Chapter 91 - Carotid endarterectomy Flashcards
CEA first done in
1950’s
CEA should be done in asymptomatic stenosis 60-99 if
1) periop stroke/death < 3% 2) 3-5 years life expectancy
POISE trial key point
Vascular disease patients benefit from perioperative beta blockers goal HR 60-80
Heparin use in perioperative CEA
1) no level I evidence 2) OHSU suggest use in crescendo TIA 3) perioperative prevent thrombosis (use with ASA)
General anesthesia vsersus local anesthesia for carotid surgery GALA
1) protamine does not increase perioperative stroke risk
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
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
Statin benefits
1) reduce stroke 2) reduce restenosis 3) reduce MI and CV events
Injury to greater auricular nerve
numbness of earlobe
Measuring stump pressure
1) clamp CCA and ECA 2) needle connected to pressure line placed into distal CCA below bifurcation
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
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
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)
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
Nerve injury with digastric division
1) spinal accessory - tendinous portion of SCM in upper third 2) glossopharyngeal - deep to digastric
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
Muscles that insert to the styloid process
1) Styloglossus 2) stylopharyngeus 3) stylohyoid muscle
Nerve injury in styloidectomy
Facial nerve
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
ligaments holding the mandible in socket
1) capsular ligament 2) lateral ligament
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
Shunt types
1) pruitt-inahara 2) javid 3) argyle pruitt less likely to maintain physiological flow javid higher risk of embolism
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%
Stump pressure
did not correlate well with EEG or TCD use
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
