Traumatic dissections of the extracranial internal carotid artery

Abstract

Traumatic dissections of the extracranial internal carotid artery (ICA) in 18 patients aged 19 to 55 years were studied. All had suffered blunt head or neck injury of marked or moderate severity; motor-vehicle accidents were the leading cause of the injury. Delayed focal cerebral ischemic symptoms were the most common presenting symptoms. Less commonly noted was focal unilateral headache associated with oculosympathetic paresis or bruit. Following a head injury, the abrupt onset of focal cerebral symptoms after a lucid interval should raise the suspicion of arterial injury, particularly when computerized tomography fails to show abnormalities that would explain the evolving neurological deficits on the basis of direct trauma to the brain. Unilateral headaches, oculosympathetic palsy, and bruits also help in establishing the diagnosis. Focal cerebral ischemic symptoms may develop months or years after the initial trauma. These delayed symptoms are caused by embolization from a thrombus within a residual dissecting aneurysm. Common angiographic findings, in decreasing order of frequency, are: aneurysm, stenosis of the lumen, occlusion, intimal flap, distal branch occlusion (embolization), and slow ICA-to-middle cerebral artery flow. Although two patients died as the result of massive cerebral infarction and edema and some were left with severe neurological deficits, most made a good recovery. Residual dissecting aneurysms and occlusion seem to occur more frequently with traumatic dissections than with spontaneous dissections of the extracranial ICA.

Endovascular Repair of Extracranial Carotid Artery Dissection: Current Status and Level of Evidence

“…The treatment of extracranial carotid artery dissection with anticoagulation has been proved to be effective, with an approximate 50%-70% arterial recanalization rate and a 10% risk of late neurologic deficits (32)(33)(34)(35)(36)(37)(38)(39). However, the high incidence of stroke within 30 days of the dissection (21%-41%) and the approximately 20% mortality rate make a compelling argument for alternative, more successful treatment strategies for overcoming these medical impasses (37).…”

Blunt Cerebrovascular Injuries

“…12 The most common mechanism causing CAI is hyperextension resulting from the stretching of the carotid artery over the lateral articular processes of C1-C3. [13][14][15][16][17][18] Vertebral artery injuries are likely a combination of direct injury, due to associated fractures of the vertebrae involving the transverse foramen through which the artery courses, and hyperextension-stretch injury due to the tethering of the vertebral artery within the lateral masses of the cervical spine. Regardless of mechanism, there is intimal disruption of the carotid or vertebral artery.…”

“…This time frame appears to range from hours up to 14 years, but the majority of patients seem to develop symptoms within 10 to 72 hours. [3][4][5]17,18,20,21 Diagnosing BCVI during this "silent period" affords the opportunity for treatment prior to neurologic sequelae.…”

Traumatic Cervical Internal Carotid Artery Occlusion in an Infant-Case Report-

“…Type 2 injury, as in our case, is considered to result from dissection or subintimal hemorrhage of the carotid wall. 2,6) Obstructions are often located at or just above the bifurcation of the common carotid artery in this type of traumatic ICA occlusion, in contrast to the ICA occlusion due to atherosclerotic change. 4,11) Traumatic ICA occlusion often leads to a poor outcome and the mortality is 37%, regardless of the mechanism of occlusion.…”

“…Neurological deficits appear at more than 6 hours after trauma. 2,4,[6][7][8]11) Delayed onset may be a consequence of progressive occlusion caused by dissection or subintimal hemorrhage. 2,6) Embolism is another cause of neurological deterioration after traumatic ICA occlusion, even in patients with sufficient collateral circulation.…”