Chapter 91 - Carotid endarterectomy Flashcards by Gary Yang

CEA first done in

1950’s

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CEA should be done in asymptomatic stenosis 60-99 if

1) periop stroke/death < 3% 2) 3-5 years life expectancy

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POISE trial key point

Vascular disease patients benefit from perioperative beta blockers goal HR 60-80

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Heparin use in perioperative CEA

1) no level I evidence 2) OHSU suggest use in crescendo TIA 3) perioperative prevent thrombosis (use with ASA)

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General anesthesia vsersus local anesthesia for carotid surgery GALA

1) protamine does not increase perioperative stroke risk

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Dextra use in platelet

1) Polysaccharide inhibits platelet aggregation 2) control embolic episodes both preop and postop 3) can be used post-CEA to control platelet aggregation for 24 hours

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Asymptomatic carotid artery progression study (ASAPS) on statin use in carotid

1) lovastatin reduces carotid artery intima-media thickness 2) lower rate of combined CV events 3) no change to stroke rate

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Statin benefits

1) reduce stroke 2) reduce restenosis 3) reduce MI and CV events

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Injury to greater auricular nerve

numbness of earlobe

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Measuring stump pressure

1) clamp CCA and ECA 2) needle connected to pressure line placed into distal CCA below bifurcation

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Eversion carotid endarterectomy Debakey etheredge kieney

DeBakey but only partial transection Etheredge revised it with complete transection below bifurcation Kieney modified 1985 oblique ICA excision and everted alone then reattach after standard endarterectomy done on the CCA and ECA

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Pro and con of eversion endarterectomy

1) faster 2) less prone to restenosis 3) no patch needed 4) more extensive dissection harder 5) endpoint inspection suboptimal complete study should be done

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EVEREST (eversion CEA vs standard trial study)

1) 1400 patients 2) no difference in outcome 3) higher incidence of perioperative complication with eversion 4) higher incidence of restenosis with standard (confirmed by metaanalysis)

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Strategies for higher exposure of a carotid

1) nasotrachial intubation (displaces mandible anteriorly 1-2 cm) 2) divide digastric 3) resect styloid process (gains 4-5 mm) 4) anterior subluxation of mandible

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Nerve injury with digastric division

1) spinal accessory - tendinous portion of SCM in upper third 2) glossopharyngeal - deep to digastric

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Steps to resect styloid process

1) divide posterior belly of digastric 2) divide styloid apparatus muscle insertions 3) divide styloid process with raunger 4) ligate occipital artery behind inferior border of digastric

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Muscles that insert to the styloid process

1) Styloglossus 2) stylopharyngeus 3) stylohyoid muscle

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Nerve injury in styloidectomy

Facial nerve

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Anterior subluxation of mandible

1) described in 1984 2)place circumdental wires around mandibular cuspid and bicuspid teeth 3) corresponding wires placed on contralateral maxillary teeth 4) sublux mandible anterioly and twist wire together to hold fixation 5) osteotomy through vertical ramus of mandible if needed

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ligaments holding the mandible in socket

1) capsular ligament 2) lateral ligament

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Methods to determine when to shunt

1) stump pressure 2) EEG 3) somatosensory evoked potential 4) TCD to measure MCA flow 5) cerebral oximetry 6) awake surgery

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Shunt types

1) pruitt-inahara 2) javid 3) argyle pruitt less likely to maintain physiological flow javid higher risk of embolism

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AbuRahma meta analysis on stroke rate for CEA with shunting

1) 1990-2010 routine shunt: 1.4% never shunt 2% awake 1.1% EEG or stump pressure 1.6% TCD 4.8%

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Stump pressure

did not correlate well with EEG or TCD use

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Rate of stroke in abnormal EEG without shunt

9% EEG is overly sensitive

SSEP for monitoring

not reliable

TCD first introduced

Schneider 1988

TCD abnormality correlation with EEG criteria

60% only not very reliable to predict cerebral ischemia

Awake surgery shunt rate

5-15% lower than any other modalities

Patch rupture with vein

0.5-4%

Aneurysmal degeneration of vein patch

17%

GSV \< this diameter more prone to rupture

3.5 mm

Patch vs no patch

Patch associated with better outcome and less stroke risk One study showed that microvascular techniques is better in primary closure but hard to reproduce

Patch material

Saphenous may be associated with more blow up and aneurysm dacron associated with more stroke and thrombosis but has since then been reengineered

EVEREST trial on completion defects that increase risk of stroke

Plaque extension greater than 2 cm into ICA

Post-CEA stroke causes

1) perioperative arterial thrombosis 2) embolization 3) cerebral ischemia during clamping 4) intracerebral hemorrhage

What to do if post-op neuro deficit in OR

1) immediate exploration and interrogation of patch with duplex ultrasound 2) if defect found then open and remove clot and redo 3) if defect found but no clot then replace with vein patch or replace whole segment with interpositional PTFE (ringed 6mm)

What to do if post-op neuro deficit in recovery

1) immediate duplex interrogation 2) if defect of thrombosis then OR 3) if not then CT 4) if CT negative then IR

Benefit of CEA based on NASCET, ECST, ACAS, ACST on risk reduction

TABLE 91.1

Population studies on perioperative CVA and death % after CEA

1.0-4.0%

Risk of MI after CEA

40-50%

Surgical CAD rate in CEA candidates

20%

Cranial nerve injury in CEA

TABLE 91.3 Permanent nerve injury 0.5-1.1% transient injury 5-20%

Hypoglossal nerve dysfunction

1) ipsilateral tongue weakness 2) deviation to affected side with protrusion 3) difficulty masticating

Course of hypoglossal nerve

1) descends from hypoglossal canal (anterior condylar foramen) medial to ICA 2) course lateral to ECA

Vagus/recurrent laryngeal injury

1) paralysis of ipsilateral vocal cord in paramedian position 2) hoarseness 3) loss of effective cough

Superior laryngeal nerve course

1) from vagus near jugular foramen 2) obliquely to larynx posterior to ECA/ICA 3) divides into internal and external branches

Injury to external branch of superior laryngeal nerve

1) loss of tensioning of ipsilateral vocal cord 2) early fatigability of voice 3) difficult with voice modulation at high registers

Injury to internal branch of superior laryngeal nerve

1) decreased sensation at laryngeal inlet 2) mild swallowing difficulty

Marginal mandibular branch injury

1) branch of facial nerve 2) drooping of ipsilateral lower lip 3) minimal functional consequence

Course of the marginal mandibular nerve

1) course along anterior border of parotid gland between platysma and deep cervical fascia 2) across masseter muscle and ramus of mandible

Glossopharyngeal nerve injury

1) mild dysphagia to recurrent aspiration 2) normally provides sensory and motor innervation to larynx

Spinal accessory nerve course

1) exit jugular foramen 2) posterior to stylohyoid muscle 3) enter cephalic extent of stenocleidomastoid

Injury of spinal accessory

1) shoulder droop and pain 2) scapular winging 3) difficulty abducting shoulder (weak trapezius)

Cutaneous sensory nerve in CEA field

1) greater auricular (60% injury) - most superior part of incision 2) transverse cervical (69% injury) - most inferior part of incision

injury to greater auricular nerve

numbness of angle of mandible and lower part of ear

Injury of transverse cervical nerve

anesthesia of anterior neck skin

Treatment of hypotension post CEA

1) fluid 2) phenylephrine target within 20 mmHg of preop

Treatment of hypertension post CEA

1) IV sodium nitroprusside 2) nitroglycerin if MI 3) resume antihypertensives evening of surgery target within 20 mmHg of preop

Cerebral hyperperfusion syndrome key points

1) several days after CEA 2) severe hypertension 3) incidence 0.4 - 7.7% 4) symp: migraine, seizures, hemorrhagic stroke 5) mortality rate 75-100%

Cause of hyperperfusion syndrome

Disordered intracerebral autoregulation sudden increase regional cerebral blood flow

Timeframe between bilateral CEA that is associated with hyperperfusion

3 months

Wound infection rate after CEA

0.09-0.15%

Bleeding after CEA

0.7-3%

Rate of significant carotid disease in cardiac surgery patients

3-14%

Rate of stroke after cabg

2% overall 3% in asymptomatic 50-99% 5% in bilateral 50-99% 7-11% in carotid occlusion

Cleveland clinic on combined CEA/CABG vs staged CABG then CEA

Stroke rate 2.8% combined vs 14% staged not all studies suggest this

When to do combined CEA/CABG

1) severe 3VD 2) LM disease 3) critical AS 1) carotid occlusion? 2) symptomatic carotid with \> 50% stenosis

carotid web

thin membrane of tissue extending from posterior wall of the ICA into lumen nidus for thrombus better seen on CTA

When should ECA endarterectomy be done

1) ICA occlusion 2) persistent ipsilateral hemispheric symptoms risk of stroke higher if contralateral disease

Current guideline standards for stroke rate after symptomatic and asymptomatic carotid CEA

symp \< 6% asymp \< 3% acceptable

Chapter 91 - Carotid endarterectomy Flashcards

(71 cards)