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.

A 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).

A 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).

A 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