Carotid Endarterectomy

The curriculum requires us to describe 'the management of elective carotid artery surgery with general or regional anaesthesia'.

Carotid endarterectomy appeared as an SAQ in 2019 (88% pass rate), where marks were lost on specific reasons for intra-operative haemodynamic instability.

The question was repeated as a CRQ in 2023, with a more modest 70% pass rate.

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Carotid stenosis is implicated in 20 - 30% of strokes
Carotid endarterectomy (CEA) aims to remove atheromatous plaque at, or around, the carotid bifurcation

It is preventative surgery with the aim of preventing disabling or fatal stroke in those with carotid stenosis
The combined perioperative risk of mortality or major stroke is 2 - 5% i.e. this is high risk surgery

Patients should be in a stable neurological condition following acute, non-disabling stroke or TIA.

Symptomatic patients with:

≥50 - 99% carotid stenosis
The benefits are considerable if >70% stenosis but only marginal if 50 - 69% stenosis

Asymptomatic patients with:

≥60 - 99% carotid stenosis
(As they are at increased risk of stroke on best medical treatment alone)

The effectiveness of CEA in stroke prevention is greatest if performed within 48hrs of symptoms, and certainly within 2 weeks

Pre-assessment should not cause undue delay with regards to timing of surgery
History and examination should focus on:

Elucidating risk factors and comorbidities associated with vascular disease e.g. HTN, DM, smoking, obesity and hyperlipidaemia
A thorough neurological examination, as the patient will have already suffered symptoms inc. TIA or stroke
Ascertaining as to whether there are contra-indications to a local technique, which include profound respiratory disease or contralateral recurrent laryngeal nerve palsy

Pre-operative counselling is important in patients undergoing CEA under local anaesthesia

Investigations

Bloods: FBC | U&E | Clotting
ECG
Review of TTE, which will have often been performed as part of the investigations for recent stroke
Further investigations as dictated by individual risks and comorbidities

Optimisation

Patients are at high risk of MACE and post-operative pulmonary complications, renal dysfunction, cognitive dysfunction and chronic pain
Individual cardiorespiratory risk factors should be optimised within the available timeframe
Patients are likely to be on at least aspirin monotherapy
A single dose of 75mg clopidogrel the night before surgery is associated with a reduced incidence of post-operative thrombotic events

There is debate about the optimal technique for CEA
Regardless of technique, the aims are to:

Maintain adequate oxygenation and cardiovascular stability
Provide analgesia
Provide good operating conditions including cerebral monitoring

The GALA Trial (2008) did not find either general or regional technique to be superior with regards to risk of stroke, MI or mortality at 30 days

General anaesthesia	Regional anaesthesia
Airway control	Accurate, immediate neurological assessment (gold standard)
Optimised cerebral blood flow by manipulating PCO₂/PO₂	Prevents unnecessary shunt insertion i.e. only in those demonstrating altered neurology
Neuroprotection from reduced CMRO₂	Shorter hospital stay
Patients tend to prefer GA	Avoids complications of GA e.g. aspiration, PONV, cardiorespiratory complications
	Allows arterial closure at a own MAP, which may reduce risk of post-operative haematoma
Precludes effective neurological monitoring	Complications of regional block inc. failure and need for GA or LA toxicity
Increased use of shunts which increases risk of post-op. stroke via emboli or thrombosis	Need for sedation or conversion negates the benefits of LA
Increased intra-op. hypotension & post-op. hypertension	Difficult airway access if needs converting
	Patient stress and pain during block increases risk of myocardial ischaemia
	Requires cooperative patient who can lie flat and sit still

General anaesthetic technique

No evidence to support IV or gas induction as superior
Generally a reinforced ETT taped to contralateral side
Appropriate eye protection given propensity for surgeons to treat the face as an arm rest
In general avoid long-acting opioids as may cloud post-operative neurological assessment
Some suggestion to extubate deep (to avoid haemodynamic dyscrasia during extubation) but then stay in theatre until normal neurology is ensured
Local anaesthetic infiltration of wound

Regional anaesthetic technique

Block over C2 - C4 dermatomes is required
Options include:

Superficial cervical plexus block
Deep cervical plexus block
Combined superficial & deep cervical plexus block
Cervical epidural, if you're feeling extra-spicy - it is technically challenging and has a high complication rate
Local anaesthetic infiltration alone

Considerations include:

Surgical issues

High lesions requiring high dissection or vigorous retraction can be difficult to block
Crossover innervation by contralateral cervical plexus may require infiltration of midline LA
The carotid artery itself (branch of glossopharyngeal n.) is exquisitely sensitive to manipulation and is difficult to block; LA injected into carotid sheath may overcome this

Ensure appropriate pre-operative counselling about expectations
Ensure comfortable positioning and temperature
Use transparent drape to reduce claustrophobia
Regular checks of cerebral function throughout, both pre- and post-cross-clamping

Monitoring

AAGBI as standard
Arterial line in contralateral arm
Wide-bore access in contralateral arm
Temperature management to ensure normothermia
Urinary catheter often not required

Neuro-monitoring

Carotid cross-clamping is performed both above and below the area of stenosis, which can cause cerebral ischaemia and focal neurology if there is inadequate collateral flow in the Circle of Willis
Placement of carotid shunts can mitigate this, yet their use is associated with increased risk of post-operative stroke from thromboembolism
Their use may be reserved for patients deemed at higher risk of cerebral ischaemia, although some surgeons place them routinely

The gold standard is the awake patient having CEA under local anaesthetic
The patient under GA cannot be reliably assessed for neurological deficits
There are a number of techniques used to monitor cerebral perfusion under GA, though none are wholly reliable:

Technique	Description	Advantages	Disadvantages
Transcranial Doppler	MCA flow measured via petrous temporal bone	Monitors for flow & emboli Can be continued post-op.	Operator dependent Unable to generate signal in 10 - 20%
Carotid stump pressure	Measure pressure in carotid stump beyond cross-clamp	Specific measure of cerebral ischaemia	Not very sensitive Doesn't monitor for emboli
(p)EEG	As standard e.g. Sedline, BIS		Affected by GA Doesn't monitor for emboli Doesn't monitor deeper (non-cortical) structures
SSEP	As standard	Monitors sub-cortical structures Useful if EEG abnormal	Affected by GA Doesn't monitor for emboli No more sensitive/specific than (p)EEG
NIRS	Measure regional saturation (rSO₂) 10 - 15% deviation from baseline indicates ischaemia	High NPV for cerebral ischaemia	Poor PPV Doesn't monitor for emboli Signal intereference

Haemodynamic considerations

Cardiovascular instability is very common during CEA; rapid, profound hypo- or hypertension can occur
Cardiovascular instability can precipitate stroke, MI or heart failure
Targets for blood pressure control include MAP within 20% of baseline, and SBP ≤170mmHg
This should be acheived with vasoactive drugs, rather than excessive fluid administration

Pathophysiology of haemodynamic instability during CEA

Impaired arterial pressure autoregulation following stroke

Reduced carotid baroreceptor sensitivity due to atherosclerosis

Effects of general or regional anaesthesia

Effects of surgery itself

Effects of patient comorbidities including old age, diabetes and anti-hypertensive medications

Bleeding - clotting balance

All patients should be taking aspirin prior to surgery ± additional clopidogrel to reduce perioperative thromboembolism
Heparin 5,000units IV is administered just prior to cross-clamping

Cerebral steal phenomenon

If hypercapnoea is allowed, it will cause preferential vasodilation of the non-operative side of the brain, as there is limited blood flow to the operative side due to carotid cross-clamping
This exacerbates the already reduced perfusion to the operative side
Prevented by ensuring normocapnoea

Oral analgesia is typicall sufficient
Regular neuro-observations are instigated from recovery onwards
Patients typically go to HDU post-operatively for monitoring and management of BP, but are often readily discharged the following day

Blood pressure control

Systolic BP should be tightly controlled, between 110mmg - 160/180mmHg

Hypertension is common (up to two thirds of patients), especially after GA

It is usually transient, peaking in the first few hours after surgery
It is related to impaired baroreceptor function
Predisposes to wound haematoma, MI and cerebral hyperperfusion syndrome

Management of post-operative hypertension includes:

Sitting the patient up
Managing pain, including that from urinary retention
Target SBP as above, or within 20% of pre-operative value
Pharmacotherapy; first line is with ɑ-blockers or β-blockers

Labetalol 10mg boluses every 2mins up to 100mg
Esmolol, metoprolol, atenolol, clonidine are other options
Direct-acting vasodilators (GTN, nitroprusside and hydralazine) and nifedipine can cause cerebral vasodilation and therefore are typically second line

Hypotension is less common

Excluding causes such as cardiogenic failure or hypovolaemia is imperative
Management may involve small fluid boluses ± phenylephrine as boluses or infusion

Overall, severe complications are rare

Post-operative bleeding and haematoma (3 - 8%) may be airway- and/or life-threatening
Myocardial infarction (2 - 3%)
Recurrent laryngeal nerve injury

Stroke can occur, with an incidence of ∽3.5%

Most are due to intra-operative embolus or post-operative thrombosis
20%, however, are due to peri-operative haemodynamic instability
Incidence is lower than the 5 - 6% rate without CEA

Cerebral hyperperfusion syndrome

Incidence 1 - 3%
Presents in the early post-operative period e.g. 2 - 7 days post-op.
Risk factors include >90% stenosis, intra-operative ischaemia/emboli, operation on the second side, prolonged post-operative hypertension and reduced cerebrovascular reserve
There is ipsilateral loss of cerebral autoregulation, causing increased ipsilateral cerebral blood flow
Manifests as:

Hypertension
Ipsilateral headache
Focal neurological deficits
Seizures

Management is with emergent control of blood pressure