Carotid Disease Flashcards
Carotid Circulation
Brain – 2% bodyweight, 15% cardiac output, 20% oxygen
75% blood supply via ICAs/25% vertebro-basilar
Little circulatory reserve – vulnerable, 3-5mins brain damage
Most ischaemic strokes – athero-sclerotic disease
Carotid bifurcation – likely site of disease
Stability = Composition of plaque
Little circulatory reserve – as no glucose or oxygen stores so vulnerable to even short deprivation in normal conditions after 3-5minutes of loss of circulation then permanent brain damage occur
Describe normal aortic arch
- coronary arteries are the first minor branches off ascending aorta
- R brachiocephalic - R subclavian - R vertebral, R common carotid
- L common carotid
- L subclavian - L vertberal
- Descending
Describe blood supply to the upper body
R Subclavian - vertebral and common carotid (bifurcates)
External carotid - face, scalp, neck - has branches
Internal - brain, eyes - wider calibre than ECA, usually lateral
_ variants (in 20% they overlap, in 10% they are reversed)
TIA or stroke?
Transient ischaemic attack (TIA)
Symptoms last for less than 24 hours
Cerebrovascular accident (CVA) or Stroke
Symptoms last more than 24 hours and can be permanent
Recovered CVA- Symptoms last more than 24 hours but there is gradual recovery.
What are the two classifications of strokes?
Haemorrhagic stroke (15%) or ischaemic stroke (85%)
Haemorrhagic stroke
Bleed within or outside the brain
Intracerebral haemorrhage (bleeding inside the brain)
Subarachnoid haemorrhage (bleeding into the subarachnoid space that surrounds the brain)
Subdural haematoma (bleeding into the subdural space)
Epidural haematoma (bleeding into the space between the skull and the dura matter)
Ischaemic stroke
Blood supply to part of the brain is decreased leading to death of brain tissue
Thrombosis (local clot)
Embolism (Embolus/clot travelling from elsewhere in the body)
Systemic hypoperfusion (General decrease in blood supply)
Cerebral venous sinus thrombosis
Stroke in relation to the carotid territory is an ischemic stroke. Can be embolic or thrombotic.
Risk Factors - stroke
Hypertension
Hyperlipidaemia
Cigarette smoking
Diabetes
Family history of cerebrovascular disease
Obesity
Inactive life style
History of myocardial infarction
Exercise and weight control – more effective at preventing strokes than multiple pharmological interventtions
Carotid disease symptoms (~20% of ischemic stroke)
TIA - <24 hours, temporary neurological deficit
CVA - >24 hours, permanent neurological deficit
Carotid territory - forebrain, cerebral cortex
Paresis
Parasthesia
Amaurosis fugax
Retinal emboli
Speech problems - dysphasia
Vertebro-basilar territory - hind brain, cerebellum
Visual blurring
Dizziness/Vertigo
Ataxia
Motor/sensory changes
Memory problems
Confusion/behavioural changes
Plaque Deposition
Majority of atherosclerotic disease is found at the carotid bifurcation, then intracranially and then vertebrals before arch. Temperaol window – MCA.
Carotid territory symptoms (anterior)
Hemiparesis- Weakness in one side (unilateral) of body (Contralateral)
Monoparesis- Weakness in one limb (Contralateral)
Hemiplegia- Paralysis of one side of body (Contralateral)
Unilateral paraesthesia- Numbness, tickling, burning sensation down one side of body (Contralateral)
Amaurosis fugax- Curtain or shadow affecting all or part of field in one eye (Ipsilateral)
Retinal emboli – Blurry vision or partial/complete loss of vision (Ipsilateral)
Homonymous hemianopia- Loss of lateral field of vision in both eyes (Contralateral to field lost)
Receptive Dysphasia- Difficulty understanding verbal or written instructions (Contralateral to dominant hand)
Expressive Dysphasia- Difficulty executing speech or written word i.e. sentences come out jumbled (Contralateral to dominant hand)
Aphasia- Unable to comprehend verbal/written word and unable to speak or write (Contralateral to dominant hand)
Dysarthria- Mechanical problem with speech when associated with hemiparesis/paraesthesia (Contralateral)
Visual fields
Opposite sides of the brain receive visual information from the opposite hemifield
Vertebro-basilar symptoms (posterior
Bilateral visual disturbance
Hemiparesis (Bilateral)
Bilateral parasthesia
Dysarthria due to deficit in vocal chords/larynx/tongue
Vertigo/Syncope/Light-headedness
Blackouts
Ataxia (Altered walking gait)
Memory problems
Confusion
Behavioural changes
Why Ultrasound?
Non-invasive
Inexpensive
No known morbidity risks
No inpatient stay required
No ionizing radiation or contrast
BUT operator dependent!
Radiations – risk of malignancy, contract – allegy, renal damage and complications of intravenous complications
NICE guidelines: Everyone with TIA who after specialist assessment is considered as a candidate for carotid endarterectomy should have urgent carotid imaging.[2008, amended 2019]
Ensure that people with stable neurological symptoms from acute non-disabling stroke or TIA who have symptomatic carotid stenosis of 50%to99% according to the NASCET (North American
Symptomatic Carotid Endarterectomy Trial) criteria, or 70%to99% according to the ECST (European Carotid Surgery Trial) criteria:
are assessed and referred urgently for carotid endarterectomy to a service following current national standards (see theNHS England and NHS Improvement National Stroke Service Model)
receive best medical treatment (control of blood pressure, antiplatelet agents, cholesterol lowering through diet and drugs, lifestyle advice).[2008, amended 2019]
NASCET Vs ECST
- 2 methods of grading stenosis used in large carotid trials to see if endarterectomy reduces stroke risk in symptomatic patients
- NASCET better correlates with the haemodynamic and angiography, so proposed as standard method
Carotid endarterectomy and carotid stenting
Beneficial in symptomatic patients with >50% stenosis or in asymptomatic patients with >70% stenosis (NASCET)
Carotid Duplex performed for pre-op CABG patients and CEA can be performed at same time as CABG.
Scanning Technique
Supine
Head extended and 45 degrees
Cautious with cervical spondylosis
Change position/remove pillow
Examiner Positioning
Close to patient - just behind head of patient
All controls within easy reach
Hold probe at the crystal end - so fingers are near/in contact with skin. Allows subtle movements of the probe to be made more easily
Scanning:
Greyscale sweep
CCA - Usually largest in size
R and L - different origins
No collateral branches
Low resistance to blood flow – spectral waveform above the baseline throughout diastole
Abnormal waveforms can indicate proximal disease or cardiac pathology e.g. Aortic valve regurgitation
ICA - Lateral, larger
Supplies blood to the brain and eye
Comparatively superficial
No branches in extra-cranial section
Lowest resistance to blood flow
Larger diameter than ECA, less than CCA
PSV - 60-80cm/s
ECA - medial, side branches, smaller
Smallest of the three, with numerous extracranial branches
Supplies blood to face and scalp
High resistance to blood flow – little flow in diastole (if any)
Valuable source of collaterals if severe ICA disease
ICA
ICA - Lateral, larger
Supplies blood to the brain and eye
Comparatively superficial
No branches in extra-cranial section
Lowest resistance to blood flow
Larger diameter than ECA, less than CCA
PSV - 60-80cm/s
ECA
ECA - medial, side branches, smaller
Smallest of the three, with numerous extracranial branches
Supplies blood to face and scalp
High resistance to blood flow – little flow in diastole (if any)
Valuable source of collaterals if severe ICA disease
Normal carotid waveforms
CCA- Source of blood for ICA and ECA, Usually largest in size, Low resistance to blood flow – spectral waveform above the baseline throughout diastole
Peak systolic velocities approx 80cm/sec
ICA- Supplies blood to the brain and eye, Lowest resistance to blood flow – spectral waveform remains well above the baseline with lots of diastolic flow, Larger diameter than ECA, less than CCA, Peak systolic velocity normally approx 60-80 cm/sec
ECA- Smallest of the three, with numerous extracranial branches, Supplies blood to face and scalp, High resistance to blood flow – little flow in diastole (if any)
Valuable source of collaterals if severe ICA disease, (Temporal tap!)
What is temporal tap?
The temporal tap maneuver is used to identify the external carotid artery. By tapping gently on the patient’s superficial temporal artery while imaging the external carotid artery, the sonographer can observe waveform artifacts of the same frequency as the tapping.
Vertebral Arteries
Low resistance to blood flow Peak systolic velocity normally approx 40 cm/sec
Often asymmetrical
Cephalad flow direction
Valuable source of collateral flow in severe ICA disease
Subclavian arteries
Supply upper limbs
R and L - different origins
Thoracic outlet syndrome
Subclavian Steal syndrome
Carotid scanning process
Carotid duplex should be a bilateral scan and include a basic assessment of the vertebral arteries.
*All results and calculations to refer to the NASCET method of measurement
*The following four velocities to be measured and recorded:PSV and EDV in CCA 1-2cm below bifurcation
PSV and EDV in ICA at point of highest velocity, i.e. stenosis jet or ICA distal to bulb in the absence of significant disease
*All velocities to be measured at a Doppler angle of 45–60°, with proper correction/calibration applied using the angle correction cursor
ACCURATELY record
Highest peak systolic velocities in the CCA, ICA and proximal ECA
End diastolic velocities in the CCA and ICA
Track up the ICA as far as possible, recording velocities as appropriate
Use b-mode to assess plaque characteristics
Exercise caution in the case of suspected occlusion
Do not rely on velocity criteria alone - use greyscale, colourflow, power Doppler. Tortuosity/coiling/kinking could cause velocity increase
Plaque morphology
lipid, collagen, blood, thrombus, calcification – different echogenicity
Surface characteristics - smooth, irregular, ulcerated
Composition = ‘stability’ of a plaque = risk of embolization
Treatment decisions
Limitations/Pitfalls
Deep or tortuous vessels, high bifurcations
Short thick necks, obesity, beards
Arrythmias
Swallowing, coughing, senility, temperament
Calcification
Level of operator experience
Other Pathology
Dissection
Aneurysm
Carotid Body Tumour
Inflammatory Arteritis
Fibromuscular dysplasia
Arterio-venous malformation
Internal jugular vein thrombosis
Lymphadenopathy
Soft tissue mass
Carotid pseudoaneurysm
Usually caused by trauma, including surgery! Post-CEA/stab wounds
All three layers of the arterial wall are no longer intact
There may be thrombus present
The ‘hole’ in the artery may be large or very narrow. There may be a connecting channel from carotid to aneurysm chamber
Inflammatory arteritis/ Takayasu’s arteritis
Inflammation causing stenosis or occlusion of arteries
Intimal dissection
Intimal layer separating from medial
What if the Duplex is normal?
Patient has had a stroke, Duplex normal.
?Cardioembolism
Risk factors: AF, LV disfunction, tumors, prosthetic valves, endocarditis
ECG
Trans thoracic/ oesophageal echo.
?intra-cranial pathology – CTa/ MRa for all ?stroke patients
Treatment options for stenosed or occluded carotid arteries?
Endarterectomies
Patient under GA
Incision along blocked artery from behind ear to collar bone
Clamp off carotid artery
Open artery, place shunt or temporary bypass to keep blood flow to brain
Remove plaque between arterial walls
Sow patch onto artery to keep it patent - synthetic or made of own vein
Close incision with sutures, temporary drain left in wound
