see also:

• vascular surgery
• aortic dissection
• thoracic aortic aneurysm
• abdominal pain in ED
• atherosclerosis and primary prevention

• do not confuse with aortic dissections which are sometimes called dissecting aneurysms & are due to blood entering media & splitting the aortic wall
• may be either:
  • true aneurysms (most) - localised dilatation involving all 3 layers of arterial wall
  • pseudoaneurysm - collection of flowing blood that communicates with arterial lumen but is not enclosed by the normal vessel wall but rather contained by adventitia or surrounding soft tissue. These are due to defect in arterial wall or a leaking anastomosis as a late complication of AAA repair.
• AAA:
  • most involve aorta below renal arteries, the aorta here is normally < 2cm & if > 3cm is regarded as being a AAA because at this size, rupture may occur & it never occurs less than 3cm.

• non-specific degenerative AAA's:
  • most AAA's
  • may have genetic basis
• specific causes of remainder of AAA's:
  • infection
  • trauma
  • CT diseases
  • arteritis

• rare before 50yrs age, but found in 2-4% ppl > 50yrs age
• ave. age at Dx is 65-70yrs
• men > women
• at risk groups:
  • pts femoral or popliteal artery aneurysms - 35-40% prevalence of AAA
  • FH AAA:
    • 10-20x risk if 1st degree relative with AAA
    • 20-25% prevalence if brother of a pt with AAA
  • elderly with PVD - 10-15% prevalence of AAA
  • smokers
  • men aged > 65yrs - 5-10% prevalence of AAA
  • aged > 50yrs - 2-4% prevalence
• acute AAA events in a 12yr study period of 92,000 population ¹⁾:
  • NONE occurred in those under age 55 yrs
  • per 100,000 population per year
    • 55 in men aged 65–74 years (274 in male smokers)
    • 112 at age 75–84 years
    • 298 at age 85 years or above
  • 73% were in men
  • 66% of all events occurred in those aged 75 years or more
  • 96% of 28 events in men aged less than 75 years occurred in ever‐smokers
  • 93% of women had hypertension

• progressively enlarge, ultimately resulting in rupture & potentially fatal haemorrhage which may be either:
  • temporarily tamponaded at rupture site
  • free intraperitoneal rupture (10-30%)
  • into GIT
  • into IVC
• ave. growth rate is 0.2-0.5cm per year, with larger ones expanding more rapidly than smaller ones
• rate of expansion is highly variable & unpredictable
• risk of rupture:
  • size:
    • most are > 5cm when rupture
    • of 24000 consecutive autopsies, 473 AAA's were found, 9.5% of AAA's < 4cm were ruptured, 23-25% of AAA's 4.1-7.0cm were ruptured, 46% of AAA's 7.1-10.0cm were ruptured & 60% of AA's > 10cm were ruptured.
• other complications of AAA's:
  • embolus of clot ⇒ occlussion of distal vessels
  • aortic thrombosis (rare)
  • local pressure effects
  • 5% have local inflammatory effects ⇒ peri-aortic fibrosis which may obstruct ureters, etc.

• maybe the cause of unexplained raised D-Dimer pathology test
  • note there are many causes of a raised D-Dimer
  • average yearly increase in AAA diameter was positively correlated with plasma D-dimer (r=0.39, p<0.001). Plasma D-dimer was independently associated with AAA progression after adjusting for other risk factors, including initial AAA diameter²⁾³⁾

• most are asymptomatic until they rupture!!
• pain in abdomen, back or flank - gradual onset, vague, dull quality, usually constant but may be throbbing
• acute or severe pain suggests imminent rupture
• pulsatile, expansile mass above umbilicus (bifurcation of aorta), if tender, suggests imminent rupture
• abdominal bruit (5-10% pts)
• femoral pulses are usually normal unless ileofemoral occlusive disease or hypotension from rupture
• emboli may cause acute painful lower limb with absent pulses
• microemboli may cause livedo reticularis, painful, cyanotic toes with palpable pedal pulses “blue toe syndrome”
• large, long-standing AAA may cause vertebral body erosion & severe back pain
• duodenal obstruction causing vomiting & weight loss
• inflammatory AAA's may cause ureteric obstruction & ureteral colic

• classic triad BUT many only have one or two of these features & some will have unusual features & none of the classic triad:
  • pain:
    • abdomen, back or flank
    • usually acute, severe, constant
    • may radiate to chest, thigh, inguinal region or scrotum
    • may be accompanied by N/V
  • hypotension:
    • may be an initial syncope or near-syncope with sudden h'age, then BP & cerebral perfusion returns to normal temporarily due to compensatory mechanisms.
    • often late & sudden,
    • occurs in 50-66% pts
  • pulsatile abdominal mass:
    • may be difficult to feel if:
      • pt. obese
      • AAA is small
      • abdominal guarding present
      • significant distension due to ileus
      • pulsations may not be palpable if hypotensive
• other S/S's:
  • ecchymoses
    • of ant. abdominal wall, flank, thigh, inguinal area, scrotum, penis, perineum, or perianal area
  • occasionally, rupture into retroperitoneum may become sealed & contained for weeks/months:
    • abdominal/back pain which gradually improves or resolves
    • femoral nerve neuropathy from pressure against iliopsoas muscle:
      • hip/thigh pain & pain on hip extension (+ve psoas sign)
      • weakness of quadriceps & diminished patellar reflex
      • decreased sensation ant/medial thigh
    • inguinoscrotal mass resembling ing. hernia
    • incarceration of previously reducible ing. hernia due to pressure effects
    • obstructive jaundice due to compression of CBD
    • at risk of sudden progression of rupture & h'age at any time
  • rupture into GIT (aortoenteric fistula) ⇒ sudden GIT bleed & death
    • types:
      • primary - usually 3rd/4th parts duodenum:
      • secondary - late complication of AAA repair; much more common than primary;
    • bowel wall erosion may cause an initial leakage of intestinal fluid ⇒ local infection/abscess
    • may cause abdo/back pain, fever, signs of i/abdo. infection or GIT bleeding
    • initial bleeding from erosion of vessels in bowel wall may be minor & precede the massive bleeding by several days or weeks ⇒ consider this possibility in any pt > 50yrs with unexplained GIT bleed.
  • rupture into inf. vena cava (aortocaval fistula) or other veins (aortovenous fistula):
    • may have concomitant retroperitoneal bleed ⇒ presents as normal ruptured AAA
    • no bleed ⇒ S/S of large AV fistula:
      • hyperdynamic circulation - tachycardia, wide pulse pressure, increased cardiac output
      • dilated heart & eventual high output cardiac failure:
        • SOB, raised JVP, pulm. oedema
        • raised renal venous pressure ⇒ decreased renal perfusion ⇒ ARF
      • diminished arterial blood flow and venous congestion distal to fistula:
        • cool lower extremity with oedema/cyanosis, dilated superficial veins & poor pulses
        • haematuria due to distension & rupture of bladder mucosal veins
        • rectal bleeding
      • may have abdo/back pain;
      • 80-90% of aortocaval fistulae have palpable AAA's
      • 75% have continuous abdo. bruit, with 25% having palpable abdo. thrill

• see abdominal pain in ED
• renal colic
• “acute abdomen”:
  • pancreatitis
  • intestinal ischaemia
  • diverticulitis
  • cholecystitis
  • appendicitis
  • perforated viscus
  • bowel obstruction
• musculoskeletal back pain - esp. dangerous misdiagnosis as pts are often discharged home
• acute myocardial infarction (AMI/STEMI/NSTEMI)

• plain XRay is rarely used however, evidence of AAA seen in 66-75% pts (esp. on lateral views):
  • curvilinear calcification of aortic wall demonstrating dilated aneurysm
  • paravertebral soft tissue mass
  • rarely, vertebral body erosion
  • with rupture, loss of psoas or renal outlines may occur
• a negative Xray does not exclude AAA

• virtually 100% sensitive in detecting AAAs provided that a technically adequate study can be obtained
• measurements of aortic diameter are very accurate
• often used in non-emergent pts & used to follow pts with known aneurysms
• in emergent AAA's has advantage of being rapid at bedside in resus. room
• cannot reliably detect whether AAA has ruptured as sensitivity for extraluminal blood is low
• CT must be used to determine likelihood of rupture
• if pt is unstable with AAA on US then immediate surgery is appropriate

• virtually 100% sensitive in detecting AAA
• provides accurate measurement of size
• less subject to technical problems & interpretation errors than US
• often used to help plan elective surgery as it can demonstrate:
  • proximal & distal extent of AAA
  • status of renal & visceral arteries
  • unsuspected pathologic condition
• IV contrast helps distinguish patent lumen from mural thrombus & can demonstrate periaortic fibrosis because soft tissue around inflammatory AAA's often enhances
• oral contrast helps differentiate bowel loops adjacent to aorta from extravasated blood
• in emergent situations, no contrast is used as may delay Sx
• 77-100% sensitive in detecting retroperitoneal h'age but false positives occur due to tumour, LNs, inflammatory soft tissue or bowel loops adjacent the aorta being identified as blood, and false negatives may occur too!!
• CT cannot determine whether rupture is imminent or whether AAA is cause of pt's pain

• has no place in emergent AAAs
• may help plan elective AAA Sx

• 2 Mx philosophies for elective repair:
  • repair all AAA's soon after Dx if in good health as even small ones will rupture
  • selective (used esp. if health not so good):
    • repair AAA's if either:
      • symptoms develop
      • documented rapid expansion occurs
      • threshold size exceeded - usually 5.5cm
    • monitor remainder with serial US or CT
      • on discharge, instruct to seek medical care immediately if abdominal, back or flank pain develops
      • follow up in surgery OP
• elective AAA repair:
  • mortality rate ~5% (compared with 80% mortality if ruptures)
  • survivors have excellent prognosis with long term survival close to general population, but this is generally limited by associated cardiac disease.
  • endovascular vs surgical repair:
    • endovascular repair has 30 day mortality of 1.8% compared with 4.3% for surgical repair but has higher late mortality according to this study⁴⁾

• pt is unstable until aorta is cross-clamped in operating room
• roles of ED are:
  • diagnosis:
    • clinical +/- bedside US in resus. room
    • if pt stable & AAA cannot be diagnosed at bedside, then consider urgent CT abdo.
  • large bore IV access lines, minimal fluid resuscitation, send blood for 10U cross-match
  • attempts to fully resuscitate in ED should be avoided as they are fruitless & waste time
  • fully correcting hypovolaemia prior to cross-clamping aorta may be harmful
  • prolonged hypotension is also harmful, so current aim is for systolic BP 90-110 although the BP needed to maintain vital organ perfusion varies between patients.
  • if pt is hypertensive due to pain or underlying HT, do not attempt to lower BP as there is no evidence that lowering BP as for aortic dissection is beneficial & there is risk of precipitous hypotension developing.
  • expedition of arrangements for surgery - notify surgery, anaesthetic teams & theatre ASAP
    • UNLESS Sx contraindicated by:
      • life expectancy very short due to underlying illness
      • poor quality of life
    • NB. cardiac arrest does not necessarily preclude Sx as ~20% of such pts survive after Sx
    • Sx mortality is 15-70% depending on centre, pre-op.hypotension & low h'crit
    • untreated mortality is 100%

• due to contamination of graft at Sx, spread of contiguous infection, haematogenous seeding
• may lead to:
  • leakage of blood from anastomosis
  • pseudoaneurysm formation
  • local signs of infection or palpable false aneurysm - esp. if distal limb of an aortofemoral graft
  • low grade fever, vague abdo/back pain
  • secondary aortoenteric fistula formation - can take years to develop
• Ix:
  • CT scan - collections of fluid/gas around graft
  • labelled WBC's - some false positives

• if GIT bleed in pt with PH AAA repair then it should be considered
• if unstable with masssive bleed ⇒ urgent laparotomy
• if stable then consider:
  • CT scan
  • upper GIT endoscopy to find another cause of bleed & avert emergent Sx

• at site of leaking anastomosis due to infection, aortoenteric fistula or degeneration of native vessel
• may cause:
  • pulsatile mass in abdomen or groin
  • distal emboli
  • rupture & life threatening h'age
• Ix:
  • CT, angiography or US

• unexplained fever
• abdominal pain
• GI bleeding