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== Aortic == * Aetiology ** Ascending aorta - typically degenerative or the sequela of prior dissection ** Infra-renal: * Distribution: ** Majority in infra-renal segment - 30% of all aortic aneurysms ** 1% of men 55-64 have a AAA > 4cm, which increases with advancing age by 2-4% per decade * Natural history ** Natural history is of progressive enlargement (2-3mm per year) leading to increased risk of rupture * Rupture risk: ** Maximal AAA diameter is the standard basis ** RFs for rupture: female, larger initial AAA diameter, smoking, lower FEV1, higher mean BP. Saccular morphology. ** Imaging characteristics for increased risk of rupture: dissection, mural thrombus, dissection of the peripheral calcification of the aneurysm sac. ** Risk of rupture declines when smoking is ceased and HTN is controlled. ** * Diagnosis ** History *** Typically asymptomatic *** Can get NSAP and/or lower back pain *** Sometimes feel pulsations *** Can sometimes see a pulsatile mass ** Examination *** Pulsatile mass, most commonly supra-umbilical and in the midline, but the location is variable *** Remember to check for POPA and femoral artery too ** Imaging *** USS has excellent sensitivity and specificity - good for screening and surveillance. Not an ideal method for detecting rupture (sensitivity might be lower than 50%). *** CT - better reproducibility of diameter measurements than USS. Best pre-op preparation. *** MRI - good, but does not detect aortic wall calcification, which can be important. Only really useful in inflammatory aneurysms where it helps show the extent. *** Angiography - only used where detailed characterisation of an aneurysm is required or for intervention, or in the case or pre-operative embolisation of an accessory renal artery prior to EVAR. * Screening: ** See bottom of this page for full table ** Rough consensus: *** One-off USS screening for all men at age 65 *** Screen first-degree relatives of those with AAA once they reach 50 years old *** Selective screening for those at high risk (women >65 who smoke, have CVA or FHx *** Generally, those who screen negative initially are at very low risk of developing a AAA later * Surveillance ** Those with infra-renal AAA 4-5.4cm should have an USS every 6-12 months * Medical therapy ** Lots of things (ACE inhibitors, beta blockers, statins, anti-platelets) have slowed AAA growth in mice, but none have worked in humans to date * Indications for repair ** Consider: operative risk (use VSGNE risk index), rupture risk, morbidity due to rupture ** Symptomatic *** Thrombosis *** Embolization of mural debris - lower extremity ischaemia/trash foot syndrome *** Compression of adjacent organs *** Aortic dissection *** Rapid expansion/impending rupture *** Frank rupture - haemodynamic instability **** Consider direct to theatre. Alternative is rapid resus with permissive hypotension and rapid CTA **** CT: heterogeneous mural thrombus, loss of fat planes around aorta, periaortic inflammation, retroperitoneal haematoma ** Asymptomatic *** Aneurysm diameter >5.5cm in men and 5.0cm in women (UK Small Aneurysm Trial showed very low risk of rupture for <5cm: 2.5% annually) **** Use risk factors for rupture (above) to personalise decision **** The real issue is timing rather than eventual necessity of repair - over 80% of patients in the ADAM trial with aneurysms 5-5.4cm EVENTUALLY underwent repair **** However earlier repair (<5.5cm) provides no survival benefit compared with surveillance and subsequent repair once it gets >5.5cm *** 12-month growth rate of 10mm or greater in either gender *** Saccular aneurysms *** Dissection of mural thrombus *** Fracture of saccular calcification * Surgery ** See 'Open AAA repair' page for discussion on choice between open vs EVAR
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