FRCA Notes

Open AAA Repair

Resources

  • The aim of AAA repair, be it open or via EVAR, is to buttress the weak, aneurysmal segment with a strong, synthetic graft
  • Access to the aorta for open repair is typically transperitoneal i.e. via midline laparotomy, which provides both rapid and effective surgical access
  • A retroperitoneal approach is also described with an incision via the left flank, though it is often reserved for those with a hostile abdomen

  • After the aneurysm is exposed, a cross-clamp is applied to the abdominal aorta

  • Once clamped, the anterior wall is incised and the graft sutured to both ends of the aorta
    • Grafts may be straight 'tubes' or bifurcated 'trousers'
  • A fem-fem crossover or other graft may be necessary to re-vascularise ischaemic limbs at the end of surgery

  • The main goal is to stratify and minimise risk of morbidity and mortality ahead of a high-risk procedure
  • For emergency patients a rapid, targeted pre-assessment should take place

Risk assessment

  • There are a number of risk assessment tools available for the patient due to undergo elective AAA repair
  • Anecdotally the Glasgow Aneurysm Score,  V-POSSUM,   Carlisle's calculator (he has a word or two to say about risk prediction models) and the British Aneurysm Repair score are more popular
  • The recommendation from NICE (2020) is to use...  none of them, owing to a lack of "high enough predictive accuracy at predicting postoperative outcomes"
  • Patients could be stratified via operative mortality into low (1 - 3%), moderate (3 - 5%) and high (5 - 10%) groups
  • Ultimately, these patients will be discussed at a Vascular MDT where appropriate surgical interventions and perioperative planning can occur

  • Perhaps unsurpisingly the presence of cardiovascular, renal or cerebrovascular disease will increase your perioperative morbidity and mortality
    • So too COPD and diabetes mellitus
  • Overall, however, it is coronary artery disease which is the leading cause of morbidity after AAA repair
    • 70% of patients undergoing AAA repair have existing coronary artery disease

  • According to the ACC/AHA guidelines (2007), EVAR is classified as either intermediate-risk if infra-renal or high-risk if complex

Investigations

  • Bloods: FBC | U&E | Clotting | Group and cross-match (6 units in our local vascular centre)
  • ECG
  • ±CXR
  • ±Urinalysis
  • Transthoracic echo.
  • CPET testing including spirometry (or other functional capacity assessment tool of choice)

Optimisation

  • All patients should commence statins and aspirin
  • Control arterial BP
  • Smoking cessation
  • Continue β-blockers if already taking
  • Continuation vs. cessation of antiplatelet agents such as clopidogrel need risk/benefit discussions and may involve liaison with other teams e.g. Cardiology
  • Treat anaemia and low haematocrit as they are associated with worse outcomes
  • Optimise COPD to reduce risk of perioperative pulmonary complications
  • Consider stopping NSAIDs or other nephrotoxic drugs for patients undergoing EVAR as high risk of peri-operative AKI (use of contrast, para-renal stents etc.)

Monitoring

  • Standard AAGBI monitoring applies but with an ECG-flavoured twist; either 5-lead monitoring or the CM5 configuration should be used are more sensitive in the detection of myocardial ischaemia
  • Arterial line
  • Central line
  • Temperature monitoring; maintenance of normothermia is key to aid haemostasis, although avoid lower body warming during cross-clamp application
  • Urinary catheter
  • Cardiac output monitoring e.g. with oesophageal doppler may be unreliable when the aorta is clamped
    • Although pulse contour analysis techniques are increasingly popular, their use hasn't been fully evaluated yet

Anaesthetic

  • In elective cases, a thoracic epidural is typically placed before induction for intra- and post-operative analgesia
  • Typically not used for intra-operative analgesia until after cross-clamp release and haemostasis as it may cause profound hypotension due to sympathetic blockade
  • Induction and maintenance is as per routine practice; propofol/remi TCI with pEEG monitoring is preferred in my trust
  • The effects of aortic cross-clamping have been discussed already

Clotting, bleeding & fluid therapy

  • 75 - 150 units/kg of IV heparin (e.g. 5,000IU for the fictional 70kg patient) is given to prevent thrombosis associated with stasis distal to the aortic cross-clamp
  • Although targeting an ACT of 2 - 2.5x baseline ± protamine reversal is described, this is not current practice in my institution

  • Blood should already be cross-matched in the realms of 6 (elective) to 10 (emergency) units
  • Warming and rapid infusion systems for introducing said blood should be available, as should cell salvage
  • As these patients are vasculopaths with ailing cardiovascular systems, a transfusion threshold haemoglobin concentration of 80g/L is suitable
  • Other products should be given as indicated e.g. by viscoelastic haemostatic assays

  • Fluid loading with crystalloids/colloids prior to the cross-clamp being applied may help reduce post-clamping hypotension
    • This can be titrated to haemodynamic indices e.g. a CVP of 10 - 12cmH2O

Intra-operative complications

  • The big worry is intra-operative myocardial ischaemia/infarction
  • Heart failure
  • Graft failure
  • Major haemorrhage

  • Higher level care in an HDU or ITU setting is required
  • Regular neurovascular observations on lower limbs
  • Analgesia is via the previously sited thoracic epidural, in addition to simple analgesics e.g. paracetamol and opioids as necessary

  • A quasi-ERAS protocol of early mobilisation, physiotherapy and VTE prophylaxis is used

Post-operative complications

  • The risk of acute coronary events is still present
  • Acute kidney injury (see below)
  • Pulmonary complications inc. respiratory failure and pneumonia
  • If cross-clamping was supra-coeliac, liver failure and paraplegia are also risks

Pathophysiology

  • The main cause of renal complications after AAA repair are:
    • Decreased renal blood flow
    • Decreased renal perfusion pressure (i.e. outside autoregulatory range), exacerbated by increased renal vascular resistance (+30%) associated with cross-clamping

  • Other pathophysiological processes contributing to ATN/AKI include:
    • Myoglobin release from ischaemic tissues
    • Ischaemia-reperfusion injury
    • Decreased renal cortical blood flow
    • Prostaglandin imbalance
    • Increased RAAS activation

Risk factors

Patient factors Procedural factors
Age >70yrs Perioperative dehydration
Diabetes mellitus Perioperative use of aminoglycosides
Cardiac failure Repeat IV contrast load within 7 days
Pre-operative eGFR ≤60ml/min (CKD stage 3a) Complex EVAR
ACE-I or ARA therapy
Perioperative use of diuretics
  • NB postoperative dialysis rates are similar in patients with suprarenal or infrarenal aneurysms

Measures to protect against AKI

  • Prevent intra-operative dehydration
  • Limit IV contrast dose
  • Omit nephrotoxic drugs
  • Maintain adequate MAP
  • Drugs; NAC is the most robustly supported, followed by sodium bicarbonate
    • No consistently demonstrable benefit from dopamine, mannitol or loop diuretics

  • A European Society of Vascular Surgery report (2008) showed the UK mortality rate after open AAA repair was the highest in Europe and Australasia (7.9% vs. 3.5%)
  • Thus the AAA-QIP programme was developed with the aim of reducing UK mortality after AAA repair
  • Mortality is now significantly lower; overall elective AAA repair mortality was 2.4% in 2012