Carotid Disease Flashcards

(33 cards)

1
Q

Carotid Circulation

A

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

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2
Q

Describe normal aortic arch

A
  • 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
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3
Q

Describe blood supply to the upper body

A

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)

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4
Q

TIA or stroke?

A

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.

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5
Q

What are the two classifications of strokes?

A

Haemorrhagic stroke (15%) or ischaemic stroke (85%)

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6
Q

Haemorrhagic stroke

A

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)

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7
Q

Ischaemic stroke

A

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.

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8
Q

Risk Factors - stroke

A

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

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9
Q

Carotid disease symptoms (~20% of ischemic stroke)

A

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

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10
Q

Plaque Deposition

A

Majority of atherosclerotic disease is found at the carotid bifurcation, then intracranially and then vertebrals before arch. Temperaol window – MCA.

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11
Q

Carotid territory symptoms (anterior)

A

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)

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12
Q

Visual fields

A

Opposite sides of the brain receive visual information from the opposite hemifield

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13
Q

Vertebro-basilar symptoms (posterior

A

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

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14
Q

Why Ultrasound?

A

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]

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15
Q

NASCET Vs ECST

A
  • 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
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16
Q

Carotid endarterectomy and carotid stenting

A

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.

17
Q

Scanning Technique

A

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

18
Q

Scanning:

A

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

19
Q

ICA

A

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

20
Q

ECA

A

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

21
Q

Normal carotid waveforms

A

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!)

22
Q

What is temporal tap?

A

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.

23
Q

Vertebral Arteries

A

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

24
Q

Subclavian arteries

A

Supply upper limbs
R and L - different origins
Thoracic outlet syndrome
Subclavian Steal syndrome

25
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 1-2 cm 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
26
Plaque morphology
lipid, collagen, blood, thrombus, calcification – different echogenicity Surface characteristics - smooth, irregular, ulcerated Composition = ‘stability’ of a plaque = risk of embolization Treatment decisions
27
Limitations/Pitfalls
Deep or tortuous vessels, high bifurcations Short thick necks, obesity, beards Arrythmias Swallowing, coughing, senility, temperament Calcification Level of operator experience
28
Other Pathology
Dissection Aneurysm Carotid Body Tumour Inflammatory Arteritis Fibromuscular dysplasia Arterio-venous malformation Internal jugular vein thrombosis Lymphadenopathy Soft tissue mass
29
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
30
Inflammatory arteritis/ Takayasu's arteritis
Inflammation causing stenosis or occlusion of arteries
31
Intimal dissection
Intimal layer separating from medial
32
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
33
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