Thrombosis of the Internal Carotid Artery Secondary to Soft Palate Injury in Children and Childhood

Abstract

Trauma to the soft palate is a uncommon event during childhood. Stroke following intraoral trauma is also rare, but has been well documented by the current literature as a potentially serious complication. In this article, we report 2 cases of posttraumatic internal carotid artery thrombosis depicted by imaging studies. We discuss pathogenesis, and the literature is reviewed.

Complications of Airway ManagementDiscussion

“…Mediastinitis and internal carotid thrombosis have also been described after oropharyngeal perforations, but these are exceedingly rare. 46,47 …”

Soft palate perforation during orotracheal intubation facilitated by the GlideScope videolaryngoscope

“…More serious complications of soft palate perforations include internal carotid artery thrombosis or pseudoaneurysm, thrombosis of the internal jugular vein, and mediastinitis [11][12][13]. Perforations near the midline (which occurred in the present case) are less likely to result in carotid artery injury, as contrasted with lateral lesions, which are anatomically closer to the internal carotid artery as it courses posteriorly to the tonsillar fossa [14].…”

Traumatic Thrombosis of Internal Carotid Artery Sustained by Transfer of Kinetic Energy

“…The middle cerebral artery is most frequently involved and examination shows contralateral hemiplegia, homonymous hemianopsia, and aphasia. 8 In our case, neurologic impairments occurred on the second day after the trauma caused by the kinetic energy of the bullet. Although the patient was hemodynamically stable and neurologically intact on the first day of his hospitalization, a distinct motor deficit had developed on his right upper and lower extremities, without ipsilateral amblyopia or aphasia on the second day.…”

“…In the literature, neurologic deficits have been described to appear at 1 hour to 6 days after trauma, which may depend on the migration of thrombus fragments. 3,8,9 First, the complete occlusion of the ICA occurred, then this occlusion could be compensated by a patent circle of Willis and no deficits would occur. If the collateral circulation is no longer capable of compensating the ischemia, the neurologic deficits would start.…”