eMedicine Specialties > Emergency Medicine > Cardiovascular

Dissection, Carotid Artery

David Zohrabian, MD, Emergency Physician, Emergent Medical Associates, Valley Presbyterian Hospital, Van Nuys, California

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.

Arterial dissection. A, Tear and elevation of the intima from the wall of the artery, resulting in luminal stenosis. The illustration shows stasis of flow in the false lumen beneath the elevated intima. This condition creates a blind pouch that predisposes the patient to thrombus formation. B, Subadventitial dissection represents hemorrhage between the media and the adventitia. The artery may become dilated as a result of thickening of the arterial wall, with some degree of luminal narrowing. Elevation of an intimal flap is not a common finding associated with this type of dissection. The hemorrhage may extravasate through the adventitia, resulting in pseudoaneurysm or fistula formation.

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

Differential Diagnoses

Workup

Laboratory Studies

• If a physician is considering spontaneous internal carotid artery dissection, laboratory studies are irrelevant for diagnosis. However, if contrast-enhanced CT or arteriography is planned, a baseline creatinine is appropriate to obtain.
• If surgery is planned, the patient's blood type, complete blood count, and coagulation profile (prothrombin and activated partial thromboplastin time) should be obtained.
• Baseline coagulation studies may be appropriate in certain settings prior to initiation of anticoagulation therapy or in cases where a patient is already taking anticoagulation therapy at the time that dissection is identified.

Imaging Studies

• Helical computed tomographic angiography
  • Helical CT angiography (CTA) now has an established role in the diagnosis of internal carotid artery dissection, and the increased use and availability of high-resolution multidetector scanners has fast replaced angiography and possibly MRA as the diagnostic modality of choice. CTA may be the first and possibly the only modality used for screening and diagnostic purposes for trauma patients who fit general screening criteria (based on signs, symptoms, and mechanism) for carotid artery dissection and who will already be undergoing CT scan for another indication. Helical CTA is fast and noninvasive, and previous limitations when compared to conventional angiography are steadily declining. When obtaining a CTA of the neck, the physician must specifically request for the study to rule out internal carotid artery dissection.
  • When performing a noncontrast CT, dissection of the internal carotid artery may be inferred from indirect findings, which include soft-tissue swelling, hematoma adjacent to the internal carotid artery, and infiltration of perivascular fat planes. Also, fracture or fracture/dislocation of the cervical bones should raise suspicion for internal carotid artery injury. Noncontrast CT scan is not an adequate screening or diagnostic test for internal carotid artery dissection.
  • The hallmark of injury to the internal carotid artery using CT angiography is a change in the caliber of the vessel. Other findings indicating a dissection may include oval, irregular, or slitlike cross section of the vessel lumen. In comparison to conventional angiography, CTA has the added benefit of imaging extravascular structures.⁹ Also, axial images can be reconstructed for 3-dimensional viewing and are obtained automatically in the newer-generation CT scanners.
  • CTA is nearly always sufficient to confirm the diagnosis of carotid artery dissection,¹⁰ and even early studies (1996) with CTA achieved 100% sensitivity and specificity with arterial angiography.¹¹
• Magnetic resonance angiography
  • Magnetic resonance angiography (MRA) may have already replaced conventional angiography for the diagnosis of internal carotid artery dissection. Some institutions use MRI and MRA as the first and only imaging modality when suspecting carotid artery dissection.
  • MRI scans with fat saturation can show intramural blood, the pathological hallmark of dissection,¹¹ and mural expansion, thus confirming the diagnosis of carotid artery dissection.¹⁰ This is visualized as a semilunar hyperintensity (the mural hematoma) partially surrounding a circular hypointense signal (the residual lumen).
  • MRA may fail to detect intramural hematoma within the first 24-48 hours after occurrence of carotid artery dissection.¹²
  • Other MRA signs of dissection include irregular vessel margins, filling defects, extravasation of contrast, vascular occlusion, and caliber changes of the vessel. The latter sign is important and appreciated on axial views, but 3-dimensional reconstructed views allow study from any angle.
  • Improved resolution, speed, noninvasiveness, absence of irradiation, and good negative predictive value make MRA an excellent screening and diagnostic tool and in most cases superior to angiography.
• Conventional angiography
  • Conventional angiography was the criterion standard for the diagnosis of internal carotid artery dissection. Conventional angiography has a 1% overall risk of complications; it is invasive, resource-intensive, and costly; and should be reserved for patients in whom suspicion for internal carotid artery dissection remains high despite negative results with other imaging modalities or when endovascular or surgical management is planned.
  • Angiography may miss dissections when the false lumen does not opacify with contrast medium.¹¹
  • The pathognomonic finding for a carotid artery dissection is an intimal flap and double lumen, secondary to an intramural hematoma. This finding is rarely detected.
  • The most common angiographic finding is termed the "string sign," which is a long, tapered, narrowing column of contrast material in the distal segment of the internal carotid artery.^10,11
  • The other angiographic patterns indicative of carotid artery dissection that are more commonly found include arterial stenosis, aneurysm formation, and arterial occlusion.¹¹
  • Despite the above, there still remain some indications as well as physician or institution preference to performing carotid angiography.
• Doppler ultrasonography (DUS), or duplex scanning
  • This modality is soon becoming an extension of the physical examination and has an increasing role in the diagnosis of a myriad of medical and surgical cases. With its increasing resolution, applicability, speed, and ease-of-use, Doppler ultrasonography can currently be used for the initial assessment of patients with suspected carotid artery dissection and is usually already at the bedside in trauma cases for focused assessment with sonography for trauma (FAST).
  • DUS has the lowest cost and highest safety profile of all the imaging modalities presented, and reported sensitivities are as high as 96% in diagnosing carotid artery dissections in patients who suffered stroke.³
  • An abnormal blood flow pattern can be appreciated in up to 90% of patients with carotid artery dissection, but the actual site of injury is usually not seen because of limited ability to evaluate past the carotid bulb.
  • The most common DUS finding in carotid artery dissection is high resistance flow pattern or absence of signal in a totally occluded artery.¹¹
  • The pathognomonic DUS finding for carotid artery dissection is the demonstration of a membrane in the longitudinal and axial view.¹¹
  • A recent prospective review found ultrasound to have a 31% false-negative rate in patients with carotid artery dissection presenting with Horner syndrome.¹ Abnormalities found by duplex scanning should always be followed up with another imaging modality.
  • Unlike angiography, DUS is able to demonstrate a false lumen even if thrombosed.¹¹

Other Tests

• These supplementary tests may be needed for evaluation of patients with a possible internal carotid artery dissection.
  • Electrocardiography
  • Echocardiography
  • Neuroimaging such as contrast and noncontrast CT, or MRI of the brain
  • Electroencephalography

Treatment

Prehospital Care

Cervical spine immobilization, which is usually appropriate, should be performed in the setting of any significant traumatic injury that could involve the neck.

Emergency Department Care

Patients with internal carotid artery dissection can present in various ways and with nonspecific complaints but, in all cases, the emergency physician should maintain a high index of suspicion. If included in the differential diagnosis, internal carotid artery dissection should be pursued until clinically ruled out. Depending on the likelihood of dissection, patient characteristics, neurologic status, and hemodynamic stability, medical management may occur during or after the diagnosis is made. As in all medical care decisions, benefits versus risks of treatment should be taken into account and input from endovascular and surgical consultants should help management decisions.

• Although it depends on the patient's presentation, an initial CT of the head is usually warranted. A negative scan, or findings that do not correlate with the patient's symptoms and signs, should be followed up by a more definitive imaging modality such as MRA, CTA, or conventional angiography depending on the institution.
• A general consensus does not exist for the management of internal carotid artery dissection, but surgical, endovascular, and medical options may depend on the type of injury, anatomic location, mechanism of injury, coexisting injuries, and comorbidities. Therefore, after the diagnosis is made, the risk versus benefit of antithrombotic therapy should be weighed, especially in cases of high-impact trauma, and vascular surgery or interventional radiology consultations should be obtained.
• Anticoagulation with intravenous heparin followed by warfarin has generally been accepted as medical management to prevent thromboembolic complications.
• Antiplatelet therapy has also been used alone especially when systemic anticoagulation is contraindicated.
• Candidates for angioplasty and stent placement include patients with persistent ischemic symptoms despite adequate anticoagulation, patients with contraindication to anticoagulation therapy, iatrogenic dissection during intravascular procedures, and patients with significantly compromised cerebral blood flow.¹³
• Surgery has a limited role in the management of carotid artery dissections.

Consultations

The risk and benefit of initiating antithrombotic therapy must be weighed for each patient with carotid artery dissection. Consultation with one or more of the following services may be useful, particularly in difficult situations such as multiple trauma, traumatic brain injury, preexisting brain lesion, or upper GI bleed.

• Neurology
• Vascular surgery
• Neurosurgery
• Interventional radiology

Medication

The goal of medical management, using antithrombotics, is to prevent progressive neurologic deficits. Antiplatelet and anticoagulation therapies have been used in combination or separately with antiplatelet therapy being recommended in most patients with dissection. Current literature continues to demonstrate improved outcomes with systemic anticoagulation.

Anticoagulants

These agents prevent thrombus formation and decrease the number of emboli following arterial dissection. Anticoagulation therapy also aids intimal healing, decreases smooth muscle cell proliferation, and decreases intimal thickening.

Unfractionated heparin

Potentiates activity of antithrombin III. Does not actively lyse thrombi but inhibits further thrombogenesis. Prevents reaccumulation of a clot after spontaneous fibrinolysis. aPTT of 1.5-2 times control value (50-80 s) is therapeutic.

Dosing

Adult

Load 80 U/kg IV, then mix infusion as follows: 25,000 U in 250 mL D5W (100 U/mL); start at 18 U/kg/h; adjust dose based on coagulation testing (INR, aPTT)

Pediatric

Load 50 U/kg/h IV, then 25 U/kg/h infusion

Interactions

Digoxin, nicotine, tetracycline, and antihistamines may decrease effects; NSAIDs, aspirin, dextran, dipyridamole, and hydroxychloroquine may increase toxicity

Contraindications

Documented hypersensitivity; subacute bacterial endocarditis; active bleeding; history of heparin-induced thrombocytopenia

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

In neonates, preservative-free heparin recommended to avoid possible toxicity (gasping syndrome) by benzyl alcohol, which is used as preservative; caution in severe hypotension and shock

Warfarin sodium (Coumadin)

Interferes with hepatic vitamin K–dependent carboxylation. Used for prophylaxis and treatment of thromboembolic disorders. Usually prolongs PT in 48 h.

Dosing

Adult

Loading dose: 10 mg PO qd for 2-4 d; adjust daily dosage to desired PT or INR (usually in range of 2-3)

Pediatric

0.05-0.34 mg/kg/d PO; adjust dose according to desired INR; infants may require doses at or near high end of this range

Interactions

Drugs that may decrease anticoagulant effects include griseofulvin, carbamazepine, glutethimide, estrogens, nafcillin, phenytoin, rifampin, barbiturates, cholestyramine, colestipol, vitamin K, spironolactone, oral contraceptives, and sucralfate
Medications that may increase anticoagulant effects include oral antibiotics, phenylbutazone, salicylates, sulfonamides, chloral hydrate, clofibrate, diazoxide, anabolic steroids, ketoconazole, ethacrynic acid, miconazole, nalidixic acid, sulfonylureas, allopurinol, chloramphenicol, cimetidine, disulfiram, metronidazole, phenylbutazone, phenytoin, propoxyphene, sulfonamides, gemfibrozil, acetaminophen, and sulindac

Contraindications

Documented hypersensitivity; severe liver or kidney disease; open wounds or GI ulcers

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Do not switch brands after achieving therapeutic response; caution in active TB or diabetes mellitus; patients with protein C or S deficiency are at risk of developing skin necrosis

Enoxaparin (Lovenox)

Produced by partial chemical or enzymatic depolymerization of unfractionated heparin (UFH). Binds to antithrombin III, enhancing its therapeutic effect. Heparin-antithrombin III complex binds to and inactivates activated factor X (Xa) and factor II (thrombin).
Does not actively lyse but is able to inhibit further thrombogenesis. Prevents reaccumulation of clot after spontaneous fibrinolysis.
Advantages include intermittent dosing and decreased requirement for monitoring. Heparin anti–factor Xa levels may be obtained if needed to establish adequate dosing.
LMWH differs from UFH by having a higher ratio of antifactor Xa to antifactor IIa compared with UFH.
Prevents DVT, which may lead to pulmonary embolism in patients undergoing surgery who are at risk for thromboembolic complications. Used for prevention in hip replacement surgery (during and following hospitalization), knee replacement surgery, or abdominal surgery in those at risk of thromboembolic complications, or in nonsurgical patients at risk of thromboembolic complications secondary to severely restricted mobility during acute illness.
Used to treat DVT or PE in conjunction with warfarin for inpatient treatment of acute DVT with or without PE or for outpatient treatment of acute DVT without PE.
No utility in checking aPTT (drug has wide therapeutic window and aPTT does not correlate with anticoagulant effect).
Average duration of treatment is 7-14 d.

Dosing

Adult

1 mg/kg administered SC q12h in conjunction with oral aspirin (100-325 mg daily); maximum antifactor Xa and antithrombin activities occur 3-5 h postadministration
CrCl <30 mL/min: 1 mg/kg SC qd

Pediatric

Not established

Interactions

Platelet inhibitors or oral anticoagulants such as dipyridamole, salicylates, aspirin, NSAIDs, sulfinpyrazone, and ticlopidine may increase risk of bleeding

Contraindications

Documented hypersensitivity; major bleeding; thrombocytopenia

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Decrease dose if CrCl <30 mL/min; if thromboembolic event occurs despite LMWH prophylaxis, discontinue drug and initiate alternate therapy; elevation of hepatic transaminases may occur but is reversible; heparin-associated thrombocytopenia may occur with fractionated low-molecular-weight heparins; 1 mg of protamine sulfate will reverse effect of approximately 1 mg of enoxaparin if significant bleeding complications develop; cases of epidural/spinal hematomas have been reported in adults receiving spinal or epidural anesthesia (holding 2 doses prior to LP or surgery is recommended)

Antiplatelets

These agents may be used in trauma patients in whom anticoagulation may be contraindicated. An earlier Cochrane review found that the available evidence does not reliably establish whether or not anticoagulation is better than antiplatelet drugs in patients with dissection.

Aspirin (Ecotrin, Empirin, Bayer, Anacin)

Blocks prostaglandin synthetase action; inhibits prostaglandin synthesis preventing formation of platelet-aggregating thromboxane A2. Acts on hypothalamus heat-regulating center to reduce fever.

Dosing

Adult

81-325 mg PO qd for platelet inhibition

Pediatric

10-15 mg/kg/dose PO q4-6h; not to exceed 60-80 mg/kg/d

Interactions

Effects may decrease with antacids and urinary alkalinizers; corticosteroids decrease salicylate serum levels; additive hypoprothrombinemic effects and increased bleeding time may occur with coadministration of anticoagulants; may antagonize uricosuric effects of probenecid and increase toxicity of phenytoin and valproic acid; doses >2 g/d may potentiate glucose-lowering effect of sulfonylurea drugs

Contraindications

Documented hypersensitivity; liver damage; hypoprothrombinemia; vitamin K deficiency; bleeding disorders; asthma; because of association of aspirin with Reye syndrome, do not use in children (<16 y) with flu

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

May cause transient decrease in renal function and aggravate chronic kidney disease; avoid use in patients with severe anemia, history of blood coagulation defects, or current anticoagulant therapy

Thrombolytics

The research involving thrombolytics for the treatment of extracranial internal carotid artery dissection is limited, and, thus, its usefulness and appropriateness are yet unknown.

Alteplase (Activase)

Tissue plasminogen activator exerts effect on fibrinolytic system to convert plasminogen to plasmin. Plasmin degrades fibrin, fibrinogen, and procoagulant factors V and VIII. Serum half-life is 4-6 min but half-life lengthened when bound to fibrin in clot. Used in management of acute myocardial infarction (MI), acute ischemic stroke, and pulmonary embolism (PE). Heparin and aspirin are not given for 24 h after tPA. Must be given within 3 h of stroke onset. Exclude hemorrhage by CT scan. If hypertensive, lower BP with labetalol, 10 mg IV. Safety and efficacy of concomitant administration with aspirin and heparin during first 24 h after onset of symptoms have not been investigated.

Dosing

Adult

0.9 mg/kg IV infused over 60 min with 10% of total dose administrated as initial IV bolus over 1 min; not to exceed 90 mg; optimal dosing for AMI not yet established

Pediatric

Not established

Interactions

Anticoagulants and antiplatelets may increase risk of bleeding; may give heparin with and after alteplase infusions to reduce risk of rethrombosis; either heparin or alteplase may cause bleeding complications

Contraindications

Documented hypersensitivity; active internal bleeding; cerebrovascular accident or stroke within last 2 mo; intracranial or intraspinal surgery or trauma; intracranial hemorrhage on pretreatment evaluation; suspicion of subarachnoid hemorrhage; intracranial neoplasm; arteriovenous malformation or aneurysm; bleeding diathesis; severe uncontrolled hypertension

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Monitor for bleeding, especially at arterial puncture sites, with coadministration of vitamin K antagonists; control and monitor blood pressure frequently during and following alteplase administration (when managing acute ischemic stroke); do not use >0.9 mg/kg to manage acute ischemic stroke; doses >0.9 mg/kg may cause ICH

Follow-up

Further Inpatient Care

• Patients should be closely monitored for delayed ischemic or embolic neurologic symptoms and for the hemorrhagic side effects of antithrombotic medication.

Further Outpatient Care

• If anticoagulation therapy is initiated, continue for 3-6 months with the appropriate follow-up for international normalized ratio (INR) and PT monitoring. Target INR should between 2.0 and 3.0.
• A follow-up CT-angiogram, Duplex ultrasonography, or other angiographic imaging modalities should be obtained several months after the event to reevaluate the dissection.

Complications

• Ischemic stroke, mainly from thromboembolic complications of the initial dissection, may occur.
• Hemorrhagic stroke may be a complication secondary to anticoagulant use in some patients.
• Recurrence of dissection may occur in the unaffected artery and may be greater than 1% per year in patients with a known heritable arteriopathy.
• The usual complications associated with surgical or endovascular procedures may occur if they are used in the early management of the dissection.

Prognosis

• Prognosis of internal carotid artery dissection depends on the severity of the initial ischemic injury and the extent of collateral circulation.
• Overall, the prognosis for spontaneous internal carotid artery dissection is favorable, with about 75% of patients making a good recovery.¹ The mortality rate is about 5%. Patients who have a dissection secondary to trauma have a much higher rate of mortality and neurologic deficit on discharge.
• Recurrence risk is highest in the first month and then about 1% per year for about a decade.
• Headache has been described to persist, in some cases, for years after the dissection.

Patient Education

• For excellent patient education resources, visit eMedicine's Stroke Center. Also, see eMedicine's patient education articles Worst Headache of Your Life, Transient Ischemic Attack (Mini-stroke), and Stroke.

Miscellaneous

Medicolegal Pitfalls

• Failure to consider the diagnosis in young patients presenting with neurologic symptoms
• Failure to rule out intracranial hemorrhage prior to initiation of anticoagulation therapy
• Failure to initiate anticoagulation therapy when a thrombus is detected
• Administration of anticoagulant, especially warfarin, or antiplatelet therapy to a pregnant patient

Special Concerns

• Trauma: Do not initiate anticoagulation therapy in trauma patients without first ruling out intracranial bleeds and extracranial sources of hemorrhage.
• Pregnancy: Do not initiate anticoagulation or antiplatelet therapy in pregnant patients without consultation with an obstetrician.
• Multiple medications: Multiple drugs displace warfarin from albumin, thus increasing its anticoagulant effect.

Multimedia

Media file 1: Arterial dissection. A, Tear and elevation of the intima from the wall of the artery, resulting in luminal stenosis. The illustration shows stasis of flow in the false lumen beneath the elevated intima. This condition creates a blind pouch that predisposes the patient to thrombus formation. B, Subadventitial dissection represents hemorrhage between the media and the adventitia. The artery may become dilated as a result of thickening of the arterial wall, with some degree of luminal narrowing. Elevation of an intimal flap is not a common finding associated with this type of dissection. The hemorrhage may extravasate through the adventitia, resulting in pseudoaneurysm or fistula formation.

References

1. Schievink WI. Spontaneous dissection of the carotid and vertebral arteries. N Engl J Med. Mar 22 2001;344(12):898-906. [Medline].

2. Redekop GJ. Extracranial carotid and vertebral artery dissection: a review. Can J Neurol Sci. May 2008;35(2):146-52. [Medline].

3. Goyal MS, Derdeyn CP. The diagnosis and management of supraaortic arterial dissections. Curr Opin Neurol. Feb 2009;22(1):80-9. [Medline].

4. Cothren CC, Moore EE, Biffl WL, Ciesla DJ, Ray CE Jr, Johnson JL. Anticoagulation is the gold standard therapy for blunt carotid injuries to reduce stroke rate. Arch Surg. May 2004;139(5):540-5; discussion 545-6. [Medline].

5. Debette S, Leys D. Cervical-artery dissections: predisposing factors, diagnosis, and outcome. Lancet Neurol. Jul 2009;8(7):668-78. [Medline].

6. Baker WE, Wassermann J. Unsuspected vascular trauma: blunt arterial injuries. Emerg Med Clin North Am. Nov 2004;22(4):1081-98. [Medline].

7. Arthurs ZM, Starnes BW. Blunt carotid and vertebral artery injuries. Injury. Nov 2008;39(11):1232-41. [Medline].

8. Tobin J, Flitman S. Cluster-like headaches associated with internal carotid artery dissection responsive to verapamil. Headache. Mar 2008;48(3):461-6.

9. Stallmeyer MJ, Morales RE, Flanders AE. Imaging of traumatic neurovascular injury. Radiol Clin North Am. Jan 2006;44(1):13-39, vii. [Medline].

10. Caplan LR. Dissections of brain-supplying arteries. Nat Clin Pract Neurol. Jan 2008;4(1):34-42. [Medline].

11. Flis CM, Jager HR, Sidhu PS. Carotid and vertebral artery dissections: clinical aspects, imaging features and endovascular treatment. Eur Radiol. Mar 2007;17(3):820-34. [Medline].

12. Kim YK, Schulman S. Cervical artery dissection: pathology, epidemiology and management. Thromb Res. Apr 2009;123(6):810-21. [Medline].

13. Fava M, Meneses L, Loyola S, Tevah J, Bertoni H, Huete I. Carotid artery dissection: endovascular treatment. Report of 12 patients. Catheter Cardiovasc Interv. Apr 1 2008;71(5):694-700. [Medline].

14. Arnold M, Baumgartner RW, Stapf C, Nedeltchev K, Buffon F, Benninger D. Ultrasound diagnosis of spontaneous carotid dissection with isolated Horner syndrome. Stroke. Jan 2008;39(1):82-6. [Medline].

15. Baker WE, Servais EL, Burke PA, Agarwal SK. Blunt carotid injury. Curr Treat Options Cardiovasc Med. Apr 2006;8(2):167-73. [Medline].

16. Berne JD, Norwood SH, McAuley CE, Villareal DH. Helical computed tomographic angiography: an excellent screening test for blunt cerebrovascular injury. J Trauma. Jul 2004;57(1):11-7; discussion 17-9. [Medline].

17. Dziewas R, Konrad C, Drager B, et al. Cervical artery dissection--clinical features, risk factors, therapy and outcome in 126 patients. J Neurol. Oct 2003;250(10):1179-84.

18. Kremer C, Mosso M, Georgiadis D, et al. Carotid dissection with permanent and transient occlusion or severe stenosis: Long-term outcome. Neurology. Jan 28 2003;60(2):271-5.

19. Mazighi M, Saint Maurice JP, Rogopoulos A, Houdart E. Extracranial vertebral and carotid dissection occurring in the course of subarachnoid hemorrhage. Neurology. Nov 8 2005;65(9):1471-3. [Medline].

20. Schoenen J, Sandor PS. Headache with focal neurological signs or symptoms: a complicated differential diagnosis. Lancet Neurol. Apr 2004;3(4):237-45. [Medline].

21. Slovut DP, Olin JW. Fibromusculardysplasia. N Engl J Med. Apr 29 2004;350(18):1862-71.

22. Vertinsky AT, Schwartz NE, Fischbein NJ, Rosenberg J, Albers GW, Zaharchuk G. Comparison of multidetector CT angiography and MR imaging of cervical artery dissection. AJNR Am J Neuroradiol. Oct 2008;29(9):1753-60.

23. Volker W, Besselmann M, Dittrich R, Nabavi D, Konrad C, Dziewas R. Generalized arteriopathy in patients with cervical artery dissection. Neurology. May 10 2005;64(9):1508-13. [Medline].

Keywords

carotid artery dissection, carotid artery dissection symptoms, CAD, ischemic stroke, internal carotid artery dissection, internal carotid artery, common carotid artery dissection, stroke,
subarachnoid hemorrhage, Horner syndrome

Contributor Information and Disclosures

Author

David Zohrabian, MD, Emergency Physician, Emergent Medical Associates, Valley Presbyterian Hospital, Van Nuys, California
David Zohrabian, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, Emergency Medicine Residents Association, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

Joseph J Sachter, MD, FACEP, Consulting Staff, Department of Emergency Medicine, Muhlenberg Regional Medical Center
Joseph J Sachter, MD, FACEP is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Physician Executives, American Medical Association, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

A Antoine Kazzi, MD, Chair and Medical Director, Department of Emergency Medicine, American University of Beirut, Lebanon
A Antoine Kazzi, MD is a member of the following medical societies: American Academy of Emergency Medicine
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

David FM Brown, MD, Assistant Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital
David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, Mark J Leber, MD, to the development and writing of this article.

© 1994- by Medscape.
All Rights Reserved
(http://www.medscape.com/public/copyright)