Carotid Artery Disease

Carotid artery disease refers to the build-up of atherosclerotic plaque in one or both common 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.

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.

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

Fig 1 – Atherosclerotic plaque from a carotid endarterectomy specimen.


Classification

Carotid disease is usually classified radiologically by the degree of occlusion:

Degree of Stenosis Diameter Reduction
Mild <50%
Moderate 50-69%
Severe 70-79%
Critical 80-99%
Total Occlusion 100%

Risk Factors

The major risk factors for carotid artery disease are:

  • Age (≥65 years)
  • Smoking
  • Hypertension
  • Hypercholesterolaemia
  • Obesity
  • Diabetes mellitus
  • History of cardiovascular disease
  • Family history of cardiovascular disease

Clinical Features

Carotid artery disease will typically 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. This may include transient visual loss, termed amaurosis fugax.
  • 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.

On examination, a carotid bruit may be auscultated in the neck. However, this is associated with carotid stenosis in less than half of cases.

Other than 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 and the vertebral arteries, via the Circle of Willis.

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 (dysphagia, 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.
  • 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 presentation can occur, typically:

  • Ipsilateral CN palsy with contralateral motor or sensory defects
  • Bilateral motor or sensory deficits
  • Isolated homonymous hemianopia
  • Cerebellar dysfunction

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. It predominantly affects young (<50yrs) females and is found most commonly in the renal arteries, yet the carotid arteries can also be affected and present clinically with focal neurological deficit.

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


Investigations

Initial Investigations

Any patient suspected of ischaemic (or haemorrhagic) stroke should have an urgent CT head scan to check for infarction potentially amenable to thrombolytic treatment.  Other investigations for a patient admitted with a stroke include:

  • Fig 2 - CT scan. Hyperdense artery sign in a patient with middle cerebral artery infarction.

    Fig 2 – CT scan. Hyperdense artery sign in a patient with middle cerebral artery infarction.

    Bloods, including FBC, U&Es, clotting, lipid profile, and glucose

  • ECG (checking for any potential source of clot)
  • CXR

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 fairly accurate results as to the degree of stenosis, as well as excluding any other possible differentials.

As this investigation is cheap, non-invasive and readily available, it is ideal for use in screening asymptomatic patients with risk factors or investigating symptomatic patients who may warrant prophylactic surgical intervention

Lesions within the carotid artery should then be further characterised with CT angiography (CTA) which gives a more accurate percentage stenosis and characterises the diseased portion of the vessels for potential surgery if the USS scan shows a greater than 50% stenosis.


Management

Acute Management

All patients admitted with a suspected stroke should be resuscitated appropriately. Patients should be started 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 the inclusion criteria. 300mg aspirin OD should be started as an inpatient for 14 days.
  • Haemorrhagic stroke – referral to neurosurgery (for potential clot evacuation*) and correction of any clotting disorders.

*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 modification:

  • Anti-platelet therapy long term, typically clopidogrel 75mg OD
    • If not tolerated, trial combination therapy aspirin and dipyradimole
  • Statin therapy
  • Aggressive management of any hypertension and/or diabetes
  • Advise smoking cessation
  • Regular cardiovascular exercise and active lifestyle

Patients presenting with asymptomatic artery stenosis ≥70% or symptomatic artery stenosis ≥50% should be referred for surgical revascularisation (see below). Timely referral is important, aiming for revascularisation within 2 weeks for patients with stabilised neurology and fit for surgical intervention.

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

The mainstay of surgical treatment for ischaemic stroke prevention is via a carotid endarterectomy (CEA). A CEA involves removing the atheroma and associated damaged intima, thereby reducing the risk of future strokes or TIAs.

A recent study noted that CEA was a superior option to carotid stenting, the latter option associated with an early and sustained approximately 55% increased hazard for long-term major adverse events.

The Carotid Endartectomy

Initially the artery is isolated and clamped, before an arteriotomy is created and often a temporary bypass shunt placed for the duration of the procedure. Shunting is especially important for any contralateral occlusive disease that may other cause minimal collateral blood supply to the brain.

The plaque and diseased intima are carefully dissected from within the artery, with careful attention not to create any free edge that could result in dissection. The arteriotomy is closed with a patch graft to prevent iatrogenic stenosis and reduce the risk of re-stenosis.

The main risks of CEA surgery are stroke (2%), nerve damage to the hypoglossal, glossopharngeal or vagus nerve, myocardial infarction, local bleeding, or infection.

Fig 3 - Carotid endarterectomy, the mainstay of surgical intervention in carotid artery disease.

Fig 3 – Carotid endarterectomy, the mainstay of surgical intervention in carotid artery disease.


Complications

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

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.

Further Reading

Management of asymptomatic internal carotid artery stenosis.
Beckman JA, JAMA

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