Ruptured AAA

• Ruptured AAA carries a high overall mortality of 65 - 90%
• 75% of those with ruptured aneurysms die before reaching surgery
• Of those who undergo surgery, a further 40 - 65% die

• Mortality is most closely linked to the degree of pre-operative hypotension
• Other factors include:

• 88% of bleeds are retroperitoneal and 'contained', which is associated with better outcome
• 12% of bleeds are intra-peritoneal, aorto-caval or aorto-enteral and are associated with higher mortality

• A rapid, targeted pre-assessment should take place although the ultimate goal is to provide adequate resuscitation and avoid delays to surgery
• Clear, effective MDT communication is required
• Priorities include:
• Rapid diagnosis (if not already)
• Mobilisation of theatre staff; ideally 2 ODPs with one dedicated to cell salvage/massive transfusion
• Mobilisation of blood products via major haemorrhage protocol and/or cross-matching 10 units
• Insertion of wide-bore IV access
• If the patient suffers cardiac arrest whilst being readied for theatre, palliation is recommended as the mortality rate approaches 100%

• There are conflicting views about whether permissive hypotension or aggressive resuscitation in the pre-clamp phase is better
• Arguments against fluid resuscitation include:
• Increased BP may cause further haemorrhage
• Use of fluids causes dilutional coagulopathy, further increasing haemorrhage
• Further haemorrhage increases need for major blood transfusion and impairs the surgical field


• Arguments against permissive hypotension include:
• Longer duration of shock increases risk of cardiac and other major organ complications
• SBP at presentation is the most important factor influencing survival; SBP ≤90mmHg is associated with a >60% mortality
• SBP <70mmHg associated with organ damage


• Without definitive evidence either way, short periods of hypotension may be tolerable but any surgical delay should prompt resuscitation with blood (products)
• Resuscitation targets in this phase include:
• Cerebral perfusion enough to respond to verbal commands
• Palpable radial pulse
• Lack of chest pain (i.e. adequate coronary perfusion)
• SBP 70-90mmHg
• Fluid loading with crystalloids/colloids while the cross-clamp is being applied may help reduce post-clamping hypotension

• If severe abdominal pain consider careful titration of opioids
• Do not delay transfer to theatre for line insertion

• Belmont (Rapid Infuser)
• Cell salvage
• Arterial and central line transducers
• Syringe drivers x 2 (noradrenaline, adrenaline)
• Temperature probe, bair hugger
• Urinary catheter

• Speed is of the essence; the abdomen should be cleaned and draped whilst awake and the surgeons should be scrubbed and ready

• AAGBI monitoring, as standard
• 2 wide-bore access e.g. 14G cannulae, PA sheath
• Although invasive monitoring will be required, it may be instituted post-cross-clamping and its insertion should not delay start of surgery
• BIS may be useful to limit over-anaesthetising a critically unwell patient

• Do not start induction until surgeons scrubbed and gowned, and abdomen prepped and draped
• Induction in patients with ruptured AAA may cause cardiovascular collapse due to:
• Cardio-depressant effects of anaesthesia
• Reduced tamponade effect following relaxation of abdominal muscles
• Reduced sympathetic tone
• Reduced venous return following instigation of PPV


• Most will use a 'cardio-stable' induction technique, although cardiovascular instability is inevitable
• Consider omission of induction agents if comatose
• Options include:
• Small amount of opioid e.g. fentanyl 50µg
• Midazolam 1-2mg
• Ketamine: small aliquots only


• Titrate adrenaline boluses (e.g. 5µg/ml) to palpable radial pulse
• Have vasopressor infusions attached and running


• Knife to skin as soon as ETT confirmed to be in the trachea

• Antibiotics as per protocol (e.g. flucloxacillin + metronidazole + gentamicin 3mg/kg)
• Fluid resuscitation goals as above

• Once the clamp is applied, begin fluid resuscitation with red blood cells via a rapid infusion device
• Cautious use of FFP/cryo until clamp removed
• Anticipate ongoing blood loss despite the clamp being on owing to loss via lumbar segmental vessels
• Target Hb >100g/L


• Usual measures to reduce cardiac afterload during cross-clamping (vasodilators, negative ino/chronotropes) are not well tolerated in this cohort
• Instead, carefully titrate vasopressors during the cross-clamp period

• Close communication with surgical colleagues
• Optimise ready for clamp removal:
• Hyperventilate approx 10mins before planned unclamping (be mindful of P_aCO₂ - to - ETCO₂ gradient in some patients e.g. COPD)
• Ensure base deficit better than -10mmol e.g. administer 25 - 50ml of 8.4% sodium bicarbonate
• Check lactate; if >8 consider further filling ± bicarbonate before clamp removal
• Ensure adequate IV filling
• Give calcium in anticipation of hyperkalaemia, as well as citrate-induced hypocalcaemia


• Gradual, manual removal of the clamp
• Anticipate a degree of hypotension and titrate vasopressor infusions accordingly to maintain MAP
• A drop in BP or a failure of BP to rise in the minutes following clamp removal should prompt re-application of the clamp

• Ensure normothermia
• Maintain platelets >100 x10⁹/L
• Maintain fibrinogen >2g/L
• Maintain ionised calcium >1mmol/L
• Consider TEG-guided blood product resuscitation

• Rectus sheath catheters for analgesia
• Patients will require ITU care post-operatively, although early extubation is preferable

• Prolonged periods of hypotension and inadequate perfusion pressures can cause:
• A global ischaemic insult
• Lower limb ischaemia; regular lower limb neurovascular observations should take place
• Intra-abdominal organ ischaemia, particularly kidneys and colon
• Spinal cord ischaemia


• AKI (20-40%)
• MACE e.g. MI, arrhythmia, LV dysfunction, stroke
• Coagulopathy due to major haemorrhage and massive transfusion
• Hypothermia
• Abdominal compartment syndrome (10-55%)