Learning Center
Plans & pricing Sign in
Sign Out



•     Dilation > 1.5X normal size 2 cm
•     True = localized dilation of wall involves all layers
•     False (pseudo) = only covered by a fibrous capsule, pulsatile hematoma;
      collection of blood surrounded by adventitial only that connects with lumen.
      Can arise from defect in arterial wall or leaking anastamosis (late complication
      post AAA repair)
•     Male > Female
•     95% are infrarenal but any location possible
•     Rupture rare b/f 3cm
•     Increases with age; rare < 50 yo; 3% > 50yo
•     Atherosclerosis common: CAD, PVD
•     Family history

•    95% associated w/ atherosclerosis but NOT a cause-effect relationship
•    Degeneration more important than atherosclerosis
•    Others: infection, CT disease, trauma, arteritis
•    High risk: >65yo, Male > female, PVD, CAD, CVD, Fhx of AAA

•   Growth: 0.2 - 0.5 cm/year, extremely variable
•   Rupture: retroperitoneal, intrperitoneal, GIT
•   Emboli can form due to mural thrombi
•   Inflammatory AAA: dense fibrotic with inflammatory rxn in walls and adjacent
    retroperitoneal structures, may lead to ureteral obstruction, etc
•   Risk of rupture
                 Size is most important factor
                 NO safe size exists; small ones can rupture
                 Most are > 5cm that rupture
                 <5cm: don’t fix b/c risk of rupture low (0.3%/yr)
                 5cm - 7cm: fix (10%/yr)
                 > 7cm: fix (20%/yr)
                 growth of 0.5cm/yr is acceptable
                 growth 0.5cm/yr requires surgery

•    Almost never dissect like thoracic aneurysms
•    >50yo + Renal colic ------- MUST THINK OF AAA
•    70% Asymptomatic
•    10% Symptomatic
                 expansion pain
                 thromboembolism
                 fistula (aortoduodenal, aortocaval)
•    20% Present w/ Rupture
                   Abdominal or Back Pain
                   Pulsatile abdominal mass
                   Hypotension
                   Distal pulses may be intact
                   50% die immediately

•    Pain: abdo/flank/back, dull ache, chronic, throbing, colicky
•    Mass: abdomenal fullness, sense of pulsation
•    Incidental finding is most common
•    Pulsatile abd mass on physical examination
•    Usually at or above umbilicus (bifurcation at umbilicus)
•    Peripheral emboli
•    Peripheral cholesteral emboli: livido reticularis, blue toes syndrome (cool,
     painful, cyantoic)
•    Compression (rare) presenting with vertebral bd erosion severe back pain,
     duodenal obstruction, ureteral obstruction

•    TRIAD: abdominal pain + hypotension + pulsatile abdo mass
•    Pain
                 Abdominal, flank, back
                 Acute, severe, constant
                 Radiates to chest, thigh, groin, scrotum, back, flank
                 Mechanism of pain not well known
                 Most present acute but may present delayed b/c of a contained
                  rupture; thus, long duration does NOT r/o AAA rupture
•    Associated features
                 Nausea, vomiting, presyncope, syncope
                 Syncope may be only presentation
                 Abdominal mass in most but NOT all (esp if small AAA, or obese)
                 Hypotension inconsistent, late, only 50% (normotension doesn’t r/
                  o AAA)
                 Abdominal ecchymosis due to blood tracking
                 Femoral neuropathy: femoral nerve compression by intraperitoneal
                  or retroperitoneal blood leading to hip/thigh pain, psoas sign,
                  weak quad, absent knee jerk, reduced sensation to anteromedial
                 ? hernia: retroperitoneal hemorrhage can extend into groin/
                  scrotum and looks like a hernia
                 Hematuria: common with AV fistula; ? indication for aortography to
                  r/o AVF
                 Rupture into GIT
                         ­       may be initial presentation
                         ­       more commonly late complication of AAA repair
                         ­       usually occurs after infection/inflammation of AAA
                         ­       may present with UGIB or LGIB
                         ­       must think of in any pt with GIB and hx of AAA repair
                    MUST THINK OF AAA IN
                    ANY PATIENT THAT YOU
                    ARE CONSIDERING…
                    1. Renal colic
                    2. Acute abdomen
                    3. AMI, esp inferior
                    4. Acute back pain
                  Rupture into vena cava
                         ­      chronic inflammation, adherence of AAA to ivc, large
                                AV fistula forms increasing venous return and
                                decreasing SVR :. hyperdynamic state and possible
                                high output CHF; note presence of continous
                                murmur in abdomen; ARF b/c of decreased renal

•     Anyone > 40 yo w/ abdo, flank, back pain must think of
•     NOTE: abdo pain high usually b/c bifurcation at umbilicus :. may even present
      like inferior MI

•    AXR
                  Evidence of AAA in 70%
                  Curvilinear calcification along aortic wall
                  Paravertebral soft tissue mass
                  Erosion of vertebral body
                  Obscuration of psoas or renal outlines
                  Does NOT r/o AAA
•     ABUS
                  Best 1st line investigation
                  Nearly 100% sensitive
                  Rapid, bedside, noninvasive, sensitive
                  Operator dependant, obesity, bowel gas reduces quality, cannot
                   reliably r/o rupture; done to determine presence of AAA, not
                  Can identify intraperitoneal blood but not good for retroperitoneal
•     ABCT
                  100% sensitive
                  IV and po contrast if possible but not essential
                  Normal aortic diameter on CT r/o AAA
                  Better for detection of retroperitoneal hemorrhage than US
                  Absence of retroperitoneal blood does NOT r/o leak
•     Angiogram
                  NO role in emergent management of AAA
                  Note difference: gold standard for aortic dissection
                  May miss AAA entirely even with big AAAs

•    Role is detection and referral
•    Expandable stents have been used for high operative mortality pts
•     Early repair is one approach
•     Selective repair is another approach: repair if ...
                    Symptomatic
                    <5cm: don’t fix b/c risk of rupture low (0.3%/yr)
                    5cm - 7cm: fix (10%/yr rupture rate)
                    > 7cm: fix (20%/yr)
                    growth of 0.5cm/yr is acceptable
                    growth 0.5cm/yr requires surgery

•    Approach is ABCs, type and cross for 10 or more units, and STAT surgery
•    Think of as NEVER being stable even with normal blood pressure b/c initial
     hemorrhage often small and pt not hypotensive; however, just waiting to have
     massive hemorrhage
•    Clinical diagnosis: to OR without testing is the rule
•    ABUS, ABCT, AXR should not delay surgery especially if pt hemodynamically
•    Relatively “stable” patients may be investigated; require close observation; CT
     may fool you into thinking there is a AAA with no rupture; close ICU observation
•    Delayed fluid resuscitation as per penetrating chest trauma undecided
•    Many die post op: MI, ARF, MSOF, respiratory failure
•    Control of AAA bleeding with fogarty catheter inserted via brachial artery is an
     option only if delay in surgery
•    Thoracotomy in ED or OR may be necessary but getting to OR more imp than ED
•    NO role for preventing hypertension as with aortic dissection
•    High mortality preop, postop, no role for medical management, hypotension
     poor prognosis

•    Graft Infection
                  Contamination in OR, hematogenous spread, contiguous spread
                   from adjacent infection can lead to infection/inflammation
                  Can lead to leakage, pseudoaneurysm formation, and fistula
                  Distal limb infection may be palpable as false aneurysm in groin
                   with local signs of inflammation
                  Presents with low grade fever, mild abdo pain or back pain
                  CT shows fluid/gas around anastamosis
•    Aorto-Enteric Fistulas (AEF)
                  Early or late (years)
                  UGIB or LGIB
                  Consider in any GIB in pt with hx of AAA repair
                  Consider immediate transfer to OR on clinical basis
                  Endoscopy or CT if more stable
                  Endoscopy: UGI scope first, duodenum common location for
                   fistula, not reliable to r/o, mainly dx other pathology
                  CT: can demonstrate graft infection, not great for AEF
•     Pseudoaneurysms
                 Mass, pain in abdomen/groin
                 Distal emboli
                 May rupture
                 US, CT, angio

•    Admit all symptomatic, surgical consult
•    Incidental: refer, RTED for pain, syncope
•    Admit for w/u of possible graft infection

•     Bilateral, multiple, 50% associated w/ aortic aneurysms :. must look for
•     tx: femoral or axillary w/ grafts: carotid or popliteal w/ saphenous vein

To top