Chap 97 Carotid Disease Flashcards
what are RF for stroke
Age >55 risk doubles Sex men >women Race blacks hispanice higher risk HTN lifetime risk if BP <120 is half Fam hx Afib Smoking DLP DM Diet Obesity Alcohol if heavy Renal insufficiency
What is risk of stroke after TIA?
What is risk of recurrence after stroke?
What is risk of death after stroke?
10% in 90d
2% at 7 days
4% at 30d
12% at 1 yr
29% at 5 yr
7% at 7d
14% at 30d
27% at 1 year
53% at 5 years
What are high risk features on duplex for plaque rupture?
hypoechoic, heterogeneous
What are non atherosclerotic causes of stroke?
Carotid kinking or coiling Carotid aneurysm Spontaneous/posttraumatic dissection FMD Radiation induced arteritis Giant cell arteritis Takayasu arteritis Cardioarterial embolization
What are symptoms of stroke from hypo perfusion?
bright light amaurosis
lightheadedness or presyncopy with any preceding focal deficits
also bilat UE weakness, cognitive difficulties, decreased visual acuity
what is wallenbergs syndrome?
intracranial vert artery lesion or PICA lesion
ipsi facial pain, numbness, sensory loss, ipsi clumsiness ipsi ptosis, meiosis contra loss of temp and sensation hoarsenss loss of balance BP lability
What is a hollenhorst plaque?
retinal infarct seen on fundoscopic exam suggest cholesterol emboli
What are the NNT for ICA stenosis of 70-99 for
2 weeks
2-4weeks
4-12 weeks?
NNT 3 to prevent 1 stroke at 5 yr
NNT 6 to prevent 1 stroke in 5 year
NNT 9 to prevent one stroke in 5 year
What is sense and spec for US, CTA, MRA, contrast enhanced MRA for carotid lesions?
90, 85
75, 95
90, 85
95, 95
What is the gray-weale classification?
duplex plaque characterization Type 1 echolucent type 2 predominantly echolucent Type 3 predom echogenic Type 4 echogenic
What were the results of NASCET for >70%?
sympto patient >70% 2yr BMT 26% CEA 9% 5yr BMT28% CEA 13% significant
What are the results for NASCET 50-69%?
2yr BMT 15% CEA 9% 5yr BMT282% CEA 16% significant
What were the results for ECST 80-99?
sympto 80-99 (60-99 by NASCET criteria)
3yr
BMT 20% CEA 7%
What were the results for ACAS
asympto >60%
5 yr
BMT 11% CEA 5%
What were the results for ACST?
Asympto stenosis >60%
5yr
BMT 12% CEA 6%
What are caveats to CEA in asympto patients?
should have life expectancy of 3-5yr
women no benefit
likely no benefit if high co-morbid burden
What is the evidence for CTO?
MA no diff, 2.4 vs 3.7
What is the risk of contra CTO?
increase peri-op risk of stroke for CEA
What is the risk of protamine use in CEA?
decreased in postop bleeding, hematoma
no difference in stroke
What is the risk of dextran use in CEA?
not associated with stroke periop
CI with cardiac dz
What is difference of GA, local or block in stroke death or MI for CEA?
all the same
Describe incision for CEA.
parallel to SCM
posterior to earlobe
What are different shunts for CEa?
What is the difference?
pruitt
Javid
pruitt less cerebral embolism but less physiologic flow
What were the results of Everest?
compared eversion to patch
no difference in restenosis 4 yr
What is the evidence for patch, no patch or eversion in CEA?
patch or eversion better then no patch
primary closure increase stroke and restenosis
What are the SVS recommendations for peri-op management of anti-plt for CAS?
plavix 3 days before and 1 month after
ASA indeffinitely
What are techniques to get surgical access to high ICA lesions.
division of digastric muscle
resection of styloid process
anterior subluxation of the mandible
verticle osteotomy
describe division of the digastric.
what are the relationships of the nerves to the muscle?
NT intubation
divide posterior belly of digastric
same course as hypoglossal but sits anterior so protect the nerve
spinal accessory nerve is in upper 1/3 of muscle
glosspahryngeal lies deep
describe resection of the styli process
After digastric divided, remove insertion of styloglossus, stylopharyngeus and stylohyoid
Identify occipital artery as it runs on inferior border of digastric and don’t injure
Resect process with rongeur
What is the difference b/w shunting and non-shunting?
What are different ways to protect the brain during CEA?
MA
no diff in routine shunting and routine non-shunting
SSEP EEG TCD stump pressure none completely accurate
What are the criteria for stump pressures?
<50mmhg then 50% neuro rate if not shunted vs 10% if shunt
poor PPV
What re criteria for shunting with EEG?
50% decrease in fast background activity
increase in delta wave activity
complete loss of reg signal
overly sensitive
stroke rate 10% in patient with abnormal reg who did not have shunts
Is there a benefit to awake CEA?
shunt use 5-15%
lower rate of MI
What are the risks of using vein patch?
rupture 0.5-4%
aneurysm 20%
GSV <3.5 mm prone to rupture
What are RF for stroke with CAS?
Age >70
within 14d
angle ICA-CCA >60
lesion>10mm
What situations are better suited for CAS?
tracheostomy
prior nerve palsy
high lesions
previous radiation
What is a consequence of balloon and stent deployment in CAS?
bradycardia and hypotension
atropine 0.4-1mg
What are the recommendations for filter devices?
What are different kind of filter devices?
SVS recommends use although evidence not robust
Distal occlusion devices
cross lesion, apply suction before removing. smaller diameter sheath
proximal occlusion devices
placement of two occlusion balloons CCA and ECA with flow reversal. large death size
distal fileters. cross lesion. small sheath size. ante grade flow
What is most common complication after CAS?
embolization
Name RCT that compare CAS vs CEA
SPACE stroke/death CAS 7% CEA 6.5% non-inf not reached
EVA-3S stroke/death
CAS10% CEA 4% stopped early
CREST
stroke/death/mi
CAS 6% CEA 3% periop
no diff of ipso stroke at 4 yrs
MA
CAS higher risk then CEA 30d stroke or death
CAS lower for MI
What are the restenosis rates for CAS?
30% at 10yrs in CAVATAS vs 10% for CEA
What feature should consider protection device during CAS?
arch ulceration, exessive calcification, Bovine or type 3 arch vessel ulceration, tortuosity, calcification, inflow stenosis, fresh thrombus, angulation, long lesion incomplete circle of willis
What is most common cause of death after CEA?
cardiac
Name different nerves that can be injured in CEA and what their injury is.
hypoglossal, ipsi tongue weakness and difficulty masticating
Vagus,
recurrent laryngeal, ipsi vocal cord–hoarseness and inefffective cough
superior laryngeal, voice fatiug and difficulty with voice modulation at high registers
facial nerve, marginal mandibular branch, drooping of ipso lower lip
Glosspharygeal, mild dysphagia, recurr aspiration
Spinal accessory, shoulder drop and pain, scapular winging, weak abd
greater auricular nerve, numbness of angle of mandible and lower part of ear lobe
transverse cervical nerves, anesthesia of anterior neck skin
ansa, innervates the hyoid muscles
describe course of hypoglossal
descend medial to ICA then courses lateral to ECA usually above bifurcation, may cross at bifurcation
if need to mobilize may need to divide tethering branches of the ECA
describe course of vagus
Usually posteoti to CCA can be variable
Can lie anterior
Recurrent laryngeal usually originates in mediastium
Can arise at level of bifurcation (nonrecurrent recurrent laryngeal) and enters larynx posterior to CCA
Describe course of SLN
Originates from vagus near jugular foramen and passes obliquely to the laryns posterior to ECA and ICA
describe course of marginal mandibular branch
Anterior border of parotid b/w platysma and deep cervical fasci
What is cerebral hypo perfusion syndrome?
increased regional blood flow secondary to disordered intracerebral autoregulation and relief of high grade stenosis in setting of severe contra lesion
What symptoms can occur with CHS?
classic triad ipsi H/A, seizure, focal neuro HA frontal, pounding, face/eye pain focal neuro--hemiplegia, aphasia, vomitting ICH
What are RF for CHS?
Longstanding hypertension –High-grade-stenosis –Poor collateral blood flow –Increased peak flow velocity –Contralateral carotid occlusion –Recent contralateral CEA –Intraoperative ischaemia distal carotid pressure <40mmhg
What are the branches of the ECA?
Some American Ladies Found Our Pyramids Most Satisfactory
S: superior thyroid artery A: ascending pharyngeal artery L: lingual artery F: facial artery O: occipital artery P: posterior auricular artery M: maxillary artery S: superficial temporal artery
What are causes of carotid aneurysm?
at hero degeneration trauma dissection local infection FMD after CEA
What are symptoms of carotid aneurysm?
pulsatile mass tender or asympto horners hoarseness facial pain dysphagia rupture
What are different treatments for carotid aneurysm?
ligation (neuro 50%) can do balloon occlusion test frist EC-IC bypass reconstruction stent
What are outcomes to open vs endo for carotid aneurysm?
reconstruction stroke and mortality 10%
nerve dysfunction 20%
endo
lower stroke rate
death 2-4%
endoleaks 8%
What is the carotid body?
What does it respond to?
neural crest cell derived chemoreceptor located in the medial portion of the carotid bifurcation
changes in O2, CO2, pH
How common are carotid body tumours?
most common H&N paraganglioma
60% right side
4% malignant
What are RF for CBT?
hronic hypoxia high altitudes, smoking, COPD carney;s triad von hippel lindau;s disease NF-1 MEN type 2
What is carney’s triad?
gastric stromal sarcoma, pulmonary chondroma, paraganglioma
What are anatomical features of CBT?
splay the bifurcation
can encapsulate the adjacent arteries
most of it located deep to bifurcation
What are microscopic features?
Granular epitheloid chief cells and sustentacular supporting cells
These cells form clusters called zellballen or cell balls
This grows into the tumor
What is fontaines sign?
fixed vertically but mobile horizontally
What other test should be done for CBT?
octreotide scan to rule out other paragangliomas. measures uptake of a somatostatin analogue
What tx options for CBT?
embolization
stent
surgical
What is the grading for CBT?
Type I tumor
Small lesion nested in the bifurcation
Type II larger, splay the bifurcation but to not encase
Type III large ancapsulate the int/ext arteries and often adhere to adjacent nerves
What are other vascular tumours of the H&N?
glomus jugulare
glomus vagale
Schwannoma
What is the carotid sinus?
Carotid sinus is a sensory branch (nerve of Hering) of the glossopharyngeal nerve that terminates in carotid bifurc in a baroreceptor complex
Response to stretch
Activation of parasympathetic and inhib of sympathetic
What is carotid sinus syndrome?
Sinus hypersensitivity, Severe light headedness, syncope or drop attacks
Diagnosed by reproducing the symptom with carotid massage
Excessive brady, hypotension, (50 reduction in SBP), combination
Movement can precipitate symptoms
What are RF for CSS?
elderly, vascular dz, HTN, CADm atherosclerosis, DM
What are tx for CSS
PM
Divide nerve of hering
Strip carotid bulb or periadventitia to distance of 3cm from bifurc
93% symptoms free at 30d
What are the SVS guidelines for intervention on carotid stenosis (6)?
- sympto angio >50% or duplex >70%
- asympto >80% consider if stroke risk CAS unless decamp CHF or scarring
- CAS>BMT if high risk for CEA
- intervention within 2 weeks
- BMT for CTO
What are causes of carotid dissection?
FMD EDS Cystic medial necrosis Marfans Autosomal dominant polycystic kidney disease Osteogenesis imperfecta type I
What vascular anomalies are implicated in carotid dissection?
Redundancy
Intracranial aneurysms
Aortic root dilation
Increased arterial distensibility
What is the triad of cervical dissection?
Horners syndrome (21%)
Neck or head pain (70%)—ipsi frontotemporal
Cerebral ischemia 30%
What causes hornets syndrome?
Sympathetic fibers involved in the dissection which run along the carotid
usually without anhidrosis
What other symptoms of carotid dissection?
Unilat weakness (55%) May also get neck pain Am fugax Anisocoria Pulsatile tinnitus Cranial nerve palsy (CN IX-XII) particularly the hypoglossal
What is natural hx of carotid dissection?
60% persistent neuro
50% luminal recovery
2% annual risk of recurrent stroke
What is risk benefit of treatment?
ICH rate with AC is 0.5%, 0 without
But recurrent TIA 5% with anti plt alone whereas 0 with AC
What are indications for treatment?
Fluctuating or deteriorating clinical neurological symptoms,
CI to AC,
expanding aneurysm
after 6 month medical therapy;
Persistent high grade stenosis,
or new/persisitnet aneurysm twice d of normal
