eMedicine Specialties > Emergency Medicine > Cardiovascular

Dissection, Carotid Artery

Author: David Zohrabian, MD, Emergency Physician, Emergent Medical Associates, Valley Presbyterian Hospital, Van Nuys, California
Contributor Information and Disclosures

Updated: Oct 29, 2009

Introduction

Background

Carotid artery dissection (CAD) begins as a tear in one of the carotid arteries of the neck, allowing blood under arterial pressure to enter the wall of the artery and split its layers. The result is either an intramural hematoma or aneurysmal dilatation, both of which can be sources of microemboli, with the latter also causing mass effect on surrounding structures.

Carotid artery dissection is a significant cause of ischemic stroke in all age groups, but it occurs most frequently in the fifth decade of life and accounts for a much larger percentage of strokes in young patients.¹ Dissection of the internal carotid artery can occur intracranially or extracranially, with the latter being more frequent. Internal carotid artery dissection can be caused by major or minor trauma, or it can be spontaneous, in which case, genetic, familial, and/or heritable disorders are likely etiologies.

Although in practice dissections are labeled spontaneous in the absence of major blunt or penetrating trauma,² when associated with minor mechanism trauma they may be caused or influenced by an underlying arteriopathy.³ Patients can present in a variety of settings, such as a trauma bay with multiple traumatic injuries; the physician's office with nonspecific head, neck, or face pain; or to the emergency department with a partial Horner syndrome.

Sophisticated imaging techniques, which have improved over the last 2 decades, are required to confirm the presence of dissection. Most ischemic cerebral symptoms arise from thromboembolic events; therefore, early institution of antithrombotic treatment provides the best outcome.⁴ Once diagnosed and treated, patients with carotid artery dissection (CAD) require regular follow-up and imaging studies of both carotids as healing usually takes 3-6 months and the incidence of contralateral dissection is higher than in the general population. When diagnosed early, prognosis is usually good. A high index of suspicion is required to make this difficult diagnosis.

Pathophysiology

Although the cause of internal carotid artery dissection remains elusive, mechanical forces (trauma, blunt injury, stretching) and underlying arteriopathies (Ehlers-Danlos syndrome IV, other connective tissue disorders/aberrations) alone, or in combination, account for most of the pathophysiology. It is widely accepted that carotid artery dissection (CAD) is a multifactorial disease.⁵

Carotid artery dissection begins as a tear in the tunica intima or directly within the tunica media (possibly originating from the vasa vasorum).¹ The blood dissects along the artery to create an intramural hematoma leading to a thrombus, which can narrow the carotid artery lumen and become a nidus for distal embolization.² Sometimes, the dissection plane lies between the tunica media and tunica adventitia, resulting in an aneurysmal outpouching of the arterial wall that may also become a source of distal emboli. Aneurysmal dilatation can also cause mass effect on nearby structures such as sympathetic fibers and the lower cranial nerves.^1,2 The dilatation resulting from an internal carotid artery dissection may be termed a true, as opposed to a false, aneurysm because the wall is composed of blood vessel elements.

Frequency

United States

The annual incidence of symptomatic spontaneous internal carotid artery dissection ranges from 2.5-3 per 100,000.¹ The incidence of carotid artery dissection as a result of blunt injury (mainly high-speed motor vehicle accidents) ranges from less than 1% to 3%.⁶ The actual incidence may be higher because some dissections are asymptomatic or cause only minor transient symptoms and remain undiagnosed.

Mortality/Morbidity

Spontaneous internal carotid artery dissection has a reported mortality rate of less than 5%, although the morbidity and mortality of internal carotid artery dissection due to blunt trauma may be much higher.

• Morbidity from carotid artery dissection varies in severity from transient focal deficits to permanent cerebral or retinal ischemic injury, and even death in the setting of trauma.
• Over half of patients with spontaneous carotid artery dissection develop stroke,¹ although this may be delayed by hours or days. 
• Rates of delayed stroke due to blunt-traumatic causes of carotid artery injury range from 3% in grade I injuries to 44% in grade IV injuries.²
• In the setting of blunt trauma, 37-58% of patients have permanent neurologic deficit on discharge,⁶ although early use of antithrombotic therapy has essentially eliminated ischemic events in asymptomatic patients with carotid artery dissection.^4,7
• As in other causes of stroke in young adults, the functional outcome is generally good, and recurrence of cerebral ischemia and carotid artery dissection is rare.⁵

Sex

No gender-based difference exists for spontaneous internal carotid artery dissection, although there may be a slight male predominance when taking into account traumatic causes of carotid artery dissection.

Age

• Internal carotid artery dissection is a common cause of ischemic stroke in patients younger than 50 years and accounts for up to 25% of ischemic strokes in young and middle-aged patients.¹
• The mean age for ischemic stroke secondary to internal carotid artery dissection from blunt traumatic injury is even younger at 35-38 years old.
• Dissection of the intracranial part of the internal carotid artery is rare at any age because the intracranial carotid artery is less mobile and the skull absorbs most of the force of trauma.

Clinical

History

Patients with internal carotid artery dissection can present with nonspecific complaints and in all settings. Maintaining a high index of suspicion for carotid dissection is critical anytime a patient presents with unusual focal neurologic complaints, particularly involving the cranial nerves and after major mechanism trauma, minor mechanism stress, or impact of the neck directly. In cases of high-impact trauma, a history of cervical hyperextension, flexion, and/or rotation should alert the physician to the possibility of dissection. In patients with multiple traumatic injuries, these nonspecific symptoms may be delayed from 1-5 days postinjury.

• Even patients with seemingly minor trauma can develop dissection of the internal carotid artery. Symptoms may range from headache to hemiparesis. Precipitating events should be sought and may include chiropractic manipulation, yoga, gymnastics, sports injuries (including direct impact of high-velocity ball or other direct impact to the neck), overhead painting, coughing, or sneezing.
• Pain is the initial symptom of a spontaneous internal carotid artery dissection presenting to a physician. Head, neck, or facial pain ipsilateral to the dissection is common. The headache is usually described as constant and severe. Unilateral facial or orbital pain is also common, and 25% of patients have isolated ipsilateral neck pain. Hypoageusia, or decreased taste sensation, may also be a presenting symptom.
• In less than half of patients presenting with a carotid artery dissection unilateral oculosympathetic palsy, or a partial Horner syndrome, may develop, and these patients will experience miosis, visual disturbance, and mild ptosis that may not be detected clinically. Isolated transient vision loss may also be a presenting complaint. Irreversible blindness from an ischemic optic nerve injury is rare. Also up to 20% of patients may present with an ischemic stroke without any warning signs.
• Typical presenting symptoms are as follows:
  • Headache, including neck and facial pain, can be constant, instantaneous, gradual, throbbing, or sharp.
    • Headache is commonly ipsilateral to the dissected artery.
    • Headache usually precedes a cerebral ischemic event, unlike a headache associated with stroke, which usually follows or accompanies the ischemic event.
    • Cluster-like headache with pain centered in or around the eye has also been described in a case of spontaneous internal carotid artery dissection.⁸
    • Recurrence of neck pain suggests extension or recurrence of the dissection.
  • Transient episodic blindness, or amaurosis fugax, is caused by decreased blood flow to the retina.
  • Ptosis with miosis, which is a partial Horner syndrome, is usually painful when caused by internal carotid artery dissections.
  • Neck swelling
  • Pulsatile tinnitus can occur in up to 25% of patients with dissection of the internal carotid artery.
  • Decreased taste sensation, or hypoageusia
  • Focal weakness
  • Migrainelike symptoms such as a scintillating scotoma, which is loosely defined as a transient visual field disturbance in the form of shimmering or arcs of light.

Physical

In the setting of high-impact trauma, a history may be unobtainable, so physical signs indicating a possible internal carotid artery dissection need to be identified. Furthermore, signs may be masked in patients with concomitant head trauma, coma, or multiple traumatic injuries.

• The signs that should be appreciated when entertaining the diagnosis of internal carotid artery dissection include the following:
  • Focal neurologic deficit and frank stroke occur hours to days postinjury and may be present in up to 93% of patients at the time of diagnosis of internal carotid artery dissection secondary to high-impact blunt trauma.
  • Hemiparesis
  • Oculosympathetic palsy, or a partial Horner syndrome (ptosis with miosis), may be present in less than 50% of patients, and when accompanied by ipsilateral pain and retinal ischemia suggests an internal carotid artery dissection. The term partial Horner syndrome is used because anhydrosis is absent. The sympathetic fibers innervating the facial sweat glands are anatomically located on the external rather than internal carotid artery; thus, anhydrosis is not a finding in the setting of internal carotid dissection.
  • Cranial nerve palsy can be present in up to 12% of patients, with the lower cranial nerves affected more often than the facial, trigeminal, and oculomotor nerves.
  • Cervical bruit
  • Cervicothoracic seat belt sign, which is ecchymosis to the neck and chest, raises the incidence of cerebrovascular injuries (internal carotid or vertebral) to 3%.
  • Neck hematoma and/or ecchymosis
  • Cervical spine injuries, maxillofacial trauma, basilar skull fractures
  • Massive epistaxis
  • Evidence of near hanging injury or strangulation injury

Causes

• Heritable connective-tissue disorders
• Ehlers-Danlos syndrome type IV
• Fibromuscular dysplasia
• Cystic medial necrosis
• Marfan syndrome
• Autosomal dominant polycystic kidney disease
• Osteogenesis imperfecta type I
• Oral contraceptives
• Hypertension
• Neck manipulation or strain - This can result from intentional manipulation or from other strain that may occur during sports activities, yoga, or even from minimal activity (eg, overhead painting).
• Blunt trauma from high impact and seemingly minor mechanisms of injury
• Penetrating trauma
• Wearing a 3-point restraint seat belt during a motor vehicle crash (MVC)
• Smoking
• Respiratory tract infections

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