Dissections: Endovascular Management
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TRAUMATIC CAROTID DISSECTIONS
Dissection of the cervical and intracranial arteries occurs following disruption of the intima and media of the vessel wall. Such disruption typically results in hemorrhage into the vessel wall and subsequent reduction in the true lumen diameter of the native vessel, in turn potentially occluding the vessel. Although several disorders of collagen and vessel wall composition exist that portend a higher incidence of vessel dissection, one of the most common causes of vessel dissection is craniocervical traumatic injury. In a series of 2000 traumatic head injuries, the incidence of carotid injury was 0.5%. Given the incidence of more than 1.5 million traumatic head injuries annually, there likely exists a substantial patient population with traumatic arterial lesions potentially resulting in stroke. The incidence of carotid dissection has been reported to be 2.6 per 100, 000 persons. Dissections have been reported to be responsible for 20% of strokes in patients under 30 years of age with neurological mortality ranging from 20 to 40% and morbidity as high as 80%. It is interesting to note that traumatic lesions to the carotid artery are often missed as less than one-half of the patients will have cutaneous manifestations, and often a plethora of other severe injuries complicate the diagnosis.
Patients with acute dissection typically present with symptoms related to ischemia or thromboembolic complications. Carotid dissections may typically cause visual scotoma, contralateral hemiparesis and hypesthesia, or aphasia (with left hemispheric events). Additionally, a Horner’s syndrome (miosis, ptosis, and anhidrosis) may occur ipsilateral to the dissection as a result of damage to the sympathetic nerve fibers. Often a partial Horner’s syndrome, without anhidrosis, is appreciated as the dissection occurs distal to the common carotid artery bifurcation, usually at the C2-C3 vertebral level. Although patients with dissections typically follow a benign course if the presenting symptoms are localized to headache or neck pain, 15% may progress to severe morbidity and/or death. Vertebrobasilar artery dissections, which may accompany traumatic carotid dissections, often result in temporary loss of consciousness, cranial nerve palsies, vertigo, or bilateral motor-sensory dysfunction.
ENDOVASCULAR TREATMENT OF DISSECTIONS
Before endovascular techniques were routinely used for the treatment of arterial dissections, medical and surgical modalities were employed to treat symptomatic patients. Medical management involved anticoagulation therapy with warfarin, and surgical options were reserved for patients who had persistent neurological events despite anticoagulation therapy. These surgical approaches clearly depended on the sequelae of the dissection. For ischemic symptoms referable to severe residual arterial stenosis resulting from a healed dissection, extracranial-to-intracranial arterial bypass surgery was done to augment blood flow to a hypoperfused region. Bypass grafting in conjunction with vessel sacrifice was a treatment option in the setting of persistent emboli from dissecting aneurysms. In a review of 96 patients, 86% of the group managed without surgery did poorly versus 53% in the surgical group.
As carotid artery stenting has become increasingly popular, use of this technology has been investigated for the treatment of symptomatic carotid and VA dissections. In one report by Liu et al., stent placement was performed for symptomatic artery dissections in seven patients. All seven patients remained symptom-free during the follow-up period (average, 3.5 years). Malek et al. described similar findings in a cohort of 10 patients with carotid dissection. Interestingly, the group was able to use multiple overlapping stents to recanalize acute vessel occlusions or “string-signs” resulting from severe dissections.
Endovascular salvage procedures have recently been described for iatrogenic intracranial and extracranial dissections. The frequency of these lesions is likely to increase as more clinicians routinely practice intracranial interventional techniques. In a review of more than 3,000 neurointerventional and diagnostic procedures involving the intracranial circulation, Cloft et al. noted iatrogenic dissections in 0.4% of this cohort.165 These authors found that the clinical course was benign for most patients with iatrogenic dissections of the carotid artery. On the contrary, another group found that dissections of the intracranial VA may result in significant neurological morbidity such as Wallenberg’s syndrome, isolated lower cranial neuropathy, Horner’s syndrome, and hemisensory dysfunction. In a paper by Dorros et al., intracranial carotid angioplasty was performed for a flow-limiting petrous carotid stenosis. Following the angioplasty, the patient was noted to have a dissection that was treated with emergent deployment of a coronary stent. The patient remained asymptomatic without the need for warfarin therapy.
Dissecting aneurysms of the intracranial anterior and posterior circulation portend a high rate of recurrent hemorrhage and subsequent neurological morbidity. This poor prognosis is likely because these aneurysms occur after acute disruption of the integrity of the vessel wall, often resulting in a false aneurysm (recanalized thrombus). The incidence of VA dissecting aneurysms is difficult to determine, but some groups have found that the incidence ranges from 20 to 40%. In a report by Kurata et al., coil embolization was used to occlude dissecting aneurysms of vertebral arteries that had hemorrhaged. The patients treated had no further hemorrhages and good outcomes. It is important to note that before a dissecting aneurysm of the intracranial VA is treated, balloon test occlusion is necessary to determine tolerance to potential sacrifice of the parent vessel. Additionally, the location of the dissection in relation to the posterior inferior cerebellar artery is important to note, as well as the caliber of the contralateral VA, the posterior communicating arteries, and the presence of any vertebral origin disease. Often, anatomic constraints such as hypoplastic contralateral vertebral arteries and absent or small posterior communicating arteries may prevent vessel sacrifice of the dominant VA for treatment of a dissection. Thus, alternative interventions must be found for patients who remain symptomatic from their dissecting VA aneurysm (usually from thromboembolic debris released from the pseudoaneurysm).
An emerging technology for the treatment of dissecting aneurysms (also discussed under the section on aneurysms) is the use of low-porosity stents. Stents reconstitute the parent vessel lumen, divert the jet of blood away from the inflow zone, and attempt to re-establish laminar flow in the direction of the parent vessel. Horowitz et al. described the use of stents for the treatment of cervical and extracranial pseudoaneurysms. Our group has treated dissecting aneurysms in four patients with intravascular stents. Although excellent radiographic obliteration of the aneurysm was observed in two cases, the technique does have some limitations. In one case, stent thrombosis and subsequent brainstem infarction developed nearly 3 months after treatment in a non-compliant patient with a history of cocaine abuse. We believe the combination of not adhering to an antiplatelet regimen, in conjunction with cocaine ingestion (a potent platelet aggregator), resulted in delayed onset of stent thrombosis. Another limitation of current stent technology involves the pliability of low-porosity stents. Low-porosity stents are advantageous as they significantly reduce the inflow and outflow of blood, which (theoretically) should lead to thrombosis. Unfortunately, as porosity declines, the rigidity of the stent increases, lessening the likelihood of successfully navigating the stent through successive tortuosities.
One approach to bypassing some of the extracranial vertebral tortuosities involves performing a cut-down on the VA at the craniocervical junction or at the C1-C2 vertebral level. Once this region of the VA is adequately exposed, a sheath can be inserted into the VA. This surgical exposure allows the sheath to be inserted in close proximity to the target lesion, avoiding many tortuosities proximal to the insertion point. Thus, less mechanical energy is translated into the sheath, catheters, and stent-delivery apparatus. Additionally, the ability to maneuver the stent may be increased by the mechanical advantage gained by inserting the sheath relatively near the dissection in the intracranial circulation. Meticulous surgical technique is essential to avoid infection, injury to the VA, iatrogenic dissection during sheath insertion, and loss of sheath position in the vessel. Should the patient’s anatomy preclude the delivery of a rigid, low-porosity stent, stent-assisted coiling may be used. Although this technique has been described by others for wide-necked or fusiform aneurysms of the posterior circulation, one must be careful when deploying coils in what may be a false lumen.
Reprinted with permission from Mohr JP, Choi DW, Grotta JC, Weir B, Wolf PA (eds): STROKE: PATHOPHYSIOLOGY, DIAGNOSIS, AND MANAGEMENT (4th edition), pp. 1475-1520 (chapter 78), Copyright Elsevier 2004. Permission has been granted to reproduce this material in online electronic format for non-exclusive world English rights.
- Pham MH, Rahme RJ, Arnaout O, et al. Endovascular stenting of extracranial carotid and vertebral artery dissections: a systematic review of the literature. Neurosurgery. Apr 2011;68(4):856-866