- 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
- This may be challenging due to the proximity of the renal or mesenteric arteries
- Application of the clamp can embolise atheromatous plaques and cause a smorgasbord of physiological derangements
- 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
Open AAA Repair
Open AAA Repair
The curriculum asks for us to be able to describe 'the perioperative management of the patient for major vascular surgery'.
Resources
- The aim of AAA repair, be it open or via EVAR, is to buttress the weak, aneurysmal segment with a strong, synthetic graft
- 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