Carotid artery dissection: Difference between revisions
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===Traumatic=== | ===Traumatic=== | ||
Carotid artery dissection is more commonly thought to be caused by trauma to the head and/or neck. The probable mechanism of injury for most internal carotid injuries is rapid deceleration, with resultant [[hyperextension]] and rotation of the neck, which stretches the [[internal carotid artery]] over the upper cervical vertebrae, producing an intimal tear<ref>TC Fabian, et al. Blunt Carotid Injury. Annals of Surgery. 1996; Vol. 223, No. 5: 513-52.</ref>. After such an injury, the patient may remain asymptomatic, have a hemispheric transient ischemic event, or suffer a stroke<ref>JH Matsuura, et al. Traumatic Carotid Artery Dissection and Pseudoaneurysm Treated With Endovascular Coils and Stent Journal of Endovascular Surgery. 1997; Vol. 4, No. 4, pp. 339–343.</ref>. | Carotid artery dissection is more commonly thought to be caused by trauma to the head and/or neck. The probable mechanism of injury for most internal carotid injuries is rapid deceleration, with resultant [[hyperextension]] and rotation of the neck, which stretches the [[internal carotid artery]] over the upper cervical vertebrae, producing an intimal tear<ref>TC Fabian, et al. Blunt Carotid Injury. Annals of Surgery. 1996; Vol. 223, No. 5: 513-52.</ref>. After such an injury, the patient may remain asymptomatic, have a hemispheric transient ischemic event, or suffer a [[stroke]]<ref>JH Matsuura, et al. Traumatic Carotid Artery Dissection and Pseudoaneurysm Treated With Endovascular Coils and Stent Journal of Endovascular Surgery. 1997; Vol. 4, No. 4, pp. 339–343.</ref>. | ||
==Epidemiology and Demographics== | ==Epidemiology and Demographics== | ||
Revision as of 00:00, 4 November 2012
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| DiseasesDB | 2145 |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Carotid artery dissection is a tear in the intima of the carotid artery wall causing separation of the wall layers. The carotid artery supplies blood to the head and brain. Carotid dissection is an important cause of stroke in young adults.
Pathophysiology
Arterial dissection of the carotid arteries occurs when a small tear in the innermost lining of the arterial wall forms. Blood can enter into the space between the inner and outer layers of the vessel, causing narrowing (stenosis) or complete occlusion. Extracranial dissection of internal carotid artery is more frequent than intracranial dissection. The stenosis that occurs in the early stages of arterial dissection is a dynamic process and some occlusions can return to stenosis very quickly[1]. When complete occlusion occurs, it may lead to ischemia. Often, even a complete occlusion is totally asymptomatic because collateral circulation in the head keeps the brain well perfused. However, when blood clots form and break off from the site of the tear, the clots travel through the blood to the brain and clog one or more of the arteries directly supplying the brain, resulting in an ischemic stroke, otherwise known as an infarct. Blood clots, or emboli, originating from the dissection are thought to be the cause of infarction in the majority of cases of stroke in the presence of carotid artery dissection. Cerebral infarction causes irreversible damage to the brain. In one study of patients with carotid artery dissection, 60% had infarcts documented on neuroimaging[2][1] .
Causes
The cause of internal carotid artery dissection can be broadly categorized into two classes: spontaneous or traumatic.
Spontaneous
Once considered uncommon, spontaneous carotid artery dissection is an increasingly recognized cause of stroke that preferentially affects the middle-aged[3].
Observational studies and case reports published since the early 1980s show that patients with spontaneous internal carotid artery dissection may also have hereditary connective tissue disorders. These include Marfan syndrome, vascular Ehlers-Danlos syndrome, autosomal dominant polycystic kidney disease, pseudoxanthoma elasticum, fibromuscular dysplasia, and osteogenesis imperfecta type I. Nevertheless, although an association exists with connective tissue disorders does exist, most people with spontaneous arterial dissections do not have associated connective tissue disorders.
Traumatic
Carotid artery dissection is more commonly thought to be caused by trauma to the head and/or neck. The probable mechanism of injury for most internal carotid injuries is rapid deceleration, with resultant hyperextension and rotation of the neck, which stretches the internal carotid artery over the upper cervical vertebrae, producing an intimal tear[4]. After such an injury, the patient may remain asymptomatic, have a hemispheric transient ischemic event, or suffer a stroke[5].
Epidemiology and Demographics
- The incidence of spontaneous carotid artery dissection is low, and incidence rates for internal carotid artery dissection have been reported to be 2.6 to 2.9 per 100,000[6].
- Prevalence of hereditary connective tissue diseases in people with spontaneous dissections is highly variable, ranging from 0% to 0.6% in one study to 5% to 18% in another study.
- An estimated 0.67% of patients admitted to the hospital after motor vehicle accidents were found to have blunt carotid injury, including intimal dissections, pseudoaneurysms, thromboses, or fistulas[7]. Of these, 76% had intimal dissections, pseudoaneurysms, or a combination of the two.
Complications
Diagnosis
Symptoms
Common symptoms of carotid artery dissection include:
- Headache
- Tinnitus
- Neck pain
- Horner syndrome
- Transient loss of vision
Physical Examination
Eyes
Treatment
The goal of treatment is to prevent the development or continuation of neurologic deficits. Treatments include observation, anticoagulation, stent implantation and carotid artery ligation.
2011 ASA/ACCF/AHA/AANN/AANS/ACR/ASNR/CNS/SAIP/SCAI/SIR/SNIS/SVM/SVS: Guideline on the Management of Patients With Extracranial Carotid and Vertebral Artery Disease (DO NOT EDIT)[8]
Management of Patients with Cervical Artery Dissection (DO NOT EDIT)[8]
| Class I |
| "1. Contrast-enhanced CTA, MRA, and catheter-based contrast angiography are useful for diagnosis of cervical artery dissection. (Level of Evidence: C) " |
| Class IIa |
| "1. Antithrombotic treatment with either an anticoagulant (heparin, low-molecular-weight heparin, or warfarin) or a platelet inhibitor (aspirin, clopidogrel, or the combination of extended-release dipyridamole plus aspirin) for at least 3 to 6 months is reasonable for patients with extracranial carotid or vertebral arterial dissection associated with ischemic stroke or TIA. (Level of Evidence: B) " |
| Class IIb |
| "1. Carotid angioplasty and stenting might be considered when ischemic neurological symptoms have not responded to antithrombotic therapy after acute carotid dissection. (Level of Evidence: C) " |
| "2. The safety and effectiveness of pharmacological therapy with a beta-adrenergic antagonist, angiotensin inhibitor, or nondihydropyridine calcium channel antagonist (verapamil or diltiazem) to lower blood pressure to the normal range and reduce arterial wall stress are not well established. (Level of Evidence: C) " |
Related Chapters
References
- ↑ 1.0 1.1 Lucas, C; Moulin, T; Deplanque, D; Tatu, L; Chavot, D (1998). "Stroke patterns of internal carotid artery dissection in 40 patients". Stroke. 29 (12): 2646–2648. doi:10.1161/01.STR.29.12.2646. PMID 9836779. Unknown parameter
|author-separator=ignored (help) - ↑ VH Lee, et al. Incidence and outcome of cervical dissection; a population-based study. Neurology 2006;67:1809-1812.
- ↑ In: Neurology 2006;67:1809-1812. Mokri B. Spontaneous dissections of internal carotid arteries. Neurologist 1997;3:104–119.
- ↑ TC Fabian, et al. Blunt Carotid Injury. Annals of Surgery. 1996; Vol. 223, No. 5: 513-52.
- ↑ JH Matsuura, et al. Traumatic Carotid Artery Dissection and Pseudoaneurysm Treated With Endovascular Coils and Stent Journal of Endovascular Surgery. 1997; Vol. 4, No. 4, pp. 339–343.
- ↑ VH Lee, et al. Incidence and outcome of cervical dissection; a population-based study. Neurology 2006;67:1809-1812.
- ↑ TC Fabian, et al. Blunt Carotid Injury. Annals of Surgery. 1996; Vol. 223, No. 5: 513-52.
- ↑ 8.0 8.1 Brott TG, Halperin JL, Abbara S, Bacharach JM, Barr JD, Bush RL; et al. (2011). "2011 ASA/ACCF/AHA/AANN/AANS/ACR/ASNR/CNS/SAIP/SCAI/SIR/SNIS/SVM/SVS guideline on the management of patients with extracranial carotid and vertebral artery disease: executive summary. A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, and the American Stroke Association, American Association of Neuroscience Nurses, American Association of Neurological Surgeons, American College of Radiology, American Society of Neuroradiology, Congress of Neurological Surgeons, Society of Atherosclerosis Imaging and Prevention, Society for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Society of NeuroInterventional Surgery, Society for Vascular Medicine, and Society for Vascular Surgery". Circulation. 124 (4): 489–532. doi:10.1161/CIR.0b013e31820d8d78. PMID 21282505.