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Carotid Artery Disease

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Last updated: April 16, 2020
Revisions: 45

Last updated: April 16, 2020
Revisions: 45

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Carotid artery disease refers to the build-up of atherosclerotic plaque in one or both common and internal carotid arteries, resulting in stenosis or occlusion.

The majority of carotid artery disease is asymptomatic, but it is also responsible for approximately 10-15% of ischaemic strokes, due to plaque rupture and/or atheroembolism.

In this article, we shall look at the clinical features, investigations and management of a patient with carotid artery disease.

Fig 1 - Atherosclerotic plaque from a carotid endarterectomy specimen

Figure 1 – Atherosclerotic plaque from a carotid endarterectomy


The pathophysiology of carotid artery disease is as for atheroma elsewhere, starting with a fatty streak, accumulating a lipid core and formation of a fibrous cap. The turbulent flow at the bifurcation of the carotid artery predisposes to this process specifically at this region.

Carotid artery disease is usually classified radiologically by the degree of stenosis:

Degree of Stenosis

Diameter Reduction







Total Occlusion


Table 1 – Classification of degree of carotid stenosis depending on diameter reduction

Risk Factors

The major risk factors for carotid artery disease are age (≥65 years), smoking, hypertension, hypercholesterolaemia, obesity, diabetes mellitus, history of cardiovascular disease, and a family history of cardiovascular disease.

Clinical Features

Carotid artery disease will often be asymptomatic, however may present as a focal neurological deficit. This can take one of two forms:

  • Transient ischaemic attack (TIA) – lasts less than 24 hours before full resolution*
  • Stroke – lasts for more than 24 hours without full resolution

Much of the detailed initial assessment for a patient presenting with a stroke is typically beyond the scope of a vascular surgeon. The Oxford Stroke (Bamford) Classification provides a system to classify stroke symptoms in relation to the arterial regions involved (see Appendix).

On examination of the vascular system, a carotid bruit may be auscultated in the neck (however this is associated with carotid stenosis in less than half of cases).

Aside from the clinical features from stroke, carotid stenosis (even with complete occlusion) is likely to be asymptomatic if unilateral. This is due to collateral supply from the contralateral internal carotid artery and the vertebral arteries, via the Circle of Willis.

*This may include transient visual loss, termed amaurosis fugax

Figure 2 – Illustration demonstrating stenosis at the internal carotid

Differential Diagnoses

Atherosclerosis is the most common form of carotid artery disease. However, there can be other pathologies involved:

  • Carotid Dissection – Patients are often younger (<50yrs) and have an underlying connective tissue disease, with the event potentially precipitated by trauma or sudden neck movement
  • Thrombotic Occlusion of Carotid Artery – Thrombus can only be differentiated from atheromatous plaque on imaging and will present clinically as for atheroma
  • Fibromuscular Dysplasia – This is non-atheromatous stenotic angiopathy causing hypertrophy of the vessel wall, predominantly affecting young (<50yrs) females and, whilst most commonly in the renal arteries, the carotid arteries can be affected, presenting clinically with focal neurological deficit
  • Vasculitis – Various great vessel vasculitidies, such as Giant Cell Arteritis or Takayasu’s Arteritis, can cause carotid stenoses, however patients typically have systemic symptoms and other vessels may be affected

In addition, non-cerebrovascular conditions that manifest neurologically should be considered. These include hypoglycaemia, Todd’s paresis*, subdural haematoma, space-occupying lesion, venous sinus thrombosis, post-ictal state, and multiple sclerosis.

*Todd’s Paresis = Unilateral motor paralysis following a seizure


Initial Investigations

Any patient suspected of ischaemic (or haemorrhagic) stroke should have an urgent non-contrast CT head scan (Fig. 3), assessing for evidence of infarction potentially amenable to thrombolytic treatment.

Other investigations for a patient admitted with a stroke include:

  • Bloods, including FBC, U&Es, clotting, lipid profile, and glucose
  • ECG, especially to check for atrial fibrillation

If thrombectomy is considered in patients with evidence of ischaemia, imaging via CT head contrast angiography is also required

Figure 3 – CT head scan showing hyperdense artery sign in a patient with middle cerebral artery infarction

Follow-up Investigations

Once a diagnosis of ischaemic stroke or TIA is made, it is important to screen the carotid arteries for disease precipitating the presentation. This can be done initially with Duplex ultrasound scans*, which gives a good estimate as to the degree of stenosis, as well as excluding any other possible differentials.

Lesions within the carotid artery may then be further characterised via CT angiography, which gives a more accurate assessment of the diseased portion of the vessels prior to any potential surgery.


Acute Management

All patients admitted with a suspected stroke should be started on high flow oxygen and blood glucose optimised (target 4-11mmol); a swallowing screen assessment should also be made on admission.

Initial management depends on the nature of the stroke:

  • Ischaemic stroke –  IV alteplase (r-tPA), if patients are admitted within 4.5hrs of symptom onset and meet inclusion criteria, and 300mg aspirin (orally, or rectal if dysphasic)
  • Haemorrhagic stroke – correction of any coagulopathy and referral to neurosurgery (for potential clot evacuation*)

Thrombectomy is indicated in patients with confirmed acute ischaemic stroke and confirmed occlusion of the proximal anterior circulation on angiography, as well as consideration for intravenous thrombolysis too.

*Neurosurgery is often not advised for a haemorrhagic stroke, unless superficial lobar bleed or ventricular bleed, yet this will be at the neurosurgeon’s discretion

Long Term Management

All patients with a known stroke or TIA should also be started on cardiovascular risk factor management:

  • Anti-platelet therapy long term, typically aspirin 300mg OD for two weeks, then clopidogrel 75mg OD
    • If not tolerated, trial combination therapy aspirin and dipyradimole
  • Statin therapy, ideally high-dose atorvastatin (started after the hyperacute phase)
  • Aggressive management of hypertension and/or diabetes mellitus
  • Smoking cessation
  • Regular cardiovascular exercise and active lifestyle with weight loss

A referral to the Speech and Language Therapy (SALT) team is advised for any dysphagia or dysphasia. Physiotherapy and Occupational Therapy input is advised for any ongoing mobility issues, with many stroke patients requiring rehabilitation.

Carotid Endarterectomy

All patients with an acute non-disabling stroke (or transient ischaemic attack) who have symptomatic carotid stenosis between 50 – 99% should be referred for assessment for a carotid endarterectomy (CEA)*

CEA involves removing the atheroma and associated damaged intima (Fig. 4), thereby reducing the risk of future strokes or TIAs. The main risks of CEA surgery are stroke (2-3%), nerve damage to the hypoglossal, glossopharngeal, or vagus nerve, myocardial infarctions, local bleeding, and infection.

*CEAs are now seen as a superior option to carotid stenting, with the latter associated with an increased risk of long-term major adverse events

Figure 4 – The carotid endarterectomy procedure


Mortality of a stroke is 12% at 7 days and 19% at 30 days.

The most significant improvement from rehabilitation occurs between 4-6 weeks, yet 50% of survivors will remain dependent at 1 year. This is significantly less in patients that are fit for carotid endarterectomy, however this is a preselected cohort, and those with a high mortality post-stroke will not be candidates for CEA.

Other complications of a stroke include dysphagia, seizures, ongoing spasticity, bladder or bowel incontinence, and depression, anxiety, or cognitive decline.

Key Points

  • Most cases of carotid artery stenosis are asymptomatic, however the major sequela of the condition is ischaemic stroke
  • First line investigation is via carotid US Doppler, with confirmed cases being further assessed with CT angiography
  • Selected cases will be offered carotid endartectomy (CEA) for risk reduction management of ischaemic stroke

Appendix – The Oxford Stroke Classification

Classification Description Signs and Symptoms
Total Anterior Circulation Stroke (TACS) (20%) Large cortical stroke in middle or anterior cerebral artery areas Must have all of:
  • Motor weakness or sensory deficit of ≥2/3 areas (face, arm, leg)
  • Homonymous hemianopia
  • High cortical dysfunction (dysphasia, dyspraxia, or neglect)
Partial Anterior Circulation Stroke (PACS) (35%) Cortical stroke in middle or anterior cerebral artery areas Will present with either:
  • 2/3 TACS criteria
  • Limited motor or sensory deficit (1 of leg, arm or face)
  • High cortical dysfunction alone
Lacunar Stroke (LACS) (20%) Occlusion of the deep penetrating arteries Will present with any of:
  • Pure motor ≥2/3 areas (face, arm, leg)
  • Pure sensory ≥2/3 areas (face, arm, leg)
  • Pure sensorimotor ≥2/3 areas (face, arm, leg)
  • Ataxic hemiparesis
Posterior Circulation Stroke (POCS) (25%) Occlusion of vertebrobasilar or PCA circulation, affecting brainstem, cerebellum, or occipital lobe Variety of presentations can occur, typically:
  • Ipsilateral CN palsy with contralateral motor or sensory defects
  • Bilateral motor or sensory deficits
  • Isolated homonymous hemianopia
  • Cerebellar dysfunction