Carotid endarterectomy

Indications

Hemispheric or retinal TIA or a mild (non-disabling) stroke within 120 days AND

Ipsilateral high-grade stenosis (> 70%)

Trials

Symptomatic

NASCETrial

Asymptomatic

Unresolved controversies

Progressive STROKE (“stroke in evolution”)

Progressive retinal ischemia

Abrupt occlusion

Tandem lesions (e.g. carotid siphon and bifurcation stenosis): although this topic remains controversial, CEA in patients with tandem lesions has not been associated with increased postoperative stroke rates.

Stenosis	Relevant study	Recommendation	Risk reductionᵇ
Symptomatic narrowing	ㅤ	ㅤ	ㅤ
70–99%	NASCET	CEA	16.5 @ 2 yrs
>60%	ECST	CEA	11.6 @ 3 yrs
50–69%	NASCET	CEAᶜ	10.1 @ 5 yrs
<30%	NASCET	BMM	0.8 @ 5 yrs
<40%	ECST	BMM	CEA worse @ 3 yrs
Asymptomatic narrowing	ㅤ	ㅤ	ㅤ
>60%	ACST	CEA if age <75 yrs	5.4% @ 5 yrs
>60%	ACAS, ACSTᵈ	CEAᵈ	6.3 @ 5 yrs
>50%	VACS	± CEAᵉ	ㅤ
<90%	CASANOVA	BMMᵉ	ㅤ

ᵃ abbreviations: NASCET = North American Symptomatic Carotid Endarterectomy Trial; ECST = European Carotid Surgery Trial; CASANOVA = Carotid Artery Stenosis with Asymptomatic Narrowing Operation Versus Aspirin; ACAS = Asymptomatic Carotid Atherosclerosis Study; ACST = Asymptomatic Carotid Surgery Trial; VACS = Veteran’s Administration Cooperative Study; CEA = carotid endarterectomy; BMM = best medical management.
ᵇ Reduction in risk of all nonfatal strokes and death from any cause with CEA vs. BMM (e.g., with an absolute risk reduction of 16.5 at 2 yrs, for every 100 patients treated, 16.5 nonfatal strokes or deaths were prevented over a 2 year period).
ᶜ Surgery moderately beneficial (requires low complication rate)
ᵈ The overall health of the patient is critical
ᵉ Results equivocal

Timing of CEA after acute stroke

Can be done after 24 hrs of tPA

But have an increased risk of stroke

Generally done after 7 days post acute stroke
Before 14 days

As after 14 days the benefit would not be as great

Pre op risk factor for CEA

Hard to define

Because they are not included in studies

NASCET and ACAS:

Age >80 years,
Prior ipsilateral CEA,
Prior contralateral CEA within 4 months,
Prior neck XRT,
Tandem lesion larger than target lesion,
Other conditions that could cause symptoms (atrial fibrillation, prior stroke with persistent major deficit, valvular heart disease),
Major organ failure,
Uncontrolled hypertension or diabetes mellitus, and
Significant coronary artery disease

SAPPHIRE Trial (Stenting and Angioplasty with Protection in Patients at High-Risk for Endarterectomy):

Patients with clinically significant cardiac disease (CHF, abnormal stress test, or need for open-heart surgery), severe pulmonary disease, contralateral carotid occlusion, contralateral laryngeal-nerve palsy, previous radical neck surgery or neck XRT, recurrent stenosis after endarterectomy, and age>80 years.

ARCHeR Trial (ACCULINK for Revascularization ofCarotids in High-Risk patients)

Also included patients with tracheostomy, spinal immobility, and dialysis-dependant renal failure.

Pre-op management

Aspirin 325mg TID for at least 2 days, preferably 5 days pre-op

Patients should be kept on their Aspirin for surgery, and if not on Aspirin they should be started, in order to reduce risks of MI and TIA

Post-op management

Patient monitored in ICU with A-line

Keep patient well hydrated (run IVF≥100 cc/hr for most adults)

SBP ideally 110–150mm Hg (higher pressures are permitted in patients with chronic severe HTN)

BP frequently labile in 1st 24 hrs post-op, may be due to “new” pressure in carotid bulb

To prevent rebound hyper- or hypotension, avoid long acting agents
Hypotension

EEG – R/O cardiogenic shock
Mild hypotension: Fluids
Severe/fluid resistant: Phenylephrine

Hypertension:

Nicardipine: drug of choice
Avoid rebound hypotension

Avoid antiplatelet drugs for 24–48 hrs post-op (causes oozing);

May start these 24–72 hrs postop

Note: ASA 325mg + dipyridamole 75mg TID have been shown not to reduce the rate of restenosis after endarterectomy

But Aspirin should be continued for life after

Optional:

Reverse half of heparin with protamine 10 minutes after closing arteriotomy

Check for

Change in neurologic status due to cerebral dysfunction, including:

Pronator drift (R/O new hemiparesis)
Signs of dysphasia (especially for left sided surgery)
Mimetic muscle symmetry (assesses facial nerve function)

Pupil diameter and reaction (R/O stroke, Horner syndrome)
Severe H/A (especially unilateral) >may indicate hyperperfusion syndrome
STA pulses (R/O external carotid occlusion)
Tongue deviation (R/O hypoglossal nerve injury)
Symmetry of lips (R/O weakness of lower lip depressors due to retraction of marginal mandibular branch of facial nerve against mandible, usually resolves in 6–12 wks, must differentiate from central VII palsy due to stroke)
Check for hoarseness (R/O recurrent laryngeal nerve injury)
Assess for hematoma in operative site: note any tracheal deviation, dysphagia

Operative technique

Anaesthesia and monitoring

Most (but not all) surgeons monitor some parameter of neurologic function during carotid endarterectomy, and will alter technique (e.g. insert a vascular shunt) if there is evidence of hemodynamic intolerance of carotid clamping (only occurs in ≈ 1–4%).

General vs local/regional anesthesia:

Local/ regional

Permits “clinical” monitoring of patient’s neurologic function.
Disadvantages:

Patient movement during procedure (often exacerbated by sedation and alterations in CBF),
Lack of cerebral protection from anesthetic and adjunctive agents.

Trials

The only prospective randomized study found no difference between local and general anesthesia.
The multicenter, randomized controlled General Anesthesia versus Local Anesthesia (GALA) Trial found no significant differences in the prevention of stroke, MI, or death for either anesthetic technique.

Sub-group analysis showed trends (not statistically significant) favoring local anesthesia for perioperative death, event-free survival at 1 year, and patients with contralateral occlusion.
Local anesthesia was associated with a significant reduction of shunt insertion.

A Cochrane Database Review found no evidence from randomized trials to favour either anaesthetic technique

General anesthesia

Including barbiturates (thiopental boluses of 125–250mg until 15– 30 second burst suppression on EEG, followed by small bolus injections or constant infusion to maintain burst suppression)

EEG monitoring
SSEP monitoring
Measurement of distal stump pressure after CCA occlusion (unreliable), e.g. using a shunt if stump pressure < 25mm Hg
Transcranial Doppler
Near-infrared spectroscopy

Position

Supine, neck slightly extended and rotated slightly (≈ 30°) away from the operative side

Incision

The incision curves gently and follows the anterior border of the sternocleidomastoid muscle, and curves posteriorly at the rostral end

Keep the horizontal portion of the incision ≈ 1cm away from the mandible to avoid injury to marginal mandibular branch of facial nerve (which lies in the inferior parotid gland and supplies lip depressor) due to retraction against mandible

Retractors should not be placed deeper than the platysma to avoid injury to recurrent laryngeal nerve, which runs between the esophagus and trachea. Blunt retractors are used to avoid internal jugular vein injury

Dissection

The common facial vein (CFV) usually crosses the field over the carotid bifurcation, it is doubly ligated and divided. It leads to the internal jugular vein (IJV)

Identifying the IJV is key, dissection is carried down between the carotid artery and the IJV

Ansa hypoglossi runs superficial to the ICA and serves as a useful guide to the hypoglossal nerve (XII) which should be identified since it is at greater risk when it is not seen.

XII can arise anywhere from the carotid bifurcation to the angle of the mandible, although it is usually in the vicinity of the CFV.
Mobilization can be facilitated by dividing the small artery (sternocleidomastoid branch of the ECA) and vein that cross over it
The ansa hypoglossi can usually be spared, and if mobilized, allows medial retraction of the hypoglossal nerve out of harm’s way. If it is necessary to divide the ansa it is done close to the hypoglossal nerve to be certain it is not a branch of the vagus and to minimize neurologic deficit (the ansa has an anterior cervical limb from the cervical plexus)

The superior thyroid artery is the first branch of the ECA, and helps differentiate ECA from the ICA (the ICA is located posterior to the ECA)

The carotid bulb may be anesthetized with ≈ 2–3ml of 1% plain lidocaine using a 27 Ga needle.

This may be done routinely, or, as some prefer only if hypotension and/or bradycardia occur during dissection (indicating IX nerve stimulation)

The ICA must be exposed beyond the extent of the plaque which can be determined by gentle palpation with a moistened finger and by visualization as the area where the artery turns from yellowish to its normal pinker colour

Occlusion and arteriotomy

A vessel loop is placed around the ECA at least 2cm above the bifurcation

A vessel loop is also placed around the ICA but is looped only once

Umbilical tape with a choke is placed around the CCA 2–3cm below the bifurcation

IV heparin (usually 5,000 IU) is given 1minute prior to cross clamping 5. a temporary aneurysm clip is placed on the superior thyroid artery

The order of occlusion of the vessels is as follows (mnemonic: “ICE”):

ICA (e.g. with temporary aneurysm clip)
CCA (e.g. with a small DeBakey clamp)
ECA (e.g. with temporary aneurysm clip)

During ICA clamping, mild hypertension is maintained by the anesthesiologist

Shunt: some surgeons use some form of monitoring (EEG, BSAER, etc.) to determine if a shunt is needed—see Anesthesia and monitoring; yet others routinely use a shunt whenever possible without assessing the need

The arteriotomy is begun in the CCA with a #11 scalpel, and once the lumen is entered, Potts’ scissors carry the incision through to the ICA beyond the plaque. Stay in the midline to facilitate arteriotomy closure

Plaque removal

Plaque usually cannot be completely removed from the CCA, and thus it is usually transected with Potts’ scissors, taking care not to inadvertently incise the artery wall and to leave as smooth an edge as possible

In the ICA, great care must be made to avoid leaving an intimal flap which could become a nidus for an arterial dissection.

If necessary the intima may be tacked down by suturing from the lumen out on both ends (using double armed suture) and tying the knot outside the vessel

Arteriotomy closure and vessel release

Arteriotomy may be performed with a running Prolene suture using either

Primary closure
Patch graft to increase the caliber of the vessel and reduce the risk of re-stenosis

Synthetic patches (Dacron, PTFE) are preferred to autologous vein (risk of aneurysmal dilatation, thrombogenic surface)

Limited evidence suggests that carotid patch angioplasty may reduce the risk of perioperative arterial occlusion and re-stenosis.

The order of releasing the vessels (reverse that of the clamping order):

ECA → CCA (allows air and debris to be washed into the ECA) → ICA

Post-op complications

To justify CEA, the absolute upper limit of (significant) complication rate should be ≤ 3%.

Overall in-hospital mortality: 1%

Disruption of arteriotomy closure:

Rare, but emergent (see below)
Present as:

Swelling of neck:

Rupture may produce a pseudoaneurysm

Tracheal deviation:

Visible
Palpable
On CXR

Symptoms:

Dysphagia
Dyspnoea
Worsening hoarseness,
Difficulty swallowing

Dangers:

Asphyxiation: most immediate danger
Stroke
Exsanguination (unlikely, unless skin closure is also disrupted)

Late (often delayed weeks to months): false aneurysm.

Risk= 0.33%.
Presents as neck mass.
Risk is increased with wound infection and possibly with patch graft as compared to endarterectomy alone

Stroke

Intra-op or post-op rate: 5%
Ischaemic

Embolic

Most common cause of minor post-op neurologic deficit)
Due to denuded media of endarterectomy

Postoperative ICA occlusion

Most common cause of major post-op stroke, but may be asymptomatic
Due to

Hypercoagulable state induced by heparin (predictable in patients whose platelet count drops while on heparin. No known therapy for this condition
The endarterectomized surface is highly thrombogenic for 4 hrs following endarterectomy (Sundt recommends not reversing heparin)
Closure, according to Sundt's series

Patch graft closure:

0.8% incidence, associated with major stroke in 33% and minor stroke in 20%

Primary closure:

4% in Sundt’s experience
2–5% in literature

Intracerebral hemorrhagic (ICH) (breakthrough bleeding):

Occurs in < 0.6%.
Due to cerebral hyperperfusion
Timing:

First 2 weeks post op
Most fq at 3–4 days post-op

Location: often in basal ganglion
Patients at greatest risk are those with

Severe stenosis
Limited hemispheric collateral flow

Post-op TIAs:

Due to

ICA occlusion (most)
Some may be due to microemboli
Hyperperfusion syndrome produces a 1% incidence of post-op TIAs

Treatment

If TIA occurs in recovery room

Emergency CT (to R/O hemorrhage) → Angiogram recommended to assess for ICA or CCA occlusion (vs. emboli)

If TIA occurs later, consider emergent Oculopneumoplethysmography' (OPG)

If abnormal → emergent surgery (if neurologically intact, pre-op angiogram is appropriate)
OPG:

Fast, relatively inexpensive, noninvasive investigation
Measurement of ocular systolic pressures in order to make determinations regarding the presence of hemodynamically significant carotid artery stenoses.

Seizures:

Usually focal in onset with possible generalization
Timing: most occur late (post-op day 5– 13)
Incidence of ≈ 0.4% to 1%
Due to

Cerebral hyperperfusion
Emboli
Intracerebral haemorrhage

Treatment

Difficult to control initially
Lorazepam
Phenytoin

Late restenosis:

Identifiable restenosis occurs in ≈ 25% by 1 yr

Half of these reduce luminal diameters by> 50%.

Causes

Within 2 yrs: fibrous hyperplasia,
After 2 yrs: atherosclerosis

Cerebral hyperperfusion syndrome (AKA normal pressure hyperperfusion breakthrough):

Due to

Return of blood flow to an area that has lost autoregulation due to chronic cerebral ischemia typically from high-grade stenosis (Controversial)

Presentation

Ipsilateral vascular H/A or eye pain that subsides within several days
Seizures (± PLEDs on EEG, more common with Halothane®, due to petechial haemorrhages)

May cause ICH
Timing: Most occur several days post-op

Hoarseness:

The most common cause is laryngeal oedema and not superior nor recurrent laryngeal nerve injury

Cranial nerve injury:

Most common complication after CEA

Incidence of up to 8–10%

Hypoglossal nerve

Tongue deviation towards the side of injury:
Incidence ≈ 1% (with mobilizing XII to allow displacement).
Presentation

Unilateral injury may cause speaking, chewing and swallowing difficulties.
Bilateral injuries can cause upper airway obstruction.

The presence of a unilateral palsy is a contraindication to doing contralateral endarterectomy until the first side recovers.

May last as long as four months

Vagus or recurrent laryngeal nerve

Unilateral vocal cord paralysis:
1% risk

Mandibular branch of facial nerve

Loss of ipsilateral lip depressor

Headache

Hypertension:

May develop 5–7 days post-op.
Longstanding HTN may occur as a result of the loss of the carotid sinus baroreceptor reflex

Managing post-op complication

Fixed post-op deficit in distribution of endarterectomized carotid

Timing

If deficit occurs immediately post-op (i.e., in PACU)

Recommend immediate re-exploration without delay for CT or angiogram

(Case reports of no deficit when flow re-established in ≤ 45 mins).

If later onset, workup is indicated.

Technical considerations for emergency reoperation:

Isolate the 3 arteries (CCA, ECA, & ICA)
Occlude CCA 1st, then ECA, and ICA last (to minimize emboli)
Open arteriotomy, check backflow; if none, pass a No. 4 Fogarty catheter into ICA, gently inflate and withdraw (avoid intimal tears)
If good backflow established, close with patch graft
Remove tortuous vessel loops and kinks before closing

Immediate management (unless ICH or SDH are likely) includes

Fluids (e.g. Plasmanate®) to improve rheology and to elevate BP
Pressors (e.g. phenylephrine) to elevate SBP to ≈ 180mm Hg
Oxygen
Heparinization (may be controversial)

Theoretical benefits of radiographic evaluation include:

Identifies ICH or SDH that might require treatment other than re-exploration of the surgical site, elevating BP, etc.

Angiogram:

Identifies whether ICA is occluded, or if deficit is from another cause (e.g. emboli from endarterectomy site) that would not benefit from re-exploration or possibly endovascular treatment

Disruption of arteriotomy closure, management

OPEN WOUND

If there is any stridor, it is critical to do this before trying to intubate (although ideally performed in O.R., the delay may be decisive).
Evacuate clot (start with a sterile gloved finger) and stop bleeding, preferably without traumatizing the artery; a DeBakey clamp is optimal

INTUBATION

High priority, may be difficult or impossible if trachea is deviated (open wound immediately).
Preferably done by anesthesiologist in controlled setting (i.e., O.R.) unless there is acute airway obstruction

Call O.R. and have them prepare set-up for endarterectomy, and take patient to O.R.

To be sorted

An appropriately examined, investigated (may include MRA or catheter angiogram to identify level of stenosis), consented and marked patient is taken to theatre and placed prone with the neck extended and the head rotated towards the contralateral side.

Surgery is commonly undertaken awake to allow for neurological monitoring. An incision (the length of which is dependent on the site and extent of stenosis) is made along the medial edge of sternocleidomastoid and dissection continues through platysma.

The carotid sheath is palpated under the medial edge of sternocleidomastoid and is exposed. Following dissection of the common, internal, and external carotid arteries, vessel loops are passed around each artery. The patient is heparinised. Proximal and distal clamps are placed prior to arteriotomy. The patient is continually assessed neurologically from clamping onwards. Microdissectors are used to dissect plaque free from the vessel wall. The site is then irrigated with heparinised saline prior to closure (usually with a patch to avoid focal stenosis at closure). Clamps are released sequentially (proximal first) to confirm haemostasis prior to drain insertion and closure.