Introduction

Arterial dissections are produced either by intramural hemorrhage, which is probably due to bleeding from the vasa vasorum, or by penetration of blood into the arterial wall through a primary intimal tear. When the arterial wall is torn, blood frequently accumulates between the layers of the artery, and a “false lumen” is produced. The blood pressure in the false lumen increases and causes narrowing of the true lumen of the artery and a local thrombus can occur. The thrombus may secondarily causes embolization to the distal arteries. (₁, ₂)

Typical radiologic findings represent different stages of the disease, including a tapered occlusion of the internal carotid artery (ICA) or a long irregular stenosis with sudden reconstitution of the lumen often combined with an aneurysmal dilatation mostly near the base of the skull.

Carotid artery dissection (SCD) can happen after neck trauma, or spontaneously together with diseases such as fibromuscular displasia, Marfan syndrome, migraine, atherosclerosis, infection (syphilis). (₃, ₄) It is seen frequently in young adults. Extracranial SCD is more frequent in the 4 th decade, whereas intracranial SCD is more frequent in the 2 nd and 3 rd decades.

Case report

A 54 years old male patient referred with frequent syncope attacks. Bilateral murmur was found in the carotid artery during physical examination and carotid artery USG and MR angiography was performed. 70-90% narrowing in the right internal artery and dissection in the left main carotid artery was established in the patient, in which history did not reveal trauma (Figure 1).

Figure 1

Figure 1: Dissection in the left main carotid artery (MR angiography).

Anticoagulation therapy with a combination of heparin and clopidrogel was started. Surgical therapy was planned for the case, after the frequency of the syncope attacks increased.

The patient was operated under elective conditions, the left carotid artery was exposed and the internal and external branches were selectively identified. A longitudinal incision was performed on the carotid artery. The dissected plaque in the carotid artery was spotted (Figure 2).

Figure 2

Figure 2: Dissected plaque in the carotid artery.

As the stump pressure was not adequate (30 mmHg), intracarotid shunt was placed. Dissected plaque was endarterectomizedy. Carotid artery incision was closed with saphenous patch plasty.

Discussion

Carotid artery dissection is an important risk factor in the development of stroke in people below age 40. It can be frequently seen spontaneously in healthy people or with traumas like manipulations of the neck. It can be seen rarely in elderly people following atherosclerosis. (₃, ₄, ₅) It is more frequent in men (1, 5/1). It usually presents with headache, transient ischemic attack or stroke. Horner syndrome may be seen in 50% of the patients. Cranial nerve paralysis may be seen in over 10% of the patients. Doppler ultrasonography, carotid artery angiography, magnetic resonance imaging (MR), magnetic resonance angiography (MRI) may be used for diagnosis. MR and MRI combination gives better results compared to other diagnostic methods.

Anticoagulation therapy in SCD includes heparin, warfarin or clopidogrel. Anticoagulation therapy reduces thrombus formation, smooth muscle cell proliferation and decreases intima thickness. Antithrombocyte therapy must be started at the same time with anticoagulation therapy. (₅) Prognosis is usually good in SCD. Recanalization usually occurs between 7-30 days. In the healing process, fibromuscular dysplasia in the arteries, and as in residual mural defects, residual vascular anomalies may be seen. In such cases, recurrent or contralateral dissection risk increases. Recurrence risk in 10 years is 11%. Recurrence is seen more often in young patients compared to the elder ones. But prognosis is better in young patients and in extracranial dissection. Whereas in intracranial SCD the mortality rate is 75%. (₅, ₆)

Prognosis is usually good, recanalization occurs within 7-30 days. Anticoagulation must be started immediately for emboli originating from the thrombus. For therapy; carotid artery ligation, intracranial or extracranial by-pass, intracarotid stent, arterial reconstruction may be considered as well.(₃,₄,₅,₆)

Surgical intervention has been used for the repair of spontaneous dissections, but it is technically challenging and is associated with higher morbidity and mortality than the repair of atherosclerotic lesions of the carotid (₇, ₈, ₉). In one recent series, the surgical treatment of SCD in 49 patients was associated with a 12% incidence of stroke and death and a 58% incidence of cranial neuropathy. (₉) No examples of stroke or death associated with endovascular treatment of SCD have been reported in the literature.

According to the literature, acute carotid dissection should be treated predominantly by a conser- vative approach with anticoagulation for 6 months. Deteriorating or fluctuating neurologic symptoms and early occlusion of the dissected ICA might be an indication for early intervention to restore normal blood flow and to prevent further thromboembolic or ischemic damage. (₈)

We, in our case, considered surgical treatment (thrombectomy, endarterectomy) more appropriate, because of the recurrent syncope attacks, intensive thrombus in the region and no response to anticoagulation therapy. On the other hand, if SCD had not happened due to atherosclerosis, and was caused by manipulation of the neck, then, placing stent in the early period would have been more appropriate.

Correspondence to

Dr.Osman Tiryakioglu
Bursa Yüksek Ihtisas Eğitim ve Arastirma Hastanesi
Kalp ve Damar Cerrahisi Kliniği
16320 Bursa/Turkey
Tel: +90 224 3605050
E-Mail: tiryaki64@hotmail.com