAR •1 to 2% 30 days post-op •3.5% after 4 Years (AAA related mortality only)
- 12. Comparing EVAR to open repair Advantages No difference Disadvantages • Can be performed without general anaesthesia • Long term all cause mortality • Higher rates of complication • Shorter postoperative stay by on average 5 days • Graft stenosis or infection • Secondary intervention more likely to be required. This is successful in 84% of cases • Lower 30 day mortality (odds ratio 0.46) • More expensive ≈ £12,000 for EVAR compared to ≈ £10,000 for open repair • Lower long term aneurysm related mortality (hazard ratio 0.39) (Lovegrove, R.E. et al. 2008) • In younger patients open repair may be a longer term solution
- 13. Ruptures EMERGENCY! • 100% mortality if untreated! • Sudden & severe abdominal pain • radiation to back and groin. • Shock • ΔΔ acute pncreatitis Acute management •Call a vascular surgeon or anaesthetist •wide bore IV access •If the shock is severe give blood •keep systolic BP ≤100mmHg •ECG & blood amylase/lipase •Crossmatch blood •Take the patient to theatre for open repair Size of AAA Risk of rupture per year 4cm or less Low risk 4 - 5cm 1 in 100 per year 5 - 6cm 1 in 12 per year 6 - 7cm 1 in 6 per year Over 7cm 1 in 4 per year or higher
- 14. Prevention • Control of risk factors • Ultrasound screening roughly halves AAA related mortality in men over the age of 65. (Fleming, C. et al.2005). • UK AAA screening program • Starting spring 2009. • For men aged 65 years and older. • http://aaa.screening.nhs.uk/.
- 16. References • Allaire, E., Schneider, F., Saucy, F., Dai, J., Cochennec, F., Michineau, S., Zidi, M., Becquemin, J-P., Kirsch, M. & Gervais, M. (2009) New insight in aetiopathogenesis of aortic diseases. European Journal of Vascular & Endovascular Surgery. 37(5), 531-537 • Lovegrove, R.E., Javid, M., Magee, T.R. & Galland, RB (2008) A meta- analysis of 21178 patients undergoing open or endovascular repair of abdominal aortic aneurysm. british journal of surgery. 95(6), 677-684 • Sakalihasan, N., Limet, R. & Defawe, O D. (2005) Abdominal aortic aneurysm. Lancet. 365(9470), 1577-1589 • Vardulaki, K.A., Walker, N.M., Day, N.E., Duffy, S.W., Ashton, H.A. & Scott, R.A. (2000) Quantifying the risks of hypertension, age, sex and smoking in patients with abdominal aortic aneurysm. British Journal of Surgery. 87(2), 195-200
Editor's Notes
- For it to be an abdominal aortic aneurysm (AAA) it must occur between the level at which the aorta crosses the diaphragm (T12) and the bifurcation into the common iliac arteries at L4. The main reason why you are interested in aneurysms is that they can rupture! If untreated this has a 100% mortality rate AAAs typically grow at a rate of about 1-2 mm per year but can also grow in sporadic spurts
- The main risk factors are on the left hand side. Unfortunately, other than stopping smoking, there is not a whole lot you can do about them. Several studies have found diabetes to be protective against AAA progression. It is thought that this is due to the thicker and stiffer aortic wall seen in diabetics.
- True aneurysms can be either saccular or fusiform in shape (Saccular are more prone to rupture) False or pseudoaneurysms occur when there is a small leak in the aortic wall. Blood leaks out, clots and forms a haematoma. This encapsulates the original tear and stops blood leaking out but still communicates with the vessel below. Common to all is thrombus formation within the lumen
- The media of the aortic wall contains elastin for distensibility and collagen for tensile strength. This is crucial for pulse propagation! The number of elastin lamellae within the media of the aortic wall decreases as you progress form the thoracic to abdominal aorta. This is thought to underlie the fact that AAAs are 3X more likely than thoracic abdominal aneurysms. Marfans – mutation in Fibrilin encoding gene Loeys Dietz – Mutation in TGF beta signalling pathway Ehlers Danols – Mutation in collagen encoding gene The formation of AAAs is usually regarded as a complex interaction of factors rather than a single underlying cause.
- The most recent research is concentrating on the enzymatic degradation of the extracellular matrix proteins within the aortic media. The diagram shows a summary of the current theory: Thrombus formation within the lumen traps neutrophils. These then secrete protease enzymes (most importantly MMPs) which diffuse into the aortic media. The proteases degrade elastin, collagen and also kill vascular smooth muscle cells (VSMCs) VSMCs normally produce an inhibitor of MMPs. Therefore by removing these cells, protease action goes ahead unchecked. Angiogenesis within the adventitia is a common finding in abdominal aortic aneurysms (usually totally devoid of vaso vasorum). These blood vessels bring in a concentrate even more protease producing leukocytes. Net Result: Decreased elastin, collagen and smooth muscle. This leades to a weakened aortic wall and possible aneurysm formataion/progression.
- If the patient has a particularly large abdomen, ultrasound may not be able to pick up the AAA. CT may be a better option.
- The main complication of EVAR repair