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Vascular Surgery > Chap 97 Carotid Disease > Flashcards

Chap 97 Carotid Disease Flashcards

1
Q

what are RF for stroke

A 
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
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2
Q

What is risk of stroke after TIA?
What is risk of recurrence after stroke?
What is risk of death after stroke?

A

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

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3
Q

What are high risk features on duplex for plaque rupture?

A

hypoechoic, heterogeneous

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4
Q

What are non atherosclerotic causes of stroke?

A 
Carotid kinking or coiling
Carotid aneurysm
Spontaneous/posttraumatic dissection
FMD
Radiation induced arteritis
Giant cell arteritis
Takayasu arteritis
Cardioarterial embolization
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5
Q

What are symptoms of stroke from hypo perfusion?

A

bright light amaurosis
lightheadedness or presyncopy with any preceding focal deficits
also bilat UE weakness, cognitive difficulties, decreased visual acuity

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6
Q

what is wallenbergs syndrome?

A

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
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7
Q

What is a hollenhorst plaque?

A

retinal infarct seen on fundoscopic exam suggest cholesterol emboli

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8
Q

What are the NNT for ICA stenosis of 70-99 for
2 weeks
2-4weeks
4-12 weeks?

A

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

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9
Q

What is sense and spec for US, CTA, MRA, contrast enhanced MRA for carotid lesions?

A

90, 85
75, 95
90, 85
95, 95

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10
Q

What is the gray-weale classification?

A 
duplex plaque characterization
Type 1 echolucent
type 2 predominantly echolucent
Type 3 predom echogenic
Type 4 echogenic
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11
Q

What were the results of NASCET for >70%?

A 
sympto patient >70%
2yr
BMT 26%  CEA 9%
5yr
BMT28%  CEA 13%
significant
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12
Q

What are the results for NASCET 50-69%?

A 
2yr
BMT 15%  CEA 9%
5yr
BMT282%  CEA 16%
significant
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13
Q

What were the results for ECST 80-99?

A

sympto 80-99 (60-99 by NASCET criteria)
3yr
BMT 20% CEA 7%

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14
Q

What were the results for ACAS

A

asympto >60%
5 yr
BMT 11% CEA 5%

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15
Q

What were the results for ACST?

A

Asympto stenosis >60%
5yr
BMT 12% CEA 6%

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16
Q

What are caveats to CEA in asympto patients?

A

should have life expectancy of 3-5yr
women no benefit
likely no benefit if high co-morbid burden

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17
Q

What is the evidence for CTO?

A

MA no diff, 2.4 vs 3.7

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18
Q

What is the risk of contra CTO?

A

increase peri-op risk of stroke for CEA

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19
Q

What is the risk of protamine use in CEA?

A

decreased in postop bleeding, hematoma

no difference in stroke

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20
Q

What is the risk of dextran use in CEA?

A

not associated with stroke periop

CI with cardiac dz

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21
Q

What is difference of GA, local or block in stroke death or MI for CEA?

A

all the same

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22
Q

Describe incision for CEA.

A

parallel to SCM

posterior to earlobe

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23
Q

What are different shunts for CEa?

What is the difference?

A

pruitt
Javid

pruitt less cerebral embolism but less physiologic flow

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24
Q

What were the results of Everest?

A

compared eversion to patch

no difference in restenosis 4 yr

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25
Q

What is the evidence for patch, no patch or eversion in CEA?

A

patch or eversion better then no patch

primary closure increase stroke and restenosis

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26
Q

What are the SVS recommendations for peri-op management of anti-plt for CAS?

A

plavix 3 days before and 1 month after

ASA indeffinitely

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27
Q

What are techniques to get surgical access to high ICA lesions.

A

division of digastric muscle
resection of styloid process
anterior subluxation of the mandible
verticle osteotomy

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28
Q

describe division of the digastric.

what are the relationships of the nerves to the muscle?

A

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

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29
Q

describe resection of the styli process

A

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

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30
Q

What is the difference b/w shunting and non-shunting?

What are different ways to protect the brain during CEA?

A

MA
no diff in routine shunting and routine non-shunting

SSEP
EEG
TCD
stump pressure
none completely accurate
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31
Q

What are the criteria for stump pressures?

A

<50mmhg then 50% neuro rate if not shunted vs 10% if shunt

poor PPV

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32
Q

What re criteria for shunting with EEG?

A

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

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33
Q

Is there a benefit to awake CEA?

A

shunt use 5-15%

lower rate of MI

34
Q

What are the risks of using vein patch?

A

rupture 0.5-4%
aneurysm 20%
GSV <3.5 mm prone to rupture

35
Q

What are RF for stroke with CAS?

A

Age >70
within 14d
angle ICA-CCA >60
lesion>10mm

36
Q

What situations are better suited for CAS?

A

tracheostomy
prior nerve palsy
high lesions
previous radiation

37
Q

What is a consequence of balloon and stent deployment in CAS?

A

bradycardia and hypotension

atropine 0.4-1mg

38
Q

What are the recommendations for filter devices?

What are different kind of filter devices?

A

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

39
Q

What is most common complication after CAS?

A

embolization

40
Q

Name RCT that compare CAS vs CEA

A

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

41
Q

What are the restenosis rates for CAS?

A

30% at 10yrs in CAVATAS vs 10% for CEA

42
Q

What feature should consider protection device during CAS?

A 
arch ulceration, 
exessive calcification, 
Bovine or type 3 arch
vessel ulceration, 
tortuosity, 
calcification, 
inflow stenosis, 
fresh thrombus, 
angulation, 
long lesion
incomplete circle of willis
43
Q

What is most common cause of death after CEA?

A

cardiac

44
Q

Name different nerves that can be injured in CEA and what their injury is.

A

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

45
Q

describe course of hypoglossal

A

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

46
Q

describe course of vagus

A

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

47
Q

Describe course of SLN

A

Originates from vagus near jugular foramen and passes obliquely to the laryns posterior to ECA and ICA

48
Q

describe course of marginal mandibular branch

A

Anterior border of parotid b/w platysma and deep cervical fasci

49
Q

What is cerebral hypo perfusion syndrome?

A

increased regional blood flow secondary to disordered intracerebral autoregulation and relief of high grade stenosis in setting of severe contra lesion

50
Q

What symptoms can occur with CHS?

A 
classic triad
ipsi H/A, seizure, focal neuro
HA frontal, pounding, face/eye pain
focal neuro--hemiplegia, aphasia, vomitting
ICH
51
Q

What are RF for CHS?

A 
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
52
Q

What are the branches of the ECA?

A

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
53
Q

What are causes of carotid aneurysm?

A 
at hero degeneration
trauma
dissection
local infection
FMD
after CEA
54
Q

What are symptoms of carotid aneurysm?

A 
pulsatile mass
tender or asympto
horners
hoarseness
facial pain
dysphagia
rupture
55
Q

What are different treatments for carotid aneurysm?

A 
ligation (neuro 50%)
can do balloon occlusion test frist
EC-IC bypass
reconstruction
stent
56
Q

What are outcomes to open vs endo for carotid aneurysm?

A

reconstruction stroke and mortality 10%
nerve dysfunction 20%

endo
lower stroke rate
death 2-4%
endoleaks 8%

57
Q

What is the carotid body?

What does it respond to?

A

neural crest cell derived chemoreceptor located in the medial portion of the carotid bifurcation

changes in O2, CO2, pH

58
Q

How common are carotid body tumours?

A

most common H&N paraganglioma

60% right side
4% malignant

59
Q

What are RF for CBT?

A 
hronic hypoxia
high altitudes, smoking, COPD
carney;s triad
von hippel lindau;s disease
NF-1
MEN type 2
60
Q

What is carney’s triad?

A

gastric stromal sarcoma, pulmonary chondroma, paraganglioma

61
Q

What are anatomical features of CBT?

A

splay the bifurcation
can encapsulate the adjacent arteries
most of it located deep to bifurcation

62
Q

What are microscopic features?

A

Granular epitheloid chief cells and sustentacular supporting cells
These cells form clusters called zellballen or cell balls
This grows into the tumor

63
Q

What is fontaines sign?

A

fixed vertically but mobile horizontally

64
Q

What other test should be done for CBT?

A

octreotide scan to rule out other paragangliomas. measures uptake of a somatostatin analogue

65
Q

What tx options for CBT?

A

embolization
stent
surgical

66
Q

What is the grading for CBT?

A

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

67
Q

What are other vascular tumours of the H&N?

A

glomus jugulare
glomus vagale
Schwannoma

68
Q

What is the carotid sinus?

A

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

69
Q

What is carotid sinus syndrome?

A

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

70
Q

What are RF for CSS?

A

elderly, vascular dz, HTN, CADm atherosclerosis, DM

71
Q

What are tx for CSS

A

PM
Divide nerve of hering
Strip carotid bulb or periadventitia to distance of 3cm from bifurc
93% symptoms free at 30d

72
Q

What are the SVS guidelines for intervention on carotid stenosis (6)?

A
  1. sympto angio >50% or duplex >70%
  2. asympto >80% consider if stroke risk CAS unless decamp CHF or scarring
  3. CAS>BMT if high risk for CEA
  4. intervention within 2 weeks
  5. BMT for CTO
73
Q

What are causes of carotid dissection?

A 
FMD
EDS
Cystic medial necrosis
Marfans
Autosomal dominant polycystic kidney disease
Osteogenesis imperfecta type I
74
Q

What vascular anomalies are implicated in carotid dissection?

A

Redundancy
Intracranial aneurysms
Aortic root dilation
Increased arterial distensibility

75
Q

What is the triad of cervical dissection?

A

Horners syndrome (21%)
Neck or head pain (70%)—ipsi frontotemporal
Cerebral ischemia 30%

76
Q

What causes hornets syndrome?

A

Sympathetic fibers involved in the dissection which run along the carotid
usually without anhidrosis

77
Q

What other symptoms of carotid dissection?

A 
Unilat weakness (55%)
May also get neck pain
Am fugax
Anisocoria
Pulsatile tinnitus
Cranial nerve palsy (CN IX-XII) particularly the hypoglossal
78
Q

What is natural hx of carotid dissection?

A

60% persistent neuro
50% luminal recovery
2% annual risk of recurrent stroke

79
Q

What is risk benefit of treatment?

A

ICH rate with AC is 0.5%, 0 without

But recurrent TIA 5% with anti plt alone whereas 0 with AC

80
Q

What are indications for treatment?

A

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

Vascular Surgery (53 decks)

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