Cerebrovascular Disease Flashcards
Contraindications to TPA in ischemic stroke
Multiple randomized controlled trials have supported the safety and efficacy of intravenous alteplase (0.9 mg/kg; maximum dose of 90 mg) for confirmed ischemic strokes of less than 3 hours duration.
Contraindications
- Age older than 80 years and a history of diabetes are contraindications for patients with a history of ischemic stroke of 3 to 4.5 hours duration
- Concurrent intravenous abciximab administration
- blood pressure of 185/110 mm Hg or higher
- intracranial hemorrhage on CTA
- a history of stroke, severe head trauma, or intracerebral or intraspinal surgery within 3 months
- gastrointestinal bleeding within 21 days
- concurrent usage of low-molecular weight heparin/thrombin or factor Xa inhibitors
Indications for treating carotid dissection
Indications for surgical or endovascular repair of traumatic carotid dissection
- is fluctuating or deteriorating neurologic symptoms despite optimal medical management
- a contraindication for antithrombotic therapy
- or symptomatic/expanding carotid aneurysm
Carotid Body tumors: % sporadic vs hereditary
Carotid body tumors (CBT) are sporadic in 75% of cases; however, 25% are associated with familial history and/or underlying germline mutations.
When to get genetic testing for carotid body tumors
Genetic testing is recommended in all patients with multi-focal tumors, CBT associated with paraganglioma, CBT associated with pheochromocytoma and or a positive family history.
Carotid Body Tumors are associated with what gene?
The succinate dehydrogenase complex subunit D (SDHD) gene is the most common gene associated with familial paraganglioma. This autosomal dominant, highly penetrant mutation involves the genes encoding 3 subunits of the mitochondrial complex II (succinate dehydrogenase), a component of the Kreb cycle metabolic pathway. These hypoxia-related pathways can be activated by chronic hypoxia (e.g., living at high altitude), leading to increased neural crest call proliferation with decreased apoptosis. Patients with familial CBT tend to be younger (mean age 35 years), have bilateral involvement, and may have associated pheochromocytoma and/or other paraganglioma
Management of acute stent thrmbosis during transfemoral or TCAR procedure
Acute thrombosis of the ICA during carotid stenting is a devastating complication with insufficient data to provide level 1 recommendations. The most recent consensus documents and observational data suggest that the most appropriate first step in this patient who is acutely neurologically decompensated is to attempt to disaggregate the platelet plug and thrombus with administration of intra-arterial abciximab and thrombolytic therapy directly into the ipsilateral carotid artery. Endovascular salvage attempts may ensue, including suction thrombectomy, repeat stenting, and balloon angioplasty. While conversion to CEA may ultimately be required, immediate conversion may also be too time-consuming and physiologically stressful for the patient.
What is cerebral hyperperfusion and how is ot managed?
Cerebral hyperperfusion is an uncommon but potentially life-threatening complication following carotid revascularization, particularly in patients undergoing revascularization (carotid stenting) opposite of severe stenosis or contralateral occlusion.
Characterized by severe hypertension and unilateral migraine-like headache, if left untreated symptoms can progress to seizures and intracerebral hemorrhage, which is associated with mortality rates as high as 75% to 100%. There is no role for heparin in cerebral hyperperfusion syndrome, given the risk of intracerebral hemorrhage. As this clinical scenario is associated with cerebral edema and likely results from dysfunction of the cerebral autoregulation, the primary goal is to strictly control the blood pressure in the postoperative period, using vasodilators such as sodium nitroprusside, nicardipine, nitroglycerin, and others. Most clinicians attempt to maintain the blood pressure to within 20 mm Hg of the preoperative level.
What is the ischemic penumbra?
The ischemic penumbra is the zone of viable, but injured, tissue surrounding an infarct
Segments of the vertebral artery
The vertebral artery is typically divided into 4 segments:
V1 (preforaminal): origin to the transverse foramen of C6;
V2 (foraminal): from the transverse foramen of C6 to the transverse foramen of C2/
V3 (atlantic, extradural or extraspinal): from C2 to the dura/
V4 (intradural or intracranial): from the dura to their confluence to form the basilar artery.
Signs of posterior circulation stroke
Posterior circulation strokes may present with symptoms such as balance disturbances, vertigo, nausea/vomiting, blurred vision or diplopia/oculomotor dysfunction, facial numbness, altered consciousness, or dysarthria. Lymphocele may occur due
Shamblin Classification
The anatomic extent of the carotid body tumor described is consistent with a Shamblin III. The Shamblin classification of carotid body tumors describes the extent of the tumor and correlates with the difficulty of surgical resection and the probability of arterial reconstruction and cranial nerve injury. Class I tumors are localized and are generally resected with a very low probability of carotid artery reconstruction or nerve injury. Class II tumors are adherent to or partially circumscribe the carotid artery. Class III tumors encase the common, external, or internal carotid artery. Resections of large Class II tumors and Class III tumors have a higher probability of necessitating carotid resection and reconstruction and are associated with a higher probability of cranial nerve injury. Preoperative embolization of large Class II and Class III tumors should be considered, but is not mandatory. Proponents of preoperative embolization of carotid body tumors cite a lower blood loss after embolization. The idea that embolization may reduce the risk of cranial nerve injury has not be supported in multiple studies. If preoperative embolization is performed, surgical resection should ensure within 24-36 hours after embolization to minimize the peri-tumor inflammation that ensues after embolization.
What normal flow abnormality can be found in the carotid bulb?
Why?
Flow reversal
Related to diameter and angle of branch vessels
Which vessel has highest diastolic component on doppler? Highest pulsatility during systole and diastole and why?
ICA
ECA, due to reflect waves from branches
What are normal blood flow velocities in the ICA in >60yo? How does it changes in younger patients?
60-90cm/sec
higher likely due to increased CO
How much does blood flow change between mid CCA and CCA near bifurcation? Where should peak CCA systolic velocity be measured?
It increases by 10-20cm/sec
2-4cm below the bulb
What are normal flow velocities in the ECA?
80-115 cm/sec
What are normal peak systolic velocities in the ICA?
usually <100 cm/sec
What things can cause elevated flow velocities? (4)
Stenosis
kinking, coiling
elevated CO
technical error (transducer error)
What features distinguish ICA from ECA? (6)
ICA usually bigger
ICA branches rare
ICA proceeds deep and post towards mastoid (ECA anteriorly)
ICA low resistance
ECA, oscillations with temporal tap
ICA less color variation from diastole to systole (ECA flickers)
What is normal intima-media thickness formula?
(0.009 x age in years) + 0.116
What is usually considered abnormal intima-media thickness?
>0.9mm
What is the international classification for carotid plaque?
type I uniformly sonolucent (>90%)
type 2 predominantly sonolucent (>50%)
type 3 predominantly echogenic (>50%)
type 4 uniformly echogenic
type 5 unclassified (poor visualization)
What method of measuring stenosis did ECST use?
(residual lumen d - original lumen d)/ original lumen d *100%
What method of measuring stenosis did ACAS/NASCET use?
(residual lumen d - lumen d normal distal)/lumen d normal distal * 100%
What parameters can characterize ICA stenosis? (3)
peak systolic velocity
VICA/VCCA
end-diastolic velocity
What can cause unexpected readings of the PSV?
low CO
hypertension
tandem lesions
contra occlusion
tortuous vessel
What can alter readings of VICA/VCCA?
external or bulb disease
At what degree of stenosis do Doppler values begin to become abnormal?
50%
What is the Washington criteria?
normal ICA PSV 125 EDV 125 EDV >140
For the SRU consensus, what cutoff values are use for PSV and ratio in carotid stenosis?
50-69% PSV 125-230, EDV 40-100, ratio 2-4
>70% to near occlusion PSV >230, EDV >100, ratio >4
near occlusion high/low/undectec
What is the incidence of stroke for an occluded ICA compared to gen pop?
same
What is the incidence of stroke for a nearly occluded ICA?
11%/year
What are features of near occlusion on US?
distal ICA small beyond stenosis
ICA smaller then ECA
What is the issue with NASCET measurement of ICA stenosis?
because the distal ICA gets smaller in near occlusion the nascet method no longer applies.
What are features of carotid occlusion on doppler?
hypoechoic/anechoic region that occupies entire lumen
no spectral, color or power dopple in lumen
occluded vessel may not be identifiable
externalization of the CCA
What is CCA externalization?
when the CCA flow pattern resembles ECA when the ICA is occluded. may not occur if ECA is serving as a large collateral.
What features on doppler indicate siphon or distal ICA occlusion?
absent diastolic flow in ICA
What scenarios can eliminate diastolic flow in the ICA
distal lesion, increase ICP, ICA dissection
How should ICA with string sign be managed?
string signs are associated with diffuse stenosis and there may not be a lesion to endarterectomize. Ligation may be the best management if causing stroke/TIA.
What are issues with measuring CCA stenosis?
PSV is variable along the CCA
How to measure CCA stenosis?
doubling of PSV to indicat4ee moderate stenosis
quad for severe >70%
How to measure origin CCA stenosis?
difficult as not visualized
ipsi/contra ratio normal 0.7-1.3
parvus tardus waveform
turbulent flow
Stenosis of the innominate artery can cause symptoms related distributions?
anterior circulation (stroke/TIA)
posterior circulation (cerebellar, brainstem strokes, dizziness)
cerebral circulation
arm ischemia
What % of arch dissection include carotid arteries?
3-7%
What % of carotid dissection resolve spontaneously? suffer disabling neuro? fatal?
70%
25%
5%
What features does carotid dissection have on US?
long tapering stenosis
visible flap
occluded artery with no calcified lesion
duplication of the carotid color flow
What features do you need to report on when assessing a carotid dissection with US?
extent
patency
stenosis
flow direction in false lumen
What features are important to assess when examining a pseudoaneurysm with US
size and location
to and fro in the neck (confirm its a pseudoaneurysm)
length and d of neck
proportion of flow/thrombosis in pseudoaneurysm
What is the most common site for AV fistula?
femoral
What are clinical findings of AVF in carotid?
neck trauma
ecchymosis
palpable hematoma
palpable or audible thrill
dilated, hyperdynamic draining vein
What can be the consequence of large AVF?
high output cardiac failure
What are US features of AVF carotid?
turbulent, pulsatile flow in jugular vein
high velocity jet between the two structures
What size and location of carotid body tumor?
1-1.5cm in adventitia at carotid bifurcation
What are US features of carotid body tumors?
highly vascular
at bifurcation
can encase ECO or ICA
If stenosis in ICA what can happen to contra PSV?
they can be increased without stenosis. ratio better assessment
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
Cerebal ischemia during CEA can be seen on transcranial doppler as?
Detection of a greater than 50% drop in middle cerebral artery velocity using transcranial Doppler is 100% sensitive for detecting cerebral ischemia.
