Aortic Aneurysm

In general, an aneurysm is a localised or diffuse dilatation which is at least 50% greater than the normal size of an artery.

An abdominal aortic aneurysm is a permanent dilation of the abdominal aorta >3cm in diameter.

true aneurysm is one where the 2 or more layers of the vessel wall forms the wall of the aneurysm (i.e. vessel wall is intact).

false aneurysm is one where a collection of blood is held close to the vessel by a wall of connective tissue (i.e. contained leak from a vessel).

fusiform aneurysm is one where the aneurysm is tapered at both ends.  A sac-like aneurysm is more rounded.

Background

  • The majority (~75-95%) of aortic aneurysms are abdominal and below the level of the renal arteries (~30% also involve the iliac arteries)
    • Of those that are thoracic, the majority are either in the ascending or descending sections (rarely found in the arch)
    • Occasionally, you can also get thoracoabdominal aneurysms.  These can be classed using the Crawford classification
  • The prevalence of AAAs is between 1.3-12.7%.  AAA frequency increases with age (25/100,000 in 50 year old men vs 78/100,000 in >70 year old men)- around 1 in 20 men >65 increasing to almost 1 in 10 >75
    • Male : Female ratio 6:1

Aetiology

  • Family history/genetics are becoming increasingly apparent as a causal factor
  • Smoking
  • Male
  • Age
  • Hypertension
  • COPD
  • Heart disease/atherosclerotic disease
  • Hyperlipidaemia
  • Rarely, other causes e.g. trauma, infection (e.g. TB, HIV); inflammatory diseases (Behcet’s, Takayasu’s); connective tissue diseases (Marfan’s; Ehlers-Danlos type IV)
  • Diabetes seems to be protective
  • Can be associated with aneurysms elsewhere e.g. popliteal aneurysms

Pathophysiology

  • In patients >50, the normal aortic diameter is 1.5cm in women and 1.7cm in men.
  • Aneurysms are thought to arise due to failure of major structural proteins of the aorta (elastin and collagen)
    • This can be genetic
    • Inflammatory processes are also thought to contribute
      • Proteases and metalloproteinases may be important, as are interleukins and various cytokines
  • Atherosclerosis (degenerative disease) is a common finding in patients with AAA.  However, not all patients with severe atherosclerotic disease will develop AAA.  The association is not thought to be causative, but there may be a common underlying process in predisposed individuals.  Some patients exhibit an inflammatory mechanism whereby vessel wall inflammation causes adhesions to adjacent structures e.g. duodenum, small bowel etc.
    • Other causes include
      • Mycotic/infective
      • Traumatic (more commonly cause false aneurysms)
      • Connective tissue disorders e.g. Marfan’s syndrome; Ehler Danlos; Tuberous sclerosis

Progression

  • Size is the best indicator of likelihood of rupture.  Note that rate of growth is also a powerful indicator.
    • <5cm have a <4% chance per annum
    • 5-6cm have a 7% chance
    • >6cm have a >20% chance (i.e. exponential increase with size)
    • a growth of >10% per year significantly increases risk

Presentation

  • Incidental- The majority of patients with an unruptured AAA will be asymptomatic and the diagnosis will be incidental either from
    • Physical examination
      • Expansile mass (i.e. expands – not just pulsatile as with normal pulses and in false aneurysms)
    • Imaging (commonly abdominal USS, but x-ray/CT/MRI also possible)
  • Patients may present with central abdominal pain, back pain, loin pain or pain in the iliac fossa/groin (rarer)
    • NB this is more common in inflammatory type aneurysms
  • Rarely, AAAs can allow thrombi to form.  These can then embolise to the lower limb causing acute ischaemia
  • Occasionally patients may have features of compression/obstruction e.g. vomiting (duodenal obstruction); oedema/DVT (IVC obstruction)
  • Rupture
    • A ruptured TAA can cause sudden onset, severe chest pain (may be similar to MI).  This can radiate to the back.  This may also deteriorate rapidly.
    • A ruptured AAA causes a ‘classical triad’ (few patients have all 3) of
      • Back/flank pain
      • Hypotension
      • Pulsatile abdominal mass
    • The patient may also feel nauseous (+/- vomit); light-headed (+/- syncope); pale/sweaty/cold; may also have bruising in flanks
    • The pulse may be weak, rapid and ‘thready’.
    • Mild cases may present with features similar to renal colic

Investigations

  • Abdominal USS is the first line imaging investigation in patients with a stable AAA.
    • CT is usually the gold-standard investigation for evaluation of the aneurysm
  • Other investigations to consider would include an ECG, CXR, bloods

Management

  • Uncomplicated aneurysm
    • <5.5cm are generally monitored
      • 3-4.4cm annually (USS)
      • 4.5-5.4cm 3-monthly (USS)
      • >5.5 (if unsuitable for surgery) 3 monthly (USS)
    • >5.5cm – consider surgery (particularly for patients with high risk of rupture e.g. large diameter, smokers, female, hypertension, family history, rapid expansion, onset of sinister symptoms/signs e.g. pain/tenderness)
      • Endovascular stent-graft repair preferred due to
        • avoids open surgery and aortic clamping
        • reduced mortality within 4 years
  • Ruptured aneurysm
    • Surgical emergency
    • ABCDE until theatre ready
    • 95% overall mortality (50% in theatre)
      • Most patients won’t survive (for those who even reach theatre, surgery mortality is 60-80%, more if there are impacting factors e.g. >80yo; shock non-responsive to resuscitation); cardiac arrest prior to/during surgery)
  • Open repair
    • Indication
      • Elective if >5.5cm or if rapidly expanding or if patient presents with pain; all emergency cases (rupture)
    • Pre-operative assessment
      • BP control
      • Smoking cessation
      • Co-morbidity/mortality assessment
    • Consent
      • 5% mortality (significant)
      • DVT; Chest infection; wound infection
      • Graft infection (~1 in 500)
    • Procedure
      • Supine position
      • Midline incision (usually)
      • Retract bowel and duodenum to right
      • Divide the posterior peritoneum and dissect the AAA
      • Define the proximal and distal neck/extent of AAA
      • Administer IV heparin
      • Apply distal then proximal aortic clamps (warn anaesthetist) before incising sac
      • Oversew arteries e.g. lumbars/IMA if patent

AAA Screening

  • Offered to all males >65 years old
  • Those with small aneurysms are monitored and those with larger ones (>5.5cm) are offered surgery
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