Module 4 : Cerebrovascular Pathophysiology Flashcards
1
Q
14 risk factors for cerebrovascular pathology
A
- hypertension
- diabetes
- smoking
- obesity/diet
- dyslipidemia
- hypercholesterimia
- sex
- age
- patent foramen ovale
- physical inactivity
- genetic predisposition/ family history
- homocystinaemia
- cardiac disease
- previous TIA or stroke
2
Q
risk factors - hypertension
A
- physical force injuries
3
Q
risk factors - diabetes
A
- chronic systemic disease with vascular atherosclerosis occurring at an early age being a primary complication
4
Q
risk factors - smoking
A
- associated with irritation of the endothelial lining
5
Q
risk factors - obesity/diet
A
- high fat high cholesterol
6
Q
risk factors - dyslipidemia
A
- abnormal levels of plasma lipids closely associated with development of atherscerlosis
7
Q
risk factors - hyperscholesterolemia
A
- genetic defect in LDL receptors
8
Q
risk factors - sex
A
- male predominance
9
Q
risk factors - age
A
- time allows for build up of plaque
10
Q
risk factors - patent foramen ovale
A
- clot or particles in the blood traveling in the right side of the heart can cross the PFO, enter the left atrium and travel out of the heart and to the brain or into coronary artery
11
Q
risk factors - genetic predisposition/ family history
A
- stroke, cardiac disease, or diabetes
12
Q
risk factors - homocystinaemia
A
- increased homocysteine level in blood which is associated with an increased risk of strokes
13
Q
2 parts of the physical examination for cerebrovascular pathology
A
- carotid auscultation for a bruit
- bilateral blood pressures
14
Q
what is a carotid auscultation for a bruit
A
- indicates abnormal flow is present
- turbulent blood flow vibrates the vessel wall and creates a bruit
15
Q
when will a bruit might not be detected
A
- in the case of a severe stenosis due to significantly diminished flow
16
Q
what is a thrill
A
- the palpable bruit
17
Q
physical exam - bilateral blood pressure
A
- difference of > 20 mmmHG between the sides indicates a possible subclavian steal
18
Q
is hemispheric/ anterior flow lateralizing or non lateralization
A
- lateralizing
19
Q
is vertebrobasilar/ posterior flow lateralizing or non lateralizing
A
- non lateralizing
20
Q
what does lateralizing mean
A
- usually stays on one side of the body
21
Q
with anterior circulation are symptoms contralateral or ipsilateral to diseased artery and why
A
- anterior circulation from the ICA supplies flow to the cerebral hemispheres and because body is often not always controlled by contralateral hemispheres
- symptoms are contralateral to the diseased artery
22
Q
what is an important exception to anterior circulation symptoms being on the contralateral side of diseased artery
A
- unilateral vision symptoms from ipsilateral side
- because of ophthalmic artery
23
Q
5 hemispheric / anterior circulation disease signs and symptoms
A
- hemiparesis/ hemiplegia
- paresthesia
- aphasia/dysphasia
- amaurosis fugax
- homonomous hemianopsia
24
Q
hemiparesis/ hemiplegia
A
- weakness or complete loss of function to one limb or one side of body
25
paresthesia
- tingling , numb, or burning sensation
26
aphasia/dysphasia
- inability to speak or comprehend language (ALWAYS LEFT)
| - speech is controlled by the left
27
amaurosis fugax
- aka transient monocular blindness
- often beginning as a black curtain coming over one (if vascular) eye vertically and sometime stopping
- ipsilateral symptom if vascular
28
homonomous hemianopsia
- blindness or visual defect in half of the field of vision in both eyes
- occurs because the right brain has visual control for the left side of both eyes and the left has visual control of the right side of both eyes
29
unilateral visual disturbances are what type of symptoms
- ipsilateral
30
bilateral visual disturbances are caused from disease of what circulation
- can be anterior or posterior
31
8 signs and symptoms of vertebrobasilar/ posterior circulation disease
- diplopia
- ataxia
- bilateral visual blurring
- drop attacks
- dysphagia
- motor/sensory disturbances
- vertigo
- subclavian steal syndrome
32
diplopia
- double vision (occipital lobe)
33
ataxia
- lack of muscle coordination which can affect walking, swallowing, eye movements, speech
34
drop attacks
- sudden fall while walking or standing that is recovered from quickly
35
dysphagia
- difficulty swallowing
36
motor/sensory disturbances
- unilateral, bilateral, or alternating
37
vertigo
- spinning or sensation that your surrounding are moving around you
38
signs and symptoms of subclavian steal
- supraclavicular bruit
- arm weakness
- decreased arm pulses
- arm pressures that are discrepant by more than 20mmHg
- usually asymptomatic
39
5 non localizing signs and symptoms
- dizziness
- syncope
+ transient loss os consciousness
- dysarthria
+ abnormal speech or difficulty with speech
- headache
- confusion
40
5 classifcations of neurological deficits
- asymptomatic
- transient ischemic attacks
- resolving/reversing/ ischemic neurological deficits
- cerebrovascular accident
- vertebrobasilar insufficiency
41
asymptomatic classification of neurological deficits
- patients present with no cerebral and retinal symptoms of vascular disease
- AUSCULTATION OF A BRUIT is most common indication for a duplex ultrasound in these patients
42
transient ischemic attack TIA class of neurological deficits
- brief episode of neurological symptoms in which cell death does not occur
- lasts 1-30minutes
- neurologic deficit last less than 24 hours an consistent with ischemia is TIA
43
resolving/reversing ischemic neurological deficit RIND
- neurologic event with symptoms lasting longer than 24 hours to within 3 weeks and with no permanent neurological damage
44
cerebrovascular accident (CVA/stroke) class of neurological deficit
- results from a loss of blood supply that has left some permanent brain damage and subsequent loss of motor, sensory or cerebral function
- may be further classified
45
what further 3 classification can be apart of cerebrovascular accident
- acute sudden onset
- unstable in evolution, symptoms come and go
- completed, no progression or resolution stable
46
vertebrobasilar insufficiency (VBI) class of neurological defect
- causes BILATERAL symptoms of visual blurring, vertigo, ataxia, and drop attacks
47
2 mechanisms of disease
- thrombosis
| - emboli
48
what is thrombosis
- formation of a blood clot over the plaque site which further decreased the lumen and contributes to ischemia or infarction
49
what is emboli
- thrombus may. break off and become and embolus
| - travels to areas downstream that are too narrow for it to pass causing ischemia and infarction
50
what is arteriosclerosis
- hardening of arteries
- directly related to age resulting in degenerative changes of the arteries that include loss of elasticity and a thickening of the intima over time
51
what is atherosclerosis
- form of arteriosclerosis
- refers to both hard and soft plaque beyond the intimal thickening of arteriosclerosis
- MOST COMMON arterial disease
- plaque builds in the arterial wall and limits or stops the blood flow by either narrowing the lumen or blocking the artery
52
What is considered to be a hemodynamically significant lesion
- a stenosis or occlusion resulting in decreased pressure or flow distal to the obstruction
- > 50% reduction in diameter
53
What tends to be the cause of atherosclerosis
- injury to the endothelial lining of the vessel wall
54
What are the 4 stages of development of atherosclerosis
- stage one = early atherosclerosis, injury
- stage two = inflammatory response
- stage three = atheromatous thickening - plaque formation
- stage four = advanced atherosclerosis - late changes
55
Stage one one of atherosclerosis
- injury could be due to a wide range of causes including
+ risk factors
+ vasculitis
+ hemodynamics stress
56
Stage 2 of atherosclerosis
- injury exposes areas of the intimacy layer allowing lipids from blood to enter leading to the fatty streak
57
Stage three of atherosclerosis
- platelets are deposited at the site and teh muscle cells become consumed with fat
- body’s attempt to repair results in teh formation of scar tissue or fibrosi leaving a tough fibrous cap overlying the soft fatty portion of the plaque
58
Stage 4 of atherosclerosis
- fibrous cap can be disturbed by hemorrhage calcification leading to further disruption of teh endothelial layer resulting in ulcerative plaque
- this type of plaque is unstable adn can release emboli into blood stream
- hemorrhage from the vast vasorum into the plaque causes ischemia leading to break down of fibrous cap and endothelium
59
Two different descriptions of plaque surface
- smooth
| - irregular
60
Smooth plaque surface
- continuous with no irregularities
61
Irregluar plaque surface
- plaque surface is discontinuous
| - ulceration is possible on these surfaces but the presence of ulcers cannot be confirmed by us
62
What is the echogenicity of plaque determine by and what 4 ways can it be described
- determined by composition of lipids, collagen, hemorrhage and calcification with the plaque
- anechoic, hypoechoic, hyperechoic, calcific
63
Anechoic plaque
- no echogenicity
| - contains lipid or intraplaque hemorrhage
64
Hypoechoic plaque
- low echogenicity
| - fibrofatty plaque
65
Hyperechoic plaque
- moderate echogenicity
- fibrous plaque
- shadowing may or may not be present
66
Calcific plaque
- highly reflective plaque with shadowing
67
What does an intraplaque hemorrhage look like
- hypoechoic regions with thin fibrous cap
| - egg shell pattern
68
normal Anterior circulation - is EDV always above the baseline and if not what are the exceptions
- not always above teh baseline
- ECA may have a short period of reversed flow at end systole
- flow reversal seen in bulb
- is ao regurge is present then long reversal in bilateral CCAs
69
Normal CCA flow
- moderate pulsatility as it supplies both high and low resistance vascular beds
- tall sharp and narrow peak
- little diastolic flow
70
Normal ECA flow
- moderate to high pulsatility as. It supplies a high resistance vascular bed
- tall shape narrow peak
- little or no diastolic flow
- possible reversal in early diastole
71
ICA normal flow
- low pulsatility and low resistance
| - broad systolic peak and forward flow throughout diastole
72
Velocity and pressure within and distal to stenosis
- velocity within the stenosis is increased with low pressure
- velocity increase is directly proportional to severity of lumen narrowing
- velocity distal to stenosis is low and pressure is high
73
In a critical stenosis what happens to the pressure and velocity
- both flow velocity and pressure is reduced
74
Where do most carotid stenosis occur
- in first 1-2cm of ICA
| - less common at prox CCA
75
What 7 factors affect stenosis velocity
- length and diameter do narrowed segments
- endothelial surface roughness
- edge ireegularity of narrowing
- flow rate
- physiologic (BP,cardiac output, peripheral resisitance)
- collateral circulation present
- normal vessel anatomy
76
What is physical factor is color Doppler imaging limited by in the carotid exam
- vessel tortuosity and shadowing from calcified plaque
77
What 6 things should you asses for each carotid exam
- CCA fro inflow/outflow obstruction and compare sides
- categorize adn image ICA disease by referring to teh criteria (ICCA/CCA ratio)
- ECA for stenosis
- vertebrals for flow direction adn possible obstruction
- SCA fro obstruction
- other pathology
- do on other side
78
Peak systolic velocity - carotid stenosis
- most important parameter but not on its own
- critical to search lumen for highest velocity
- significant ctenosis has a high pitched hissing sound
79
Carotid stenosis - end diastolic velocity
- < 50% diameter reduction = EDV remains within normal range
- > 50% reduction = increase in end diastolic velocity
- > 70% reduction = rapid rise in diastolic velocity
80
What is teh systolic velocity ratio
- comparison between with PSV in ICA / PSV in CCA
| - when CCA or Bulb have stenosis the ratio is invalid
81
NASCET and ACAS
- North American SYmptomatic Carotid Endarterectomy Trial = showed benefit from endarterectomy with > 70% diameter reduction
- Asymptomatic CArotid Atherosclerosis STudy = showed endarterectomy reduced stroke risk by 5.8% over 5yrs with >60% diameter reduction
82
How to measure stenosis (diameter reduction) for NASCET and ACAS
- measure normal lumen distal to a stenosis (D) measure diameter within stenosis (d)
- (1 - (d/D)) x 100
83
Area reduction formula
- A = area of total lumen
- a = area of stenotic lumen
- ((A-a) / A ) x 100
84
Characteristics of pre stenotic region (prox)
- increased pulsatility with severe stenosis
- waveform = sharp narrow systolic peak, low systolic velocity, little diastolic flow and reversal in early diastole
- thump sound heard
- staccatos waveform maybe
85
Characteristics of post stenotic region (immediately distal)
- flow stream spreads causing turbulence
- max disturbance within 1 cm
- turbulence disappears by 2cm
- laminar flow resumes at 3 cm
- turbulence can sometimes be only clue to stenosis present
86
Characteristics of post stenosic region (more distal)
- distal dampened waveform will be seen with severe stenosis
+ PSV lower than normal
+ systolic peak rounded
+ diastolic flow increased
- tardus parvus / pulsus parvus / pulsus tardus
87
Abnormal Doppler waveforms and velocity for CCA
- no abnormal velocity
- low to zero EDV may indicate distal CCA bif or prox ICA high grade stenosis
- hemodynamically significant stenosis will produce focal velocity increase and post stenotic turbulence
88
If >/= 30cm/sec difference noted between teh right and left CCA at multiple levels what 4 things should be considered
- proximal obstruction = prox CCA has slow upstroke adn lower velocity wave form
- vessel tortuosity = higher proximal CCA velocity
- tight distal CCA stenosis = prox CCA waveforms with quick upstroke but low velocity
- compensatory flow due to contralateral occclusion = CCA velocity much higher compared to opposite side
89
Abnormal flow and velocity in ICA
- PSV > 125 cm/s with spectral broadening
- EDV > 40 cm/s
- use the highest PSA and EDV from pre bulb CCA and first 3 cm of ICA for ICA/CCA ratio
- plaque location and characteristics should be described
- flow disturbances can be seen early postendarterectomy may disappear with remodeling
90
Abnormal flow and velocity in ECA
- high resistance branches are seen
| - PSA > 150-200 cm/s with plaque adn post stenotic turbulence = > 50% stenosis
91
ECA flow in presence of severe ICA stenosis/ occlusion
- low resist cafe flow pattern may be seen
| - result of ECA acting as collateral to supply the low resistance vessels of the brain
92
ECA flow with CCA occlusion
- ECA flow direction will often reverse in order to perfume the brain by means of supplying blood to ICA
93
What is a temporal tap
- way to help identify ECA
| - spectral trace should oscillate when you tap the superficial temporal artery
94
4 ways collateral flow changed with arterial occlusion near or distal to a stenosis
- increase velocity
- increased volume flow
- flow reversal
- decreased pulsatility
95
Three basic intracranial routes for collateral circulation
- larger inter-atrial connection through the circle of Willis
- intracranial - ectracranial anastomoses or pre-willisian anastomoses
- leptomeningeal
96
Larger inter-arterial connections through the circle of Willis - intercranial collateral
- provide pathways between the two carotids (side to side)
| - or between basilar and right or left carotid (posterior to anterior)
97
Intercranial-extracranial anastomoses or pre-willisian anastomoses - intercranial collaterals
- ECA to ICA (through ophthalmic artery)
- ECA (occipital) to vertebral (Atlantic)
- cervical branches of subclavian to vertebral/ occipital of ECA
- ECA branches across midline to pre orbital branches
98
Leptomeningeal - intercranial collaterals
- connect terminal cortical branches of main cerebral arteries across vascular border zones
- not major but can interfere with diagnosis if they become sufficiently developed
99
Extra cranial collateral flow - occluded vertebral
- enlargement of opposite vertebral
| - flow shunted to thryocervical branches
100
Extracranial collateral flow - large aortic branches occluded
- intercostal and internal mammary arteries to subclavian
101
Compensatory flow in CCAs
- when an occlusion or a very high grade stenosis exists on one side the opposite carotid artery may be supplying both sides of the brain
+ results in increased flow within the CCA ECA and ICA of compensating side
102
Can compensatory falsely increase the grade of stenosis based on absolute values alone
- yes
| - due to incoming velocities increased from compensatory flow state
103
What are the 4 characteristics that identify when a stenosis appears higher due to compensatory flow that need to be addressed
- ICA/CCA ratio is in a lower category than the velocity criteria
- image measurement is in a lower category than the velocity flow
- PSV is generally higher throughout the CCA and is higher than the contralateral side
- interpretation should induce which velocities may be falsely elevated and explained that compensatory flow is likely factor
104
Characteristic of pre-occlusive stenosis / trickle flow
- when stenosis is so sever that the blood trickles through the residual lumen
- when occlusion is bein considered one MUST set system controls for low flow
+ low wall filter
+ low PRF
+ increase color gain
+ increase sample size
+ power Doppler
105
What is a total occlusion
- occlusion is present when no flow is detected by color or spectral Doppler with appropriate settings
106
Characteristics of total occlusion
- lumen filled with plaque may be obscured by calcification
- color flow or Doppler should not be detected at all
- arterial vessel pulsation absent
- vessel = isoechoic or echogenic to surrounding tissue
- long standing occlusion = small vessel
- string sign on angiogram
- ECA may haves increased flow with a higher diastolic velocity than normal
- contralateral CCA may have compensatory increased flow
- ipsilateral CCA will have thump sound, decreased PSV and absent or reversed diastolic flow
107
Due occlusions happen more often in CCA or ICA
- ICA 10-1
108
9 things to confirm total occlusion
- decrease scale
- increase color and PW gain
- decease wall filter
- increase sample volume size but avoid ECA branches adn veins
- interrogate distal to bulb in sag with PW and color
- with ICA occlusions diastolic flow in CCA may be absent
- ICA may be filled with plaques adn motion observed with each pulse
- a downstream occlusion indicated by a staccato waveform
- intracranial ICA occlusion will demonstrate no end diastolic flow in distal ICA
109
3 indications for a posterior circulation interrogation
- suspected vertebral-basilar insufficiency (atherosclerotic stenosis, impingement)
- dissection
- subclavian steal
110
What is the primary cause of vertebral basilar insufficiency
- atherosclerosis
111
4 common sites of atherosclerosis in the posterior circulatory system
- origin of vertebral artery at subclavian artery to its entrance into foramina at C6
- intercranial just beyond C1 arch
- transverse foramina plaque development
- intercranial segments of VA and BA
112
4 causes of posterior circulation ischemia
- emboli
- cardia dysrhythmia
- impingement from osteophytes
- artery to artery steal syndromes (subclavian)
113
What are three tests to help aid in the diagnosis of posterior circulation ischemia
- duplex ultrasound = limited
- angiography = definitive test
- magnetic resonance angiography MRA
114
Vertebral artery assessment
- assessed for normality occlusion and flow direction
- flow should be antegrade and low resistance
- vertebral Artery stenosis usually occur in prox portion
- hemodynamically significant stenosis = focal velocity increase, post stenotic turbulence, possible color bruit
- flow velocities can vary from side to side as one vertebral artery (left) usually dominant
- subclavian steal may be indicated by reversed flow in VA
115
Vertebral artery with occlusion
- with distal occlusion loss of end diastolic component
- vertebral occlusion is indicated by no flow detected in Pw and color along with well visualized artery below the vein
- pendulum (bunny ear) waveform indicate early sign of subclavian stenosis or presteal
+ seed on ipsilateral side of impending reversal
116
Normal subclavian artery characteristic
- triphasic or multiphasic in some labs
- velocities typically higher than teh carotid arteries but no precise number
- compare waveforms and brachial pressures for both sides
- with hemo significant stenosis = focal velocity increase, post stenotic turbulence, color bruit
117
What 4 things to determine when assessing subclavian artery
- plaque location and characteristic
- PSV and flow characteristics
- V2/V1 PSV where V2 = stenotic PSV and V1 = normal prox PSV
- any change in spectral waveform (trihasic to biphasic to monophaisc)
118
Normal subclavian artery characteristics
- no echoes seen within artery lumen
- color Doppler filled the entire lumen wall to wall
- normal waveform triphasic/ biphasic in older people
119
Abnormal subclavian artery characteristics
- echoes seen within artery and decreased lumen measured
- color Doppler does not fill entire arterial lumen
- post stenosis turbulence can cause color mosaic
- monophasic wave form distal to stenosis delayed rise time
120
Subclavian artery with hemo significant stenosis
- focal velocity increase (>/= double that of prox arterial segment)
- spectral waveform changes (tri/multi/bi to monophasic)
- post stenotic turbulence
- color aliasing
- potential color bruit
121
3 indirect signs of hemo significant stenosis in subclavian artery when prox velocity difficult to obtain
- increased velocities with lumen reduction and post stenoitc turbulence
- spectral waveform changes rom one segment to teh next
- compare the arterial waveform at the same site in the contralateral artery
122
3 indications for subclavian steal
- patients present with arterial arm pressures differing by >20mmHg between arms
- obtain a waveform on the ipsilateral vert arter to the arm with the lower BP and note direction of flow
- reversed flow in vert combined with significant difference in pressures in arm indicate subclavian steal
123
What 3 other additional interrogations may you do in case of subclavian steal
- PW to interrogate teh ipsilateral subclavian Artery to look for increased velocity or occlusion prox to vertebral origin
- identify vessel diameter reduction
- compare bilateral axillary waveforms
124
What is subclavian steal syndrome
- subclavian steal doesn’t always produce neurological defecitys or symptoms
- if there are then is is call subclavian steal syndrome/ phenomenon and is accompanied by reversal of basilar artery if sever
125
3 medical treatments for carotid artery disease
- modify risk factors (stop smoking, lower cholesterol, lose weight)
- tissue plasminogen activator = treats ischemia strike within 3 hours of onset of symptoms
- anticoagulants = warfarin, heparin
126
6 surgical treatment of carotid artery disease
- carotid endarterectomy
- ICA resection and re-anastomoses
- carotid thrombectomy
- bypass
- vertebral Artery transposition to CCA
- direct focal repairs
127
2 endovascular treatments of carotid artery disease
- carotid angioplasty
| - carotid stent
128
Duplex exam after a carotid endarterectomy
- first exam 30 days after procedure
| - exams done in first few days may show shadowing from air entrapment associated with a synthetic patch or graft
129
7 complications after carotid endarterectomy
- restenosis/occlusion
- residual plaque
- tissue flaps
- vessel narrowing
- neointimal hyperplasia
- hematoma
- endovascular leak
- pseudoanurysm
130
Restenosis/ occlusion after carotid endarterectomy
- myointimal hyperplasia can result in focal or diffuse narrowing at teh endarterectomy site and associates with increase flow velocity and post stenoitc flow disturbance within the firth 3 years
- primary atherosclerosis si usually case of later stenoissi
131
Tissue flaps post carotid endarterectomy
- can cause flow disturbances and may lead to re stenosis or thrombosis
- usually seen at teh distal end of the endarterectomy
132
Neointimal hyperplasia post carotid endarterectomy
- smooth muscle and fibrous overgrowth of the tissue layer that replaces the intima folowin carotid intervention
133
Normal duplex finding after carotid endarterectomy
- normal intimal-media stripe not identified
- sutures appear as bright reflectors in the anterior wall
- wall thinking develops but should be minimal unless associated with a lumen reduction adn increased PSV
- luminary or only slightly disturbed blood flow
134
5 complications to carotid stents
- poor initial stent development
- restenosis by hyperplasia
- progressive stenosis distal to stent due to atherosclerosis disease
- stent positional shift
- stent kinking
135
What to asses from a standard duplex exam after carotid stents
- prox native artery
- prox stant attachment
- prox,mid,dist stents
- distal attachment site
- native arty distal to stent (1cm)
136
Normal duplex finding for carotid stents
- smooth velocity increase into stent
- slight lumen narrowing may persist at teh ends of the stent
- laminar or only slightly disturbed blood flow with abrupt increased in velocity
- PSV are unpredictable
- compare PSV from exam to exam in teh exact same location with similar angle to flow
137
What is a carotid artery dissection
- tear in intimacy lining of an artery with or without involving the outer medial wall
- blood enters the media of teh vessel through the tear and creates a false lumen
- blood flow still moves through true lumen
- occurs due to trauma, medical complication or spontaneous
- blood through the tear can clot
- falls lumen may be blind ended or reconnect to distal origins
- may remain patent or occlusion
- expansion of false lumen can narrow true lumen and cause obstruction
138
Origin of ICA dissection
- starts in the first 2-4cm of ICA
139
CCA dissection origin
- CCA dissection may be an extension of aortic dissection or from blunt trauma
140
What can teh false lumen eventually become
- dilate into a pseudoaneurysm
141
10 risk factors for causing spontaneous dissection
- hypertension’s
- fibromusclar dysplasia
- mar fans syndrome
- ehlers Danlos syndrome
- cystic medical necrosis
- strenuous exercise
- rapid neck motion
- compression by spine or mandible
- seat belt injury
142
Ultrasound findings of carotid diessection
- intimal flutter with cardiac cycle
- duplicated lumen
- narrowed true lumen with thrombosis false lumen
- disturbed flow distal to dissection
143
How is a dissection treated and what other modalities are useful in diagnosis
- anticoagulation therapy
| - MRA and angiogram
144
What is fibromuscular dysplalsia (FMD)
- non atherosclerotic arterial disease
- multiple focal stenosis followed by widening in an arterial segment
- string of pearl appearance
- affects medium and larger arteries especially Renal artery and ICA
- >90% in women in mid section ICA
- involves 2-6cm segment of mid extracranial ICA
145
FMD on ultrasound
- series of tandem stenosis and dilation
- accompanied by moderate-significant increase in PSV
- extensive turbulence
- scan as far distal in ICA especially with bruits and no atherosclerotic disease in bulb
146
Symptoms and complication of FMD
- incidental finding or neurological incident
| - encroachment on lumen caused flow reduction, collection of thrombi, emboli, dissection adn rupture
147
Imaging and treatment for FMD
- ultrasoud, MRA, Angiogram
| - symptomatic patients may be dilation of Artery
148
What is a carotid body tumor CBT
- small cluster of chemoreceptors cells at splits of carotid bifurcation and is part of autonomic nervous system
- regulated O2 levels in atrial blood, CO2 adn hydrogen ions and can signal vasoconstriction
- CBT is a paraganglioma
- rare usually unilateral and benign
- more often in females at high altitudes s
- MOST TIMES ECA SUPPLIES BLOOD if large ICA, vert and thryocervical trunk can help
149
Ultrasound appearance any symptoms of CBT
- ovoid structure 5x3x2mm
- characteristic widening or bulging of bif
- palpable mass, headache, neck pain, hoarseness
150
Complications imaging and treatment of CBT
- compression of laryngeal nerve, or invasion of surrounding vessels
- Ultrasound to asses and follow small tumors , angio pre surgery
- surgical resection, embolization with angiography
151
Two types of extracranial aneurysms
- aneurysm
- pseudoaneurysm
- very rare
152
Pseudoaneurysm
- weakened wall increase risk post endarterectomy
- may occur at carotid bypass anastomitc site
- causes = infection, tension at anasatomosis, thin walled arteries suture deterioration, improper suture technique
153
Aneurysms
- causes = atherosclerosis(most common) , dissection, trauma, previous surger
- CCA most common, ICA , ECA
- usually fusiform and located at bif of CCA or prox ICA
154
Clinical features of extracranial aneurysms
- pulsatile mass, pain, dysphasia, hoarseness, neurgolical symptoms due to embolization of thrombus from aneurismal wall
155
Treatment or extracranial aneurysms
- surgical resection
| - endovascular therapy
156
Other imaging for extracranial aneurysms
- MRA, CT, angiogram
157
What is arteritis/vasculitis
- inflammation of arterial walls
- can cause carotid narrowing or weakened artery walks that may become aneurysmal or dissected
- causes not well known but genetic, infections and toxins suspected
- treated with steroid drugs
158
4 conditions that can lead to arteritis/vasculitis
- takayasus arteritis
- temporal arteritis “giant cell arteritis”
- polyarteritis
- buergers disease
159
What is a radiation injury
- causes injury to vasa vasorum and necrosis of the vessel wall
- endothelial cells that line the wall of arteries in teh irradiated field are susceptible
- lipid contain plaques can form in teh intima once teh wall is damaged
160
5 other tests to help aid in diagnose carotid pathology
- physical exam adn history
- Doppler Ultrasound
- computed tomography CT
- cerebral arteriography (angiography)
- MRA/MRI
