Extracranial Carotid Injuries

The incidence of carotid artery dissection (CAD) in adults after blunt head and neck injury is estimated at 0.3 to 0.67%. In children, this injury seems to be significantly less common (estimated at 0.03%). However, because CAD can be clinically silent, its frequency may be underestimated. The traumatic event is usually that of hyperextension/rotation injury or a direct blow to the neck.

Extracranial CAD represents the most common location of traumatic vascular dissections in the head and neck area and is followed in frequency by the extracranial vertebral artery. Arterial dissection has been associated with several conditions including fibromuscular dysplasia, Marfan syndrome, cystic medial necrosis, oral contraceptives, and drug abuse. In connective tissue disease there is a structural defect leading to weakness in the arterial wall and predisposing to dissection either spontaneously or after a minor trauma. In other cases, environmental factors such as drug abuse can cause endothelial damage predisposing to this condition. On the other hand, traumatic dissection is also known to occur in otherwise healthy patients with no known risk factors.

CAD can be asymptomatic, especially in patients younger than 18 years of age. The dissection may remain in a subadventitial rather than subintimal plane, which may account for a delay in presentation ; a subadventitial dissection is believed to result in pseudoaneurysm with a potential for delayed presentation caused by emboli, whereas a subintimal one can lead to significant narrowing of the lumen with a more imminent clinical presentation ( Fig. 1 ). A review of the literature showed that in most cases the diagnosis was suspected and then confirmed only after a focal neurologic deficit consistent with a stroke or transient ischemic attack (TIA) in the presence of a history of trauma. Consequently, a high index of suspicion based on the mechanism of injury or physical signs and symptoms is of paramount importance to diagnose these lesions before the occurrence of severe neurologic deficit.

15-year-old boy with neck pain after football injury. ( A and B ) Lateral view of cerebral angiogram with (R) internal carotid injection shows a traumatic dissection with pseudoaneurysm of the extracranial ICA. ( C ) Lateral view of cerebral angiogram with (R) internal carotid injection at 6 months after endovascular treatment of the dissection using stent shows intimal healing and endothelialization.

One mechanism of injury that deserves a special emphasis in children is soft palate traumatic injury. Pens and sticks are the most frequent traumatic agents and the mean age of occurrence is 4 years. The proposed pathophysiology is related to an indirect compression of the internal carotid artery (ICA) against the skull base or against the upper cervical transverse process. Although CAD is rare after such an injury, it is potentially associated with high mortality and morbidity. The initial symptoms are usually mild, such as minor and transient oral bleeding, small pharyngeal wound, and tenderness at the angle of the mandible. The neurologic symptoms typically appear after a silent period that can last from a few hours to several days.

Intracranial Carotid Injuries

Although intracranial location is rare among CAD in adults, it seems to be common in children. In their review of the literature, Fullerton and colleagues found that 60% of the reported cases of CAD were intracranial. A male predominance seems to be attributable to a higher incidence of trauma among young males. Similarly, Oka and colleagues found that 25 of 45 patients who presented with intracranial carotid dissection were 18 years of age or younger. Although subarachnoid hemorrhage (SAH) is a real concern in these cases, strokes and TIAs remain the most common presenting feature.

Intracranial ICA dissection in children most commonly occurs spontaneously without any history of trauma. Among all reported cases of pediatric ICA dissection, the likelihood of intracranial dissection seems to be inversely proportional to the severity of trauma reported. Following severe trauma, 25% of the reported ICA dissections were intracranial, compared with 58% in the case of mild trauma, and 86% when no history of trauma is given. This observation favors a traumatic cause in extracranial dissections and a spontaneous cause in the intracranial ones (possibly precipitated by a minor trauma). A predisposing risk factor (collagen vascular diseases, connective tissue disorders, use of oral contraceptives, smoking, hypertension, and migraine) was reported in several cases; however, in most cases the cause remains unknown. Overall, the mortality seems to be significantly higher in intracranial dissections compared with extracranial ones.

Traumatic intracranial aneurysms are rare, comprising less than 1% of intracranial aneurysms in most large series. Histologically, they can be true aneurysms (disruption of intima and media, with an intact adventia) or false aneurysms (disruption of all 3 layers with formation of a contained hematoma). False aneurysms are considered the most common, although the relative incidence of these histologic types is unknown. Traumatic intracranial aneurysms in children are best categorized by mechanism of injury and location ( Table 1 ). Traumatic aneurysms can be caused by penetrating or nonpenetrating trauma. Aneurysms secondary to nonpenetrating trauma can be divided further into skull base and peripheral lesions. Peripheral traumatic aneurysms can again be divided into aneurysms of the distal anterior cerebral artery (ACA) secondary to trauma against the falcine edge ( Fig. 2 ), distal posterior cerebral artery secondary to trauma against the tentorial edge, and distal cortical artery aneurysms frequently associated with an overlying skull fracture ( Fig. 3 ). At the base of the skull, traumatic aneurysms most commonly involve the petrous and cavernous carotid artery and are almost invariably associated with a skull base fracture. Injury to the ICA at the skull base can cause immediate rupture, leading to a carotid-cavernous fistula or to massive epistaxis. Maurer and colleagues stated that the triad of unilateral blindness, basal skull fracture, and recurrent severe epistaxis is diagnostic of ICA injury at the skull base.

A 7-year-old boy after a motor vehicle accident. ( A ) Axial CT scan of the brain without contrast shows evidence of interhemispheric subarachnoid and intraparenchymal hemorrhage. ( B ) Lateral view of cerebral angiogram with (L) internal carotid injection illustrates a traumatic distal ACA aneurysm.

A 3-month-old baby in a suspected case of nonaccidental trauma. ( A ) Axial CT of the brain without contrast shows large (R) intraparenchymal hemorrhage. ( B ) Lateral view of cerebral angiogram with (R) internal carotid injection illustrates a traumatic aneurysm of a distal cortical branch of the middle cerebral artery. Although distal cortical aneurysms are frequently associated with skull fractures, no fracture was identified in this case.

Traumatic carotid-cavernous fistula (TCCF) is another rare entity that can occur after head injury. The estimated incidence ranges between 0.1 and 1%. In a recent study, a skull base fracture was documented in 67% of the cases, and among 312 patients with a fracture at the skull base, TCCF was found in 3.4%. TCCF most commonly results from a direct connection between the carotid artery and the cavernous sinus, leading to high-flow fistula. These lesions are unlikely to regress spontaneously and require prompt diagnosis and management. Clinically, these patients most commonly present with exophthalmos, bruit, chemosis, decreased vision, and limited ocular movements.

Extracranial Vertebral Injuries

Traumatic extracranial vertebral artery injuries may include dissections, pseudoaneurysms, or arteriovenous fistulas. Trauma remains the most common cause of dissection of the extracranial vertebral artery. Other causes include mainly vasculopathy and connective tissue disease. In some cases the dissection can be spontaneous, with no history of trauma or predisposing factors identified. In accordance with the adult literature, the most common segment involved is at the mobile C1-C2 level. The predilection for injury of this segment of vertebral artery has been observed in traumatic as well as in spontaneous cases. In most reported cases, vertebral dissections are preceded by a mild head or neck trauma. Typically, there is a history of neck hyperextension with torsion. When the dissection involves a segment below C2, an alternative mechanism must be sought because rotation between adjacent lower cervical vertebrae is minimal ( Fig. 4 ). Typically, more severe trauma with cervical spine fractures is found in these cases.

A 9-year-old boy after whiplash injury from a motor vehicle accident. ( A ) Axial and ( B ) sagittal CTA shows a dissection and intimal flap ( arrow ) of the proximal part of the right extracranial vertebral artery.

Arteriovenous fistulas involving the vertebral artery are rare lesions, defined by the presence of an abnormal shunt between the extracranial vertebral artery or 1 of its muscular or radicular branches and the adjacent perivertebral venous plexus. Approximately one-third of arteriovenous fistulas are asymptomatic, discovered incidentally after auscultation of a neck bruit. However, these lesions can have ischemic symptoms of vertigo, diplopia, and cephalgia secondary to arterial steal. The presence of myelopathy or cervical neuralgia is rare but can result after arterial blood reflux into spinal pial veins, causing venous hypertension (Foix-Alajouanine syndrome) or after root compression by engorged epidural veins. The main goal of treatment is closure of the arteriovenous fistula or pseudoaneurysm with preservation of the parent artery, frequently attained through an endovascular approach.

The natural history of extracranial vertebral artery dissection in children remains poorly understood. Late complications in children include pseudoaneurysm formation, thrombosis, and recurrent stroke. Stroke can result either from thrombosis leading to critical narrowing of the vessel or from emboli. The dynamic processes involved with vascular injury and healing may span years and result in variable outcomes. Because of the unpredictable evolution of these vascular changes, long-term clinical and radiologic follow-up are warranted.

Intracranial Vertebral Injuries

Intracranial dissection constitutes around 11% of reported vertebral artery injuries in children. Unlike intracranial carotid dissections, trauma remains the most common cause in intracranial vertebral dissections. Intracranial vertebral artery dissections also differ from extracranial dissections, which are usually associated with strokes, as mentioned earlier. Their prognosis is worse than extracranial dissections. Intracranial vertebral artery dissections are more susceptible to rupture than the extracranial segment, because the intracranial vertebral artery has thinner adventitia, and few elastic fibers in the media. SAH is commonly reported in these cases with a high risk of rebleed (in up to 30%–70% of cases in some series), resulting in high mortality and morbidity. Rare cases of nonaccidental trauma resulting in intracranial vertebral artery injury have been reported. The presence of retinal hemorrhage in these cases should be interpreted with caution as it can be simply the consequence of SAH (Terson syndrome).

Patients with vertebral artery dissections usually have a lucid interval after trauma until they present with symptoms. Ipsilateral headache, neck pain, dizziness, and neurologic deficits are the most common symptoms of vertebral artery dissections. Patients who develop neurologic deficit may have speech deficits, dysphagia, and vision defects.

Extracranial Vertebral Injuries

Traumatic extracranial vertebral artery injuries may include dissections, pseudoaneurysms, or arteriovenous fistulas. Trauma remains the most common cause of dissection of the extracranial vertebral artery. Other causes include mainly vasculopathy and connective tissue disease. In some cases the dissection can be spontaneous, with no history of trauma or predisposing factors identified. In accordance with the adult literature, the most common segment involved is at the mobile C1-C2 level. The predilection for injury of this segment of vertebral artery has been observed in traumatic as well as in spontaneous cases. In most reported cases, vertebral dissections are preceded by a mild head or neck trauma. Typically, there is a history of neck hyperextension with torsion. When the dissection involves a segment below C2, an alternative mechanism must be sought because rotation between adjacent lower cervical vertebrae is minimal ( Fig. 4 ). Typically, more severe trauma with cervical spine fractures is found in these cases.

A 9-year-old boy after whiplash injury from a motor vehicle accident. ( A ) Axial and ( B ) sagittal CTA shows a dissection and intimal flap ( arrow ) of the proximal part of the right extracranial vertebral artery.

Arteriovenous fistulas involving the vertebral artery are rare lesions, defined by the presence of an abnormal shunt between the extracranial vertebral artery or 1 of its muscular or radicular branches and the adjacent perivertebral venous plexus. Approximately one-third of arteriovenous fistulas are asymptomatic, discovered incidentally after auscultation of a neck bruit. However, these lesions can have ischemic symptoms of vertigo, diplopia, and cephalgia secondary to arterial steal. The presence of myelopathy or cervical neuralgia is rare but can result after arterial blood reflux into spinal pial veins, causing venous hypertension (Foix-Alajouanine syndrome) or after root compression by engorged epidural veins. The main goal of treatment is closure of the arteriovenous fistula or pseudoaneurysm with preservation of the parent artery, frequently attained through an endovascular approach.

The natural history of extracranial vertebral artery dissection in children remains poorly understood. Late complications in children include pseudoaneurysm formation, thrombosis, and recurrent stroke. Stroke can result either from thrombosis leading to critical narrowing of the vessel or from emboli. The dynamic processes involved with vascular injury and healing may span years and result in variable outcomes. Because of the unpredictable evolution of these vascular changes, long-term clinical and radiologic follow-up are warranted.

Intracranial Vertebral Injuries

Intracranial dissection constitutes around 11% of reported vertebral artery injuries in children. Unlike intracranial carotid dissections, trauma remains the most common cause in intracranial vertebral dissections. Intracranial vertebral artery dissections also differ from extracranial dissections, which are usually associated with strokes, as mentioned earlier. Their prognosis is worse than extracranial dissections. Intracranial vertebral artery dissections are more susceptible to rupture than the extracranial segment, because the intracranial vertebral artery has thinner adventitia, and few elastic fibers in the media. SAH is commonly reported in these cases with a high risk of rebleed (in up to 30%–70% of cases in some series), resulting in high mortality and morbidity. Rare cases of nonaccidental trauma resulting in intracranial vertebral artery injury have been reported. The presence of retinal hemorrhage in these cases should be interpreted with caution as it can be simply the consequence of SAH (Terson syndrome).

Patients with vertebral artery dissections usually have a lucid interval after trauma until they present with symptoms. Ipsilateral headache, neck pain, dizziness, and neurologic deficits are the most common symptoms of vertebral artery dissections. Patients who develop neurologic deficit may have speech deficits, dysphagia, and vision defects.