Aaa repair

Surgical approach

• Two main strategies: Open AAA repair vs EVAR (endovascular aneurysm repair)
  • Choice depends on anatomy (neck length/angulation, iliac access), physiology, urgency, local expertise
• Open repair (elective/urgent/ruptured): midline laparotomy or left retroperitoneal approach; aorta exposed; systemic heparin often given; aortic cross-clamp (usually infrarenal; may be suprarenal); aneurysm sac opened; thrombus evacuated; Dacron/PTFE graft (tube or bifurcated) sewn in; clamp released; haemostasis; sac closed over graft; abdomen closed (may be left open in rupture/ACS risk).
  • Major physiological insults: clamp on/off, large blood loss, hypothermia, coagulopathy, ischaemia–reperfusion, abdominal compartment syndrome
• EVAR: percutaneous or open femoral artery access; guidewires/catheters; stent-graft deployed under fluoroscopy; may need iliac extensions; completion angiography; closure devices; less physiological stress but contrast load and access complications.
  • Complications: endoleak (I–V), limb ischaemia/embolisation, access site bleeding, renal injury, spinal cord ischaemia (rare; higher with extensive coverage), conversion to open

Anaesthetic management (headline)

• Type of anaesthesia: GA for open repair; GA or regional/LA with sedation for EVAR (institution-dependent).
  • Ruptured AAA: GA almost always; aim for rapid control of bleeding and physiology-guided resuscitation
• Airway: ETT for open repair and most ruptures; EVAR may be ETT or spontaneous ventilation with airway support depending on plan and patient factors.
• Duration: Open elective typically 3–6 h; ruptured variable; EVAR often 1.5–3 h.
• Pain: Open repair very painful (laparotomy/retroperitoneal); EVAR mild–moderate (groin access, possible iliac manipulation).
• Monitoring/lines: A-line before induction, large-bore IV x2, rapid infuser; central access often; urinary catheter; temperature; ABGs; consider cardiac output monitoring; cell salvage (open).
• Key intra-op goals: maintain coronary/cerebral perfusion, anticipate clamp physiology, haemostatic resuscitation, normothermia, renal protection strategy, timely ICU/HDU handover.

Indications and definitions

• AAA = permanent dilatation of abdominal aorta ≥ 3.0 cm (or >50% normal diameter).
• Repair generally considered when: diameter ≥5.5 cm (men), ≥5.0 cm (women, often earlier due to rupture risk), rapid expansion (>0.5 cm/6 months), symptomatic aneurysm, saccular morphology, rupture/impending rupture.
• Options: EVAR (lower early morbidity, needs surveillance) vs open repair (higher early risk, durable).

Preoperative assessment (elective)

• High-risk vascular cohort: common comorbidities include IHD, heart failure, COPD, CKD, diabetes, smoking, frailty.
• Cardiac: assess functional capacity; ECG; echo if murmur/HF/poor METs; consider stress testing if it will change management; optimise anti-anginals, beta-blocker continuation (avoid new high-dose initiation immediately pre-op).
• Respiratory: COPD optimisation (bronchodilators, steroids if indicated), smoking cessation, treat infection, consider ABG if severe disease.
• Renal: baseline creatinine/eGFR; avoid nephrotoxins; plan contrast mitigation for EVAR (hydration strategy, minimise contrast).
• Haematology: FBC/coagulation, group & save/crossmatch (often 6–10 units for open; local policy), iron deficiency correction if time.
• Medication: continue statin; continue aspirin usually (surgeon-specific); manage dual antiplatelets/DOAC/warfarin with plan; ACEi/ARB often withheld on day to reduce refractory hypotension (local policy).
• Consent/communication: ICU/HDU expectation, blood transfusion, epidural risks/benefits, potential postoperative ventilation/renal replacement therapy.

Preparation and monitoring

• Monitoring: invasive arterial pressure (preferably pre-induction), 5-lead ECG with ST analysis, SpO2, capnography, temperature (core), urine output, serial ABG/lactate, glucose.
• Vascular access: 2 large-bore cannulae (14–16G) + rapid infuser; central venous access often (drug delivery/vasopressors); consider large-bore sheath if anticipated massive haemorrhage.
• Cardiac output monitoring: oesophageal Doppler, pulse contour, or TOE in selected cases (significant cardiac disease, rupture, unexplained instability).
• Blood management: cell salvage (open), TXA per local major haemorrhage protocol, fibrinogen/cryoprecipitate guided by labs/viscoelastic testing if available.
• Temperature: forced-air warming, fluid warmers, minimise exposure; hypothermia worsens coagulopathy and arrhythmias.

Anaesthetic technique

• Induction: haemodynamically stable elective—balanced induction with vasopressor readiness; ruptured—haemodynamically fragile, titrated induction, consider ketamine/etomidate, early vasopressors, avoid precipitous drop in SVR.
• Maintenance: volatile or TIVA; avoid tachycardia/ischaemia; lung-protective ventilation; consider higher FiO2 during major haemorrhage; maintain normocapnia.
• Analgesia (open): multimodal + regional where appropriate. Options: thoracic epidural (T8–T10), spinal opioid, TAP/rectus sheath catheters, IV lidocaine infusion (local practice), PCA opioid if neuraxial unsuitable.
  • Epidural benefits: improved analgesia, reduced respiratory complications, earlier mobilisation; risks: hypotension (esp. with clamp release/bleeding), epidural haematoma with anticoagulation, failure rate.
• EVAR anaesthesia: GA (airway control, immobility) vs regional/LA + sedation (faster recovery, less haemodynamic depression). Must tolerate supine, contrast, potential conversion to open.

Physiology of aortic cross-clamping (open repair)

• Clamp level matters: infrarenal (commonest) vs suprarenal/supraceliac (greater afterload, renal/visceral ischaemia).
• On clamping: ↑SVR/afterload → ↑MAP; potential ↓CO (esp. poor LV); ↑myocardial O2 demand; redistribution of blood volume; possible proximal hypertension and myocardial ischaemia.
  • Management: deepen anaesthesia, vasodilators (GTN), treat ischaemia (beta-blockade cautiously), optimise preload/contractility; avoid excessive hypertension.
• Distal ischaemia during clamp: anaerobic metabolism in lower body → lactate, acidosis, hyperkalaemia; gut ischaemia risk; renal hypoperfusion (worse if suprarenal).
• On unclamping: sudden ↓SVR and venous return + washout of metabolites → hypotension, acidosis, hyperkalaemia, arrhythmias; bleeding may worsen.
  • Management: warn team; volume loading judiciously; reduce volatile; vasopressors ready (noradrenaline/phenylephrine/vasopressin); correct K+/Ca2+/pH; slow/stepwise release if possible.

Haemorrhage and transfusion strategy

• Open repair: major blood loss from lumbar/iliac vessels, back-bleeding, coagulopathy, hypothermia, surgical field issues; rupture can be catastrophic.
• Use a major haemorrhage protocol early if needed; aim for haemostatic resuscitation (RBC:FFP:platelets guided by local policy and labs/TEG/ROTEM).
• Calcium: citrate toxicity causes hypocalcaemia → hypotension/coagulopathy; check ionised Ca and replace.
• Cell salvage: useful in elective open AAA; consider contamination risk if bowel injury (relative).

Renal protection and metabolic issues

• Risks: pre-existing CKD, suprarenal clamp, hypotension, embolisation, rhabdomyolysis (limb ischaemia), contrast nephropathy (EVAR).
• Principles: maintain perfusion pressure/CO, avoid hypovolaemia, minimise nephrotoxins, monitor urine output and ABGs; treat acidosis/hyperkalaemia; consider bicarbonate only for severe acidaemia with instability (case-by-case).
• Diuretics (mannitol/furosemide): not routine; may be used by some teams around suprarenal clamping but evidence mixed—prioritise haemodynamics.

Postoperative care

• Destination: usually ICU/HDU after open repair; EVAR often HDU/ward if uncomplicated.
• Key issues: ongoing bleeding, myocardial ischaemia/arrhythmias, renal dysfunction, respiratory failure/atelectasis, ileus, delirium, sepsis, limb ischaemia, graft occlusion, abdominal compartment syndrome (rupture/large transfusion).
• Analgesia: epidural infusion (if used) with vasopressor support as needed; otherwise PCA + multimodal; early mobilisation and chest physiotherapy.
• VTE prophylaxis: mechanical + pharmacological when safe; balance against neuraxial timing and bleeding risk.

Ruptured AAA (rAAA): specific considerations

• Presentation: hypotension, abdominal/back pain, collapse; may be transiently stable if retroperitoneal tamponade.
• Resuscitation: permissive hypotension until proximal control (e.g., target SBP ~70–90 mmHg or conscious with radial pulse; individualise—avoid in traumatic brain injury/critical coronary/cerebral ischaemia).
• Avoid: aggressive crystalloid, hypertension that disrupts clot, delays to theatre; early balanced blood products and vasopressors as needed.
• Induction: titrate to effect; have surgeon scrubbed/ready; vasopressors running; consider RSI with haemodynamic caution; anticipate immediate clamp after laparotomy.
• Coagulopathy: common (shock, dilution, hypothermia); use MHP, warming, calcium, viscoelastic-guided therapy if available.