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aortic aneurysm
A true aneurysm of the aorta is a permanent dilatation at least 50% greater than its original size involving all wall layers
A pseudoaneurysm is a rupture through the layers of the aorta held together by blood and surrounding tissues
A dissection is a disruption of the intimal layer of the aorta, with bleeding within the wall.
Untreated aneurysms of the descending and thoracoabdominal aorta exceeding 6 cm in diameter have a 14.1% annual rate of rupture, dissection, or death.
The 5 yr survival of patients managed conservatively is 10–20%
| Diameter of AAA | Annual rupture risk | Additional risk factors for rupture |
|---|---|---|
| <4 cm | 0% | Rate of expansion (>0.5 cm in 6 months) |
| 4–4.9 cm | 0.5–5% | Continued smoking |
| 5–5.9 cm | 3–15% | Uncontrolled hypertension |
| 6–6.9 cm | 10–20% | Female sex associated with higher risk of rupture for a given diameter AAA |
| 7–7.9 cm | 20–40% | |
| ≥8 cm | 30–50% |
Indications:
- rupture or acute dissection
- symptomatic enlargement: pain or compression of adjacent structures
- aneurysm enlargement >1 cm/y or rapid increase in size
- absolute size >6.5 cm or >6.0 cm in patients with connective tissue disease
Thoracoabdominal aortic aneurysms (TAAAs) are described using the Crawford classification according to the location of aneurysmal sections
- Extent I:
- from left subclavian artery
- to below diaphragm
- Extent II:
- from left subclavian artery
- to aortic bifurcation
- Extent III:
- from the lower half of descending thoracic aorta
- extending to the aortic bifurcation
- Extent IV: disease confined to the abdominal aorta

Pre-op
Pre-op assessment
- functional capacity & organ system reserve
- risk stratification
- evidence of compression of adjacent structures e.g.
- stridor / dyspnoea from encroachment onto trachea / LMB
- dysphagia from oesophageal compression
- HOV from RLN stretching
- baseline neuro deficits
Pre-op Ix: - PFT
- may need OLV
- CAD
- CPET
- anaerobic threshold of >11 ml/kg/min is often quoted as a cut-off for offering open surgery
- CT
- look for compression
- for DLT
Risk models have been used but are somewhat limited in their prediction for an individual and are not recommended by NICE
Initial resus for ruptured AAA
- avoid hypotension
- (a/w ↑ mortality)
- avoid hypertension
- could disrupt clot formation,
- targeting SBP 90–120 mmHg
- transfer should occur <30 minutes of diagnosis and is normally to the receiving hospital's emergency department resuscitation area.
- Transfer should not require blood products unless already commenced.
- Patients should not be anaesthetized for transfer or imaging as the associated loss of tone and sympathetic drive can result in irreversible cardiovascular collapse.
Optimisation:
Pre-op optimisation of vascular patients
undiagnosed COPD
short acting bronchodilator → long acting
steroid responsive: course of steroid prior to surgery
Smoking cessation
incentive spirometry
peri-op physio
Prehabilitation
A Cochrane review of RCTs comparing the impact of preoperative exercise interventions versus usual care in people having AAA repair was unable to ascertain whether prehabilitation reduced 30-day mortality, pulmonary complications, re-intervention rates or postoperative bleeding.
It may however, reduce cardiac and renal complications
Statins are protective both in the long term (reducing cardiovascular risk) but also in the perioperative period
Aspirin is continued but thienopyridine derivatives such as clopidogrel should generally be stopped in advance of open surgery due to the association with excessive bleeding and contraindication to neuraxial blockade
recent PCI → d/w cardiac
current recommendations state that initiation of β-blockers should not be considered routine in those undergoing vascular surgery and should be only started if indicated on a case-by-case basis.
Key trials on Open vs EVAR for AAA
overall: lower peri-oip mortality but survival benefits lost in following years & ↑ re-intervention rates
EVAR I, the Dutch DREAM trial and the American OVER trial concluded that although EVAR offered lower operative and 30-day mortality rates there was no survival advantage at the 5-year endpoint.
EVAR was associated with ↑ risks of
- complications,
- reinterventions
- costs
follow-up study of EVAR-1 demonstrated ↑ all cause and aneurysm-related mortality figures in the EVAR group from 8 years following follow up. This was in part attributed to secondary aneurysm sac rupture.
ACE trial demonstrated similar 30-day mortality rates between the two interventions
In 2014, the IMPROVE trial failed to prove any significant difference in 30-day mortality between EVAR and open surgery in patients with ruptured AAA.
However, those that survived who underwent EVAR
- ↓ LOS
- ↑ discharged directly home
- ↑ lead an independent life
IMPROVE trial identified that EVAR under LA is associated with a fourfold ↓ in mortality compared with GA, adjusted for age, sex, Hardman index and other factors
Complications from EVAR may be ↓ ∵
- introduction of newer stent grafts,
- improvements in
- preoperative planning,
- imaging
- perioperative care,
- more EVAR procedures done under LA instead of GA
Conclusions from the original RCTs mentioned above, may therefore be less applicable to more contemporary practice, although not all agree
The ongoing ACTION-1 trial is comparing whether ACT guided heparinisation results in more optimal coagulation than 5000 IU as a single dose and although focusing on OR, it should be applicable to EVAR
Anaesthetic technique
The anaesthetic technique for open AAA repair is built on the foundations of maintaining
- haemodynamic stability,
- normo-thermia,
- haemostasis
- adequate analgesia
Monitoring
5 lead ECG ∵ ↑ risk of CAD
Urine output and temperature monitoring are important in this group of patients, particularly when considering the pathophysiological effects of cross-clamping.
Cardiac output monitoring in combination with goal-directed fluid therapy was shown to improve postoperative outcome in high-risk general surgical patients. To date, the evidence sup-porting the use of cardiac output monitoring in open aneurysm repair is lacking
The reliability of the oesophageal Doppler and arterial pressure waveform analysis is invalidated when the aorta is clamped
BIS has garnered some support in recent times. It has been suggested that monitoring depth of anaesthesia using electroencephalographic data allows more accurate titration of anaesthetic agents without increasing the risk the awareness
Avoiding excessive doses of anaesthetic agents would be beneficial in this group of patients prone to significant haemodynamic changes, but this has yet to be proven
Evidence is emerging that suggests BIS-guided anaesthesia may be associated with a ↓ incidence of postoperative cognitive dysfunction (POCD)
Other essential equipment:
rapid infusion device
Cell salvage
POC devices e.g. VHA
Conduct of anaes
The potential cardioprotective effects of volatile anaesthetics found in cardiac surgery were not replicated when volatiles were compared with total intravenous anaesthesia (TIVA) for patients undergoing elective AAA repair
Low tidal volume ventilation with high positive end-expiratory pressure (PEEP) is associated with a reduction in post-operative pulmonary complications
PROVAR trial failed to demonstrate an improvement in intraoperative or postoperative respiratory function when using different lung protective ventilatory strategies in patients undergoing open abdominal surgery
Active warming measures should be employed to avoid the associated risks of hypothermia (oxygen consumption, myocardial dysrhythmias, coagulopathies, and postoperative wound infections). Lower body warming during aortic cross-clamping should be avoided
EA
For those undergoing open repair an epidural plus general technique has better outcomes than general plus systemic analgesia
Postoperative analgesia is usually managed with a thoracic EA that is sited before induction. Some anaesthetists prefer not to commence the epidural infusion until the end of surgery, after haemostasis and haemodynamic stability has been achieved
sympathetic blockade associated with epidural analgesia will necessitate vasopressor therapy if commenced early after aortic clamp release
Limited evidence does support the use of thoracic epidural analgesia both in terms of
- safety,
- quality of analgesia
- familiarity with the technique
When compared to systemic opioids, thoracic EA has been shown to - ↓ duration of postoperative tracheal intubation,
- provide superior analgesia
- ↓ incidences of
- postoperative MI
- gastric or renal complications
In isolation, aspirin does not confer any additional increased risk of spinal canal haematoma, but careful consideration must be given to those patients on dual or more novel antiplatelet therapies
EOT
MTP should be initiated whilst blood is sent for full cross-match (minimum 8–10 units)
Permissive hypotension and the avoidance of aggressive fluid resuscitation prior to cross-clamping minimizes surges in BP that could cause dislodgement of an intact thrombus and avoids further dilution of already depleted clotting factors
SBP of 70 mmHg is advocated provided the patient shows no signs of altered conscious state or cardiac ischaemia
RSI w/ Arterial line, & patient prepped & draped
The aim is to minimize the time between induction and application of the aortic cross-clamp
Heparinization is not usually required
Blood products
Blood loss during open aneurysm repair is highly variable
Contributing factors include those relating to the aneurysm and those relating to the surgery
Larger aneurysms, those with more complex anatomy and those associated with a hostile abdomen are associated with an increased risk of bleeding
Haemorrhage may result from
- retrograde bleeding from lumbar vessels,
- mal-positioned aortic clamps,
- leaking anastomoses
- dilutional or consumptive coagulopathies
Pre-op anaemia treated
Ideally, blood products should be transfused when haemostasis has been achieved and after the aortic cross-clamp has been released
Ideally the anesthetist should aim for
- platelet >100 x 10^9/litre,
- fibrinogen concentration >2 g/dl
- INR <1.5.
- Hb >10 g/dl while bleeding on-going
- iCa >1mmol/L
- K < 5.5 mmol/L
- lactate < 2mmol/L
- temp 36-37°C
Aortic cross clamping
Surgery involving aortic arch
DHCA
Repair of the aortic arch involves interruption to the cerebral blood supply necessitating the use of CPB with deep hypothermic circulatory arrest (DHCA). Cerebral perfusion may be maintained antegrade via cannulation of arteries as they branch from the aortic arch or via the arterial line into the right axillary, subclavian, or innominate artery, or retrograde via cannulation of the internal jugular vein.
Hypothermia is an effective technique for the protection of the central nervous system and other viscera in the presence of reduced or absent blood flow. The lower temperature reduces tissue metabolic activity and attenuates the inflammatory response to reperfusion.
The core temperature is allowed to decrease spontaneously with additional cooling from the heater/cooler on the CPB circuit. Application of topical cooling to the head is performed in some centres to minimise passive warming, although the benefits of this have been extrapolated from studies in animals. Where used, particular care should be taken to protect the patient's eyes
Opinions vary on the degree of hypothermia required. Deep hypothermia (14.1–20°C) allows 20–30 min of safe circulatory arrest time compared with 10–20 min where moderate hypothermia (20.1–28°C) is used
Profound cooling contributes to morbidity through the development of coagulopathy and an increased inflammatory response.
Anaes considerations
Invasive arterial blood pressure monitoring via the right radial artery ensures continued assessment should the aortic cross-clamp be applied proximal to the left subclavian artery.
If the right axillary artery is used for antegrade cerebral perfusion, a left radial arterial catheter may be required
Temperatures measured within the nasopharynx have been shown to most accurately reflect cerebral temperature, and monitoring is usually via probes positioned in the nasopharynx and either rectum or bladder
Pharmacological protection of the brain and spinal cord is used variably as an adjunct to hypothermia, as there is little consistent evidence.
Drugs occasionally administered include
- thiopental,
- methylprednisolone,
- magnesium,
- lidocaine.
Near-infrared spectroscopy is increasingly used during surgery involving the aortic arch to provide continuous, real-time non-invasive monitoring of anterior cerebral oxygenation. The proportion of light absorbed attributable to oxygenated and deoxygenated haemoglobin within the cerebral cortex is calculated using adhesive diodes on the forehead. Intracerebral oxygen saturation (rSO2) is calculated and should be maintained within 25% of baseline.
Inadequate cerebral perfusion should prompt assessment of cannulation sites; increased flow rate within the CPB circuit; optimised haemoglobin concentration; and, if necessary, increased hypothermia and Pco2 to promote vasodilatation.
Surgery involving descending aorta
Where a clamp can be placed distal to the left subclavian artery and there is to be no interruption to the cerebral blood supply, the use of partial left heart bypass (PLHB) is preferable
Anaes considerations
OLV
neuromonitoring
A left-sided DLT is used for ease of positioning, although external compression of the left main bronchus by the enlarged aorta may preclude this, and a right-sided DLT or single-lumen tube with bronchial blocker may be required
An arterial catheter is sited in a femoral artery, in addition to the right radial artery, to allow monitoring of distal perfusion pressure
A central venous catheter and percutaneous introducer sheath are inserted into the left internal jugular vein; insertion into the right may lead to problems with kinking once the patient is positioned
Spinal cord protection
Paraplegia after thoracic aortic surgery is a devastating and life-limiting complication, reported to occur in 4–16% of cases overall and in up to 50% of Extent II aneurysms
Perfusion insufficiency may be 2/2
- ↓ segmental arterial inflow during and after surgery
- ↑ tissue pressure ∵
- oedema
- ↑ CSF pressure,
- ↑ venous pressure limiting outflow
- ↓ arterial blood flow
- ↑ central venous pressure
→ compromising spinal cord perfusion
Replacement of diseased sections of aorta requires temporary or permanent interruption of arterial collaterals, leading to spinal cord ischaemia and subsequent reperfusion injury.
Ischaemia causes spinal oedema, hyperaemia, and inflammation, thus increasing the CSF pressure (CSFP) and compromising spinal cord perfusion pressure (SCPP).
Risk factors for spinal cord ischaemia include
- extent of the aneurysm;
- long graft >20cm
- longer duration of aortic cross-clamping;
- requirement for emergency surgery
- previous surgery to the distal aorta;
- severe peripheral vascular and atherosclerotic disease;
- perioperative hypotension;
- advanced age;
- diabetes mellitus
interventions to ↓ risk of spinal cord ischaemia, including
- minimising cross-clamping time
- sequential clamping of the aorta
- reimplantation of intercostal & lumbar segmental vessels
- (for open repair only)
- drainage of CSF to maintain SCPP,
- use of neurophysiological monitoring
Monitoring may be
- functional
- SSEP
- motor-evoked potentials
- metabolic
- CSF analysis
- physiological
- lumbar CSF pressure
- paravertebral muscle oximetry
- clinical (post-op)
- LL motor & sensory
- bowel & bladder continence
Spinal cord blood supply
The superior source vessels are branches from the left subclavian and vertebral arteries, which form the anterior and posterior spinal arteries.
Throughout its length the anterior spinal arteries receive supply from the paired intercostal and lumbar segmental arteries and then caudally from branches of the inferior mesenteric, internal iliac, and sacral arteries
reverse flow from spinal arteries may both contribute to extraprosthetic leaks after the placement of sealed or occlusive stent grafts (type II endoleaks) and ‘shunt’ blood from the spinal circulation by a low-resistance pathway
Lumbar drain
Cerebrospinal fluid drainage is effective because acute changes in the spinal cord in response to ischaemia or reperfusion may result in oedema and increased CSF pressures during the procedure and for 48–72 h (or even longer) afterwards
CSFP is maintained at 10–15 mm Hg
CSF is drained to maintain this at rates up to 20 ml/h
Monitoring of CSFP and drainage continue for up to 72 h after surgery.
An SCPP target of 70 mm Hg is used in most centres, requiring a CSFP of less than 15 mm Hg and a minimum MAP of 80 mm Hg
Where there is evidence of spinal cord ischaemia, the SCPP and MAP target can be increased in 5 mm Hg increments
The spinal drain consists of a transduced intrathecal catheter inserted at the level of L3–4 or L4–5 to reduce the risk of direct spinal cord damage
IONM
Paraplegia caused by spinal cord ischaemia significantly dampens the lower-limb potentials when compared to those of the upper limb.
MEPs disappear in the presence of neuromuscular blocking agents, and volatile anaesthetics also cause dose-dependent depression of the MEP at doses within the range used in clinical practice
TIVA is preferred if MEPs are to be used
SSEPs, although less frequently used, allow monitoring of the posterior ascending sensory columns, and are not affected by neuromuscular blocking agents or volatile anaesthetic agents.
A ↓ in MEP amplitude >50% should prompt reinsertion of intercostal arteries into the graft along with measures to improve spinal cord perfusion.
A MAP >80 mm Hg and distal aortic pressure >60 mm Hg are targeted.
Haemoglobin concentration should be maintained at or above 100 g/L
CSF may be drained at 20 ml/h
The decision for surgical intervention is usually made within 3–5 min of the change in the neurophysiological variables.
Post-op
In most cases, the aim is for primary extubation at the end of surgery and transfer to HDU/ICU
Ensure peripheral pulses are checked in lower limb for early detection and treatment of thrombosis and ischaemia before extubation.
Indications for a period of post-operative ventilation include
- profound metabolic acidosis,
- refractory hypothermia,
- respiratory failure,
- high vasopressor or inotropic support
The requirement for organ support often depends on
- complexity of the intervention,
- intra-op complications,
- patient's pre-morbid state.
multimodal analgesia to allow early weaning
→ to facilitate neuro assessment
?EA
vs spinal opioid via lumbar drain
Post-op complications
Postoperative organ dysfunction is particularly common in
- cardiovascular,
- ↑ peri-op myocardial demand → delayed myocardial ischaemia
- commonly occuring w/i first 72h post-op
- respiratory
- atelectasis
- PNA
- PE
- TRALI
- renal
- overall incidence of AKI 5-10%
- ↑ risk if
- supra-renal aortic clamp
- CKD
- nephrotoxic contrast
- ↓ renal blood flow & perfusion pressure → ATN
- no evidence to support "renoprotective drugs"
- dopamine
- N-acetyl cysteine
- furosemide
- mannitol
Neuro complication : rare
Disruption of the arterial supply to the spinal cord during cross-clamping can result in ischaemia and paraplegia
Preoperative placement of a cerebrospinal fluid (CSF) drain may be deemed necessary in patients deemed to be high-risk or spinal cord ischaemia
In general, the risk is extremely low and maintenance of adequate perfusion pressure with postoperative monitoring for evolving neurology is sufficient
Other less common postoperative complications include
- bowel ischaemia
- open repair > EVAR
- cerebrovascular disease,
- LL ischaemia
- associated surgical complications
Abdominal compartment syndrome is caused by combination of
- haematoma,
- trauma,
- oedema secondary to resuscitation and reperfusion.
Intra-abdominal pressure monitoring should be considered, as it can be difficult to diagnose and carries a significant risk of multi-organ failure.
Patients identified intraoperatively as high-risk may require a laparostomy and delayed closure.
References
Perioperative Management of Thoracic and Thoracoabdominal Aneurysms - BJA Ed
Spinal Cord Protection in Aortic Endovascular Surgery - BJA Ed