Carotid Artery Dissection

Updated: Feb 19, 2019
Author: David Zohrabian, MD, FAAEM, FACEP; Chief Editor: Barry E Brenner, MD, PhD, FACEP 



Carotid artery dissection begins as a tear in one of the carotid arteries of the neck, which allows blood under arterial pressure to enter the wall of the artery and split its layers. The result is either an intramural hematoma or an aneurysmal dilatation, either of which can be a source of microemboli, with the latter also causing a 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, or heritable disorders are likely etiologies.

Although in practice, dissections are labeled spontaneous in the absence of major blunt or penetrating trauma,[2] when they are 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; a physician’s office with nonspecific head, neck, or face pain; or an emergency department (ED) with a partial Horner syndrome.[4]

Sophisticated imaging techniques, which have improved over the past two 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.[5]

Once diagnosed and treated, patients with carotid artery dissection require regular follow-up and imaging studies of both carotid arteries. Healing usually takes 3-6 months, and the incidence of contralateral dissection is higher in these patients than in the general population. When the condition is diagnosed early, the prognosis is usually good. A high index of suspicion is required to make this difficult diagnosis.

For patient education resources, see the Brain & Nervous System Center, as well as Worst Headache of Your Life, Transient Ischemic Attack (TIA, Mini-Stroke), and Stroke.


Although the cause of internal carotid artery dissection remains elusive, mechanical forces (eg, trauma, blunt injury, and stretching) and underlying arteriopathies (eg, Ehlers-Danlos syndrome IV[6] and other connective tissue disorders and aberrations), either alone or in combination, account for most of the pathophysiology. It is widely accepted that carotid artery dissection is a multifactorial disease.[7]

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 that leads to a thrombus, which can narrow the carotid artery lumen and become a nidus for distal embolization (see the image below).[2]

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

Sometimes, the dissection plane lies between the tunica media and the 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 a 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 rather than a false aneurysm because the wall is composed of blood vessel elements.


Causes of carotid artery dissection include the following:

  • Heritable connective-tissue disorders
  • Ehlers-Danlos syndrome type IV
  • Cystic medial necrosis
  • Autosomal dominant polycystic kidney disease
  • 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 apparently minimal activity (eg, overhead painting)
  • Blunt trauma from high impact and seemingly minor mechanisms of injury
  • Penetrating trauma
  • Wearing a three-point restraint seat belt during a motor vehicle crash
  • Smoking
  • Respiratory tract infection


The annual incidence of symptomatic spontaneous internal carotid artery dissection is 2.5-3 per 100,000.[1] The incidence of carotid artery dissection as a result of blunt injuries (mainly high-speed motor vehicle accidents) ranges from less than 1% to 3%.[8] The actual incidence may be higher; some dissections are asymptomatic or cause only minor transient symptoms and remain undiagnosed.

Age- and sex-related demographics

Internal carotid artery dissection is a common cause of ischemic stroke in patients younger than 50 years and accounts for as many as 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: 35-38 years. 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.

No significant gender-based difference in frequency exists for spontaneous internal carotid artery dissection, though there may be a slight male preponderance when traumatic causes of carotid artery dissection are taken into account.


In general, the prognosis 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, 9] The reported mortality is less than 5%. Patients who have a dissection secondary to trauma have a much higher mortality on discharge.

Morbidity from carotid artery dissection ranges in severity from transient focal deficits to permanent cerebral or retinal ischemic injury. More than one half of patients with spontaneous carotid artery dissection develop stroke,[1]  though 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 deficits on discharge,[8] though early use of antithrombotic therapy has essentially eliminated ischemic events in asymptomatic patients with carotid artery dissection.[5, 10]

As with other causes of stroke in young adults, the functional outcome is generally good, and recurrence of cerebral ischemia and carotid artery dissection is rare.[7] The risk of recurrence is highest in the first month and then remains in the area of 1% per year for about a decade. Headache may persist, in some cases for years after the dissection.




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 whenever a patient presents with unusual focal neurologic complaints, particularly if the cranial nerves are involved and of the patient has sustained major mechanism trauma, minor mechanism stress, or a direct impact on the neck. Failure to consider the diagnosis in young patients presenting with neurologic symptoms is a potential medicolegal pitfall.

In cases of high-impact trauma, a history of cervical hyperextension, flexion, or rotation should alert the physician to the possibility of dissection. In patients with multiple traumatic injuries, the appearance of these nonspecific symptoms may be delayed for 1-5 days after the injury.

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.

Typical presenting symptoms are as follows:

  • Headache, including neck and facial pain – This can be constant, instantaneous, gradual, throbbing, or sharp
  • Transient episodic blindness (amaurosis fugax) – This is caused by decreased blood flow to the retina
  • Ptosis with miosis (partial Horner syndrome) – This is usually painful when caused by internal carotid artery dissections
  • Neck swelling
  • Pulsatile tinnitus [11] – This can occur in as many as 25% of patients with dissection of the internal carotid artery
  • Decreased taste sensation (hypogeusia)
  • Focal weakness
  • Migrainelike symptoms (eg, a scintillating scotoma, which is loosely defined as a transient visual field disturbance in the form of shimmering or arcs of light)

Pain is the initial symptom of a spontaneous internal carotid artery dissection presenting to a physician. Headache (including neck and facial pain) is usually described as constant and severe and is commonly ipsilateral to the dissected artery. It usually precedes a cerebral ischemic event, unlike headache associated with stroke, which usually follows or accompanies the ischemic event. Recurrence of neck pain suggests extension or recurrence of the dissection.

Unilateral facial or orbital pain is also common, and 25% of patients have isolated ipsilateral neck pain. Cluster-like headache with pain centered in or around the eye has been described in a case of spontaneous internal carotid artery dissection.[12]

Hypogeusia, or decreased taste sensation, may also be a presenting symptom.

In fewer than half of patients presenting with a carotid artery dissection, unilateral oculosympathetic palsy (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. As many as 20% of patients may present with an ischemic stroke without any warning signs.

Physical Examination

In the setting of high-impact trauma, a history may be unobtainable; consequently, it is essential to identify physical signs indicating a possible internal carotid artery dissection. Furthermore, signs may be masked in patients with concomitant head trauma, coma, or multiple traumatic injuries, making careful examination crucial.

Signs that should be looked for when the diagnosis of internal carotid artery dissection is being entertained include the following[13, 14] :

  • Focal neurologic deficit and frank stroke occurring hours to days after injury – These may be present in as many as 93% of patients at the time of diagnosis of internal carotid artery dissection secondary to high-impact blunt trauma
  • Hemiparesis
  • Oculosympathetic palsy (partial Horner syndrome; ptosis with miosis) – This may be present in fewer than 50% of patients; when accompanied by ipsilateral pain and retinal ischemia, it suggests an internal carotid artery dissection
  • Cranial nerve palsy – This can be present in as many as 12% of patients, with the lower cranial nerves affected more often than the facial, trigeminal, and oculomotor nerves
  • Cervical bruit
  • Cervicothoracic seat belt sign (ecchymosis to the neck and chest) – This raises the incidence of cerebrovascular injuries (to internal carotid or vertebral arteries) to 3%
  • Neck hematoma or ecchymosis
  • Cervical spine injuries, maxillofacial trauma, or basilar skull fractures
  • Massive epistaxis
  • Evidence of near-hanging injury or strangulation injury

The term partial Horner syndrome (see above) is used for the oculosympathetic palsy because anhydrosis is absent. The sympathetic fibers innervating the facial sweat glands are anatomically located on the external rather than the internal carotid artery; thus, anhidrosis is not a finding in the setting of internal carotid dissection.





Laboratory Studies

If a diagnosis of spontaneous internal carotid artery dissection is under consideration, laboratory studies are largely irrelevant for diagnostic purposes. However, if contrast-enhanced computed tomography (CT) or arteriography is planned, it is appropriate to obtain a baseline creatinine concentration. If surgery is planned, the patient’s blood type, a complete blood count (CBC), and a coagulation profile (including prothrombin time [PT] and activated partial thromboplastin time [aPTT]) should be obtained.

Baseline coagulation studies may be appropriate in certain settings before the initiation of anticoagulation therapy or in cases where a patient is already taking an anticoagulant at the time that dissection is identified.


Magnetic resonance angiography

Magnetic resonance angiography (MRA) may have already replaced conventional angiography for the diagnosis of internal carotid artery dissection. Some institutions use it as the first and only imaging modality when carotid artery dissection is suspected.

Magnetic resonance imaging (MRI) with fat saturation can show intramural blood, the pathologic hallmark of dissection,[15]  and mural expansion, thus confirming the diagnosis of carotid artery dissection.[16]  These findings are 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 the occurrence of carotid artery dissection.[17]

Other MRA signs of dissection include irregular vessel margins, filling defects, extravasation of contrast, vascular occlusion, and caliber changes of the vessel. The last of these signs is particularly important and is well appreciated on axial views, but three-dimensional (3D) 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, one that in most cases is superior to conventional angiography.

Helical computed tomography angiography

Helical (spiral) CT angiography (CTA) has an established role in the diagnosis of internal carotid artery dissection, and with the increased use and availability of high-resolution multidetector scanners, it is rapidly replacing conventional angiography and possibly MRA as the diagnostic modality of choice.

CTA may be the first (or even the only) modality used for screening and diagnosis in trauma patients who fit general screening criteria (based on signs, symptoms, and mechanism) for carotid artery dissection and who will already be undergoing CT for another indication. Helical CTA is fast and noninvasive, and the limitations it once exhibited in comparison with 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.

On 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. In addition, fracture or fracture-dislocation of the cervical bones should raise the index of suspicion for internal carotid artery injury. Noncontrast CT is not an adequate screening or diagnostic test for internal carotid artery dissection.

The hallmark of injury to the internal carotid artery on CTA is a change in the caliber of the vessel. Another finding that may indicate a dissection is an oval, irregular, or slitlike cross-section of the vessel lumen. In comparison with conventional angiography, helical CTA has the added benefit of imaging extravascular structures.[18] Furthermore, axial images can be reconstructed for 3D viewing and are obtained automatically in the newer CT scanners.

CTA is nearly always sufficient to confirm the diagnosis of carotid artery dissection,[16] and even early studies of CTA were able to achieve 100% sensitivity and specificity with arterial angiography.[15]

Conventional angiography

Conventional angiography was the standard modality for diagnosing internal carotid artery dissection. It has a 1% overall risk of complications; it is invasive, resource-intensive, and costly; and it should be reserved for patients in whom suspicion for internal carotid artery dissection remains high despite negative results with other imaging modalities or for patients in whom endovascular or surgical management is planned. In addition, it may miss dissections when the false lumen does not opacify with contrast medium.[15]

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.[16, 15] The other angiographic patterns indicative of carotid artery dissection that are more commonly found include arterial stenosis, aneurysm formation, and arterial occlusion.[15]

Although conventional angiography is no longer generally considered the diagnostic modality of choice for carotid artery dissection, there remain some indications for its use, and some physicians and institutions still prefer it.


Doppler ultrasonography (DUS), or duplex scanning, is becoming an extension of the physical examination and is playing an increasingly important role in the diagnosis of a myriad of medical and surgical conditions. With its improving resolution, ready applicability, speed, and ease of use, DUS can now be used for the initial assessment of patients with suspected carotid artery dissection.[19] In trauma cases, it usually is already at the bedside for focused assessment with sonography for trauma (FAST).

Of all the imaging modalities used to diagnose carotid artery dissection, DUS has the lowest cost and the highest safety profile. Reported sensitivities are as high as 96% for diagnosing carotid artery dissections in patients who suffered stroke.[3] An abnormal blood flow pattern can be appreciated in as many as 90% of patients with carotid artery dissection, but the actual site of injury usually is not seen, because DUS has only a limited ability to evaluate past the carotid bulb.

The most common DUS finding in carotid artery dissection is a high-resistance flow pattern or the absence of signal in a totally occluded artery.[15] The pathognomonic DUS finding for carotid artery dissection is the demonstration of a membrane in the longitudinal and axial view.[15] Unlike angiography, DUS is able to demonstrate a false lumen even if it is thrombosed.[15]

A prospective review found ultrasonography to have a 31% false-negative rate in patients with carotid artery dissection who presented with Horner syndrome.[1] Whenever abnormalities are found by DUS, follow-up with another imaging modality is always indicated.

Other Tests

Supplementary tests that may be needed for evaluation of patients with a possible internal carotid artery dissection include the following:

  • Electrocardiography (ECG)
  • Echocardiography
  • Neuroimaging (eg, contrast and noncontrast CT or MRI of the brain)
  • Electroencephalography (EEG)


Initial Management

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

Patients with internal carotid artery dissection may present to the emergency department (ED) in various ways and with various nonspecific complaints, but in all cases, the emergency physician should maintain a high index of suspicion. If internal carotid artery dissection is included in the differential diagnosis, the possibility should be pursued until it is clinically ruled out.

Depending on the likelihood of dissection, patient characteristics, neurologic status, and hemodynamic stability, medical management may occur during the diagnostic process or after the diagnosis is made. As in all medical care decisions, the benefits of treatment must be carefully weighed against the risks. Input from endovascular and surgical consultants should facilitate management decisions.

Initial computed tomography (CT) of the head is usually warranted, depending on the patient’s presentation. If the scan yields negative results or the findings do not correlate with the patient’s symptoms and signs, it should be followed up by a more definitive imaging modality, such as magnetic resonance angiography (MRA), CT angiography (CTA), or conventional angiography (depending on institutional preferences; see Workup).

In a prospective study that used repeated MRI over 6 months to investigate spatial and temporal dynamic changes of intramural hematomas in 10 patients with acute spontaneous internal carotid artery dissection, Heldner et al found an early postdissection volume increase with progression of the internal carotid artery stenosis in five patients.[20] Overall, spontaneous internal carotid artery dissection had a good prognosis with spontaneous hematoma resorption in all of the investigators’ patients, but early follow-up imaging may be considered, particularly in the case of new clinical symptoms.

Pharmacologic, Endovascular, and Surgical Therapy

There is no general consensus regarding optimal management of internal carotid artery dissection, but the choice among medical, endovascular,[21] and surgical options may depend on the type of injury, the anatomic location, the mechanism of injury, coexisting injuries, and comorbid conditions. Therefore, after the diagnosis is made, the risk-to-benefit ratio of antithrombotic therapy should be determined, especially in cases of high-impact trauma, and vascular surgery or interventional radiology consultations should be obtained.

Anticoagulant therapy should be initiated when a thrombus is detected. Anticoagulation with intravenous (IV) heparin followed by warfarin has generally been accepted as adequate medical management for preventing thromboembolic complications. Do not initiate anticoagulation in trauma patients without first ruling out intracranial hemorrhage (ICH) and extracranial sources of hemorrhage.

Antiplatelet therapy has also been used alone, especially when systemic anticoagulation is contraindicated. Do not initiate either anticoagulation or antiplatelet therapy in pregnant patients without consulting an obstetrician.

Candidates for angioplasty and stent placement include patients with persistent ischemic symptoms despite adequate anticoagulation, patients with a contraindication to anticoagulant therapy, patients with an iatrogenic dissection developing during an intravascular procedure, and patients with significantly compromised cerebral blood flow.[21, 22, 23]

Surgery has a limited role in the management of carotid artery dissections. The usual complications associated with surgical or endovascular procedures may occur if such procedures are employed in the early management of the dissection.

Nonetheless, a literature review study by Xianjun and Zhiming indicated that in selected patients, internal carotid artery dissections can be effectively managed with stenting or stent-graft-supported angioplasty.[21] The review included 201 patients who suffered traumatic, spontaneous, or iatrogenic internal carotid artery dissection. Endovascular treatment of these patients had a 99.1% technical success rate, with no procedure-associated mortality reported.

Perioperatively, there was an overall rate of major cardiovascular events of 4% in this review, and postoperatively, over a mean 16.5-month follow-up period, the rate of intimal hyperplasia or in-stent restenosis or occlusion was 3.3%.[21] Over a mean 20.9-month follow-up period, recurrent transient ischemic attack in the treated vessel’s territory occurred in just 2.1% of patients.

In a study of 18 selected patients with extracranial internal carotid artery dissection, Juszkat et al found carotid artery stenting to be safe and effective.[24] In all patients, stent deployment immediately restored flow in the true lumen of the internal carotid artery. Complete resolution of clinical symptoms was observed in 14 patients (78%), partial improvement in two (11%), and persistence of neurologic deficit in only two (11%).


For each patient with carotid artery dissection, the risks and benefit of initiating antithrombotic therapy must be assessed. 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 gastrointestinal bleeding:

  • Neurology
  • Vascular surgery
  • Neurosurgery
  • Interventional radiology

Long-Term Monitoring

Patients should be closely monitored for delayed ischemic or embolic neurologic symptoms and for the hemorrhagic side effects of antithrombotic medication. Ischemic stroke, mainly from thromboembolic complications of the initial dissection, may occur. Hemorrhagic stroke may occur secondary to anticoagulant use in some patients.

If anticoagulation is initiated, it should be continued for 3-6 months with appropriate follow-up for international normalized ratio (INR) and prothrombin time (PT) monitoring. The target range for the INR should be 2.0-3.0. Follow-up with CTA, Doppler ultrasonography (DUS), or another angiographic imaging modality should be done several months after the event to reevaluate the dissection. Dissection may recur in the unaffected artery; the incidence of this development may be higher than 1% per year in patients with a known heritable arteriopathy.



Medication Summary

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

Anticoagulants, Cardiovascular

Class Summary

Anticoagulants prevent thrombus formation and reduce the number of emboli after arterial dissection. Anticoagulation also aids intimal healing, decreases smooth muscle cell proliferation, and decreases intimal thickening.


Heparin potentiates the activity of antithrombin III. It does not actively lyse thrombi, but it inhibits further thrombogenesis. Heparin prevents reaccumulation of a clot after spontaneous fibrinolysis. An activated partial thromboplastin time (aPTT) of 1.5-2 times the control value (50-80 seconds) is therapeutic.

Warfarin sodium (Coumadin, Jantoven)

Warfarin interferes with hepatic vitamin K–dependent carboxylation and is used for prophylaxis and treatment of thromboembolic disorders. It usually prolongs the prothrombin time (PT) in 48 hours.

Enoxaparin (Lovenox)

Enoxaparin is a low-molecular-weight heparin (LMWH) produced by partial chemical or enzymatic depolymerization of unfractionated heparin (UFH). It binds to antithrombin III, enhancing its therapeutic effect. The heparin-antithrombin III complex binds to and inactivates activated factor X (Xa) and factor II (thrombin). LMWH differs from UFH by having a higher ratio of anti–factor Xa to anti–factor IIa.

Enoxaparin does not actively lyse thrombi but is able to inhibit further thrombogenesis. It prevents reaccumulation of clot after spontaneous fibrinolysis. Its advantages include intermittent dosing and a decreased requirement for monitoring. Heparin anti–factor Xa levels may be obtained if needed to establish adequate dosing. There is no point in checking the aPTT; the drug has a wide therapeutic window, and aPTT does not correlate with anticoagulant effect. The average duration of treatment is 7-14 days.

Enoxaparin prevents deep vein thrombosis (DVT), which may lead to pulmonary embolism (PE) in patients undergoing surgery who are at risk for thromboembolic complications. It is used for prophylaxis in hip replacement surgery (during and after hospitalization), knee replacement surgery, or abdominal surgery in those at risk for thromboembolic complications, as well as in nonsurgical patients at risk for thromboembolic complications secondary to severely restricted mobility during acute illness.

Enoxaparin is 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.

Desirudin (Iprivask)

Desirudin is a highly selective thrombin inhibitor. It inhibits fibrin formation, activation of coagulation factors, and thrombin induced platelet aggregation. This results in prolongation of the activated partial thromboplastin time.

Lepirudin (Refludan)

Lepirudin, a recombinant hirudin derived from yeast cells, is a highly specific direct thrombin inhibitor. It is indicated for anticoagulation in HIT and associated thromboembolic disease. Its action is independent of antithrombin III. Lepirudin blocks the thrombogenic activity of thrombin. It affects all thrombin-dependent coagulation assays (eg, aPTT values increase in a dose-dependent manner). Adjust the dose on the basis of aPTT ratios (target, 1.5-2.5 times normal) determined every 4 hours and then daily.

Antiplatelet Agents

Class Summary

Antiplatelet agents may be used to treat trauma patients in whom anticoagulation may be contraindicated. A Cochrane review found that the available evidence does not reliably establish whether anticoagulation is superior to antiplatelet therapy in patients with dissection.

Aspirin (Ecotrin, Empirin, Bayer, Anacin)

Aspirin blocks prostaglandin synthetase action and inhibits prostaglandin synthesis, preventing the formation of platelet-aggregating thromboxane A2. It acts on the hypothalamic heat-regulating center to reduce fever.

Clopidogrel (Plavix)

Clopidogrel selectively inhibits adenosine diphosphate (ADP) binding to platelet receptors and subsequent ADP-mediated activation of the glycoprotein (GP) IIb/IIIa complex, thereby inhibiting platelet aggregation.


Ticlopidine is second-line antiplatelet therapy for patients in whom aspirin is not tolerated or is ineffective.

Dipyridamole 200 mg/aspirin 25 mg (Aggrenox)

Dipyridamole-aspirin is a combination antiplatelet agent that takes advantage of the additive antiplatelet effects of the 2 drugs. Dipyridamole acts via the adenosine-platelet A2-receptor system, whereas aspirin inhibits platelet aggregation by causing irreversible inhibition of cyclooxygenase system, thereby reducing generation of thromboxane A2, a powerful enhancer of platelet aggregation and vasoconstriction.


Class Summary

Research into the use of thrombolytics for the treatment of extracranial internal carotid artery dissection has been limited; consequently, the usefulness and appropriateness of this approach have not yet been established.

Alteplase (Activase)

Alteplase, or tissue plasminogen activator (tPA), exerts an effect on the fibrinolytic system to convert plasminogen to plasmin. Plasmin degrades fibrin, fibrinogen, and procoagulant factors V and VIII. The serum half-life of alteplase is 4-6 minutes but is lengthened when the drug is bound to fibrin in clot.

Alteplase is used in the management of acute myocardial infarction, acute ischemic stroke, and PE. It must be given within 3 hours of stroke onset, and heparin and aspirin must not be given for 24 hours after its administration. The safety and efficacy of concomitant administration with aspirin and heparin during the first 24 hours after symptom onset have not been investigated. Exclude hemorrhage by means of computed tomography. If the patient is hypertensive, give labetalol 10 mg intravenously.

Reteplase (Retavase)

Reteplase is a recombinant tPA that forms plasmin after facilitating cleavage of endogenous plasminogen. In clinical trials, it has been shown to be comparable with tPA in achieving patency at 90 minutes. Heparin and aspirin are usually given concomitantly and afterwards.

Tenecteplase (TNKase)

Tenecteplase is a modified version of alteplase that is made by substituting 3 amino acids. It has a longer half-life than alteplase and thus can be given as a single bolus infused over 5 seconds (as opposed to the 90 minutes required for alteplase). It appears to cause less non–intracranial bleeding than alteplase but carries a comparable risk of intracranial bleeding and stroke.


Questions & Answers


How does carotid artery dissection begin?

Which conditions are a result of carotid artery dissection?

What is the association of ischemic stroke and carotid artery dissection?

Where does dissection of the internal carotid artery occur?

What is the role of minor trauma in the etiology of carotid artery dissections?

How is carotid artery dissection confirmed?

What is included in long-term monitoring of carotid artery dissection?

What are the pathophysiologic mechanisms of carotid artery dissection?

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What is the source of distal emboli in pathogenesis of carotid artery dissection?

What is the pathophysiology of carotid artery dissection aneurysmal dilation?

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What is the incidence of carotid artery dissection?

In which age groups is carotid artery dissection most common?

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What history is characteristic of carotid artery dissection?

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What is the goal of medical management of carotid artery dissection?

Which medications in the drug class Thrombolytics are used in the treatment of Carotid Artery Dissection?

Which medications in the drug class Antiplatelet Agents are used in the treatment of Carotid Artery Dissection?

Which medications in the drug class Anticoagulants, Cardiovascular are used in the treatment of Carotid Artery Dissection?