Abdominal aortic aneurysm (AAA)

Reviewed and revised 5 September 2015, including amendments suggested by Dr Jason Chuen (@OzVascDoc)

OVERVIEW

Abdominal Aortic Aneurysm (AAA) is a permanent localised or diffuse dilatation of the abdominal aorta to 1.5 times its normal diameter that involving all three layers of the vessel wall

  • normal infrarenal aortic diameters in patients >50y are 1.5 cm in women and 1.7 cm in men
  • an infrarenal aorta 3 cm in diameter or more is considered aneurysmal
  • ectasia is when aortic diameter is <50% increased

Emergency presentations of AAA include:

  • incidental finding, often of a newly discovered asymptomatic AAA
  • symptomatic or painful aneurysm due to local inflammatory state or acute dissection (true acute expansion of the aneurysm rarely if ever presents acutely otherwise)
  • contained retroperitoneal or compensated rupture (“contained leak”)
  • uncontained, decompensated rupture with hypovolaemic shock (“free rupture”)
  • distal embolisation or local thrombosis
  • other atypical presentations

AAA is relatively common, primarily affects the elderly and is often fatal

  • rare <50 years of age
  • 10% rate in men aged 65-79 years

The pathogenesis of AAA is distinct from that of dissection

CAUSES

Strongly associated risk factors:

  • Male gender
  • Age
  • Smoking
  • Hypertension
  • Genetic/familial disposition(e.g. inherited connective tissue disorders such as Marfans and Ehlers-Danlos)

Identified and postulated causes include:

  • atherosclerotic injury and associated degeneration
  • primary connective tissue degeneration
  • inflammatory arteritis with associated aneurysmal degeneration
  • traumatic injury and pseudoaneurysm
  • mycotic injury and pseudoaneurysm
  • aortic dissection-related aneurysmal degeneration

PATHOPHYSIOLOGY

Anatomy and types of AAA

  • True aneurysms of the Abdominal aorta involve all 3 layers of the vessel wall, and are defined as being >3cm in diameter or having increase >50% from baseline
  • False aneurysms (or pseudoaneurysms) are deficient in at least one layer
  • Fusiform aneurysms have a “bulbous” shape and are usually true aneurysms
  • Saccular aneurysms have a lateral out-pouching like a Berry aneurysm and are often false aneurysms
  • Most abdominal aortic aneurysms occur in the infra-renal segment (90-95%)
  • AAAs to extension above the renal arteries is rare but extension into the iliac arteries is common

Pathogenesis involves:

  • infiltration of the vessel wall by lymphocytes and macrophages
  • destruction of elastin and collagen in the media and adventitia by proteases, including matrix metalloproteinases
  • loss of smooth-muscle cells with thinning of the media
  • neovascularization

Acute events

  • pain
    • acute expansion is rarely if ever a cause of pain; pain is typically associated with inflammation or dissection
  • rupture
    • contained: leak contained within the retroperitoneal space, may be relatively haemodynamically stable
    • uncontained: free rupture into intra-peritoneal cavity resulting in shock
  • thrombosis or distal embolisation

Complications

  • death
  • major haemorrhage
  • aortic branch involvement resulting in ischaemia (e.g. renal, spinal, pancreatitis)
  • distal emoblisation (e.g. trash foot)
  • rhabdomyolysis

CLINICAL ASSESSMENT

  • asymptomatic AAA may be an incidental finding on clinical examination or imaging
  • palpation of an expansile mass
    • pass two fingers on either side of the pulsating mass and observe for separation of the fingers with each pulsation
    • may be detectable at 4-5cm diameter depending on body habitus
  • isolated pain in abdomen, epigstrium or back (contained leaks typically present with back pain)
  • ‘classic’ triad of AAA rupture (often not present e.g. guarding, obese, hypotensive or large retroperitoneal haemorrhage)
    • Pain, typically severe and predominantly located in the back
    • Signs if circulatory compromise, often the patient is frankly shocked
    • The presence of a pulsatile mass in the abdomen
  • atypical presentations in the elderly
    •  back pain (may mimic renal colic)
    • +/- radiation to the legs (mimicking sciatica)
    • chronic severe back pain (contained rupture)
  • tender AAA on palpation is an aortic emergency unless proven otherwise
  • massive GI haemorrhage raises suspicion for an aorto-enteric fistula (usually in the context of a previous AAA graft that has eroded into the GI tract)

INVESTIGATIONS

Investigations should be tailored to clinical presentation

  • see management

Bedside

  • ECG (do not delay resuscitation or transfer to operating theatre if ruptured AAA)
  • VBG and glucose

Laboratory

  • FBC
  • UEC
  • group and hold or cross match

Imaging

  • ultrasound
    • best investigation in an unstable patient as can be performed rapidly at the beside
    • can detect aneurysm and free fluid (cannot confirm fluid is due to rupture) if present
    • AAA diameter is measured as the maximum AP diameter in the transverse plane
    • imperfect sensitivity (~95%) and about 100% specific
  • CT abdomen with contrast
    • best imaging modality if diagnosis is uncertain
    • shows size and extent of AAA, demonstrates AAA leak and complications
    • imaging in unstable patients is controversial – stability is relative – patients with uncertain diagnoses and borderline stability are more likely to benefit from obtaining a definitive diagnosis with ongoing resuscitation in the CT scan room before undergoing emergency surgery
  • MRI
    • highly specific and sensitive
    • only suitable in elective settings
  • plain AXR not recommended but may show:
    • mural calcification
    • lateral may be better as right border of AAA often obscured by vertebral column

MANAGEMENT

Rupture

  • attend to ABCs
  • insert 2 x large bore peripheral IV cannulae, attached to giving sets with hand pumps or rapid infusion systems
  • target SBP ~90 mmHg to maintain end organ perfusion (analogous to the permissive hypotension approach in penetrating trauma)
  • cross-match 6+ units of blood, consider activation of massive transfusion protocol
  • obtain FBC, UEC, coagulation profile, VBG and ECG
  • provide titrated analgesia (e.g. fentanyl or morphine)
  • arrange urgent transfer to the operating theatre for definitive treatment (unless palliation is appropriate)
  • refer to vascular surgery, anaesthesia and  ICU
  • insert IDC and arterial line (unless this will cause a delay to OT – CVC in ED is not necessary)
  • a contained rupture still requires urgent repair, less acutely than an uncontained rupture and with less need for resuscitation

Acute pain

  • refer all cases to vascular surgery urgently
  • acute pain is an emergency, even in a stable patient the absence of rupture
  • assume that any pain in a patient with an AAA is due to an aortic emergency, until proven otherwise

Incidental asymptomatic AAA

  • refer to vascular surgeon if surgical candidate, urgency depends on AAA size and presence/ absence of symptoms
    • <2cm diameter is normal
    • 2-5.5 cm diameter and asymptomatic requires follow up with regular ultrasound
    • > 5.5 cm diameter requires operative intervention regardless of symptoms in patients suitable for surgery

Decision to operate on AAA, and by which procedure, depends on:

  • emergency or elective/ prophylactic
  • anatomy (not all patients have anatomy amenable to endovascular repair)
  • presence of symptoms
  • AAA diameter and growth rate
  • Operative risk (i.e. age and comorbidities)
  • Patient preferences and values

Indications for repair

  • Male with AAA >5.5 cm
  • Female with AAA >5.0 cm
  • Rapid growth >1.0 cm/year
  • Symptomatic AAA (e.g. rupture, abdominal/back pain/tenderness, distal embolisation)

Repair options

  • Open repair
    • only option for a ruptured AAA
    • involves an abdominal or flank incision, vessels above and below the aneurysm are controlled, and the aneurysm sac is opened with placement of a synthetic graft
    • similar mortality to endovascular repair in the long term (8 to 10 years) for elective repairs
    • ~20% of patients require a subsequent operation
  • Endovascular stent grafting
    • less invasive and has lower perioperative morbidity and mortality
    • involves the intraluminal introduction of a covered stent through the femoral and iliac arteries; can be performed under local anaesthesia
    • only possible in ~50% of unruptured AAAs
    • require long-term surveillance owing to a small risk of aneurysm sac reperfusion and late rupture (aka “endoleaks”)
    • 20-30% require a secondary intervention during the next 6 years

PROGNOSIS

Asymptomatic AAA

  • risk of rupture increases with size, however a AAA of any size can rupture
  • > 6 cm diameter AAA has 5 year survival rate of ~20% and ~50% rupture <1 year of diagnosis
  • mortality rate is decreased by elective repair (~5%) before rupture occurs

Ruptured AAA

  • 100% fatality unless repaired
    • Of those that survive to hospital with a ruptured AAA, mortality for surgical repair is still high, (up to 50%)
    • Mortality correlates with age, co-morbidities and hypotension

References and Links

LITFL

Journal articles

  • Al-Hashimi, M, Thompson J. Anaesthesia for elective open abdominal aortic aneurysm repair. Contin Educ Anaesth Crit Care Pain (2013) 13 (6): 208-212. [Free Full Text]
  • Frederick JR, Woo YJ. Thoracoabdominal aortic aneurysm. Ann Cardiothorac Surg. 2012 Sep;1(3):277-85. PMC3741772.
  • Gawenda M, Brunkwall J. Ruptured abdominal aortic aneurysm: the state of play. Dtsch Arztebl Int. 2012 Oct;109(43):727-32. PMC3498473.
  • Kasipandian V, Pichel AC. Complex endovascular aortic aneurysm repair. Contin Educ Anaesth Crit Care Pain (2012) 12 (6): 312-316. [Free Full Text]
  • Kent KC. Clinical practice. Abdominal aortic aneurysms. The New England journal of medicine. 371(22):2101-8. 2014. [pubmed]
  • Leonard A, Thompson J. Anaesthesia for ruptured abdominal aortic aneurysm. Contin Educ Anaesth Crit Care Pain (2008) 8 (1): 11-15. [Free Full Text]
  • Robinson D, Mees B, Verhagen H, Chuen J. Aortic aneurysms – screening, surveillance and referral. Australian family physician. 42(6):364-9. 2013. [pubmed]
  • Upchurch GR Jr, Schaub TA. Abdominal aortic aneurysm. Am Fam Physician. 2006 Apr 1;73(7):1198-204. PMID: 16623206. [Free Full Text]

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Critical Care

Compendium

Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also the Innovation Lead for the Australian Centre for Health Innovation at Alfred Health and Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of two amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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