TCVI occurs in about 1% of all blunt trauma patients. ¹ Carotid injury occurs in 0.1 to 1.55% of blunt trauma patients. Vertebral injury occurs in 0.2 to 0.77% of trauma patients.

Motor vehicle collisions account for 41 to 70% of cases. ² Other mechanisms of injury include assault, pedestrian versus vehicle, and hanging.

The injury may result from a direct vascular blow, extreme hyperextension/rotation, or laceration by bony fragments.

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  Independent risk factors for carotid artery injury include: closed head injury (with Glasgow Coma Scale [GCS] score ≤ 6), petrous bone fracture, diffuse axonal injury, and LeFort II or III fracture.

  
  
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  Cervical spine injury—C1, 2, or 3 fracture; transverse foramen fracture; or subluxation—is an independent risk factor for vertebral artery injury.

The most commonly used classification system divides TCVI into five types ( Table 9.1 ). ^{3 , 4}

Arterial dissection (type I and II injuries)

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  Results from rapid deceleration of the body with subsequent stretching of the involved vessel.

  
  
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  Two mechanisms have been proposed ( Figs. 9.1 and 9.2 ): (1) intramural hematoma formation between layers of the artery wall; and (2) an intimal tear leading to exposed subendothelial collagen, initiating platelet aggregation and leading to thrombus formation.

  
  
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  Specific segments of the carotid and vertebral arteries are more vulnerable to dissection than others:

  
  
  
  
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    Carotid: the distal cervical internal carotid artery (ICA), where the ICA is stretched over the lateral masses of the cervical spine, is at risk. Injury typically results from hyperextension and rotation to the contralateral side.

    
    
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    Vertebral: the V2 and V3 segments, as the vessel travels through the transverse foramina of C6 to C2 and around the lateral mass of C1, are at risk. V2 segment injuries typically have an associated cervical spine injury, whereas injury to V3 or V4 segments may occur in isolation.

Traumatic aneurysm (type III injuries)

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  This results from disruption of the internal elastic lamina, which weakens the vessel wall and leads to expansion of the adventitia.

  
  
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  The term pseudoaneurysm implies a complete disruption of all layers. However, dissecting aneurysms may contain a complete artery wall. So, the term traumatic aneurysm is more appropriate.

  
  
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  Traumatic aneurysms of the carotid artery typically occur in the mid- or upper cervical ICA and account for 15 to 44% of TCVIs. A portion (7.6%) of carotid injuries that initially consist only of luminal irregularity later develop into traumatic aneurysms. ⁵

  
  
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  Traumatic aneurysm accounts for only 4.8% of vertebral artery TCVIs.

  
  
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  Unlike spontaneous dissecting aneurysms, traumatic aneurysms tend to persist and often enlarge over time. ⁶

Occlusion (type IV injuries)

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  Traumatic vascular occlusion may occur at the time of the injury or may arise in a delayed fashion as the result of thrombus formation at the site of an arterial dissection.

  
  
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  Occlusion is much less common than arterial dissection.

  
  
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  Patients may present with symptoms of ischemic stroke or remain asymptomatic if good collateral circulation exists.

Arteriovenous fistulas (type V injuries)

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  Present with tinnitus, cervical radiculopathy, heart failure, hemorrhage, steal, intracranial venous hypertension, or embolic stroke.

Type I traumatic cerebrovascular injury (Fig. 9.1).

Type II traumatic cerebrovascular injury (Fig. 9.2).

Penetrating neck trauma is accompanied by vascular injury in 20% of patients. ⁷

Seventy-five percent of these vascular injuries are attributable to stabbing. Gunshot wounds account for the remainder. ⁸

The venous system is more commonly affected but less likely to require treatment.

Carotid artery injury due to penetrating neck trauma results in vessel occlusion in 36% of cases and traumatic aneurysm formation in 33% of cases. ⁹ As compared with blunt extracranial carotid injury, the rate of ischemic stroke with a penetrating injury is lower, but the mortality rate is higher. ¹⁰

Penetrating extracranial injuries can be classified by type:

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  Arterial laceration

  
  
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  Dissection

  
  
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  Occlusion

  
  
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  Aneurysm

  
  
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  Arteriovenous fistula. Fistulas may be either carotid-cavernous (discussed in the blunt intracranial injury section) or vertebral-venous in nature. The latter may present as tinnitus, cervical radiculopathy, heart failure, hemorrhage, steal, intracranial venous hypertension, or embolic stroke. Slow-flow fistulas may be followed expectantly with serial angiography every 12 months in asymptomatic and otherwise clinically stable patients. High-flow fistulas may cause brainstem or spinal cord symptoms due to pressure from arterialization of the cervical venous plexus. Posterior circulation ischemia may result from diversion of flow.

Physical examination is the most important part of the diagnostic evaluation for penetrating cervical vascular injury (see box below).

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  If physical signs of vascular injury are present, there is a 90% chance of a major arterial or venous injury. ¹¹

  
  
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  In the absence of physical signs, the risk of major vascular injury falls to 0.9%. ¹¹

Data regarding the overall incidence of blunt intracranial TCVIs is lacking. Such injuries are substantially less common than blunt extracranial injuries.

GCS score < 8 and the presence of facial fractures are independent risk factors for blunt intracranial arterial injury. ¹²

Blunt intracranial injuries may be classified by type:

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  Dissection

  
  
  
  
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    May be associated with trivial trauma or blunt injury in closed head trauma, as well as penetrating injury.

    
    
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    The most common affected sites are the supraclinoid ICA and the intradural portion of the vertebral artery.

    
    
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    Intracranial dissection may be associated with underlying vascular abnormality of the cerebral arteries, including fibroelastic thickening and congenital deficiency with disruption of the internal elastic lamina. Associated conditions that may predispose one to dissection in the setting of blunt injury include fibromuscular hyperplasia, cystic medial degeneration, Marfan syndrome, homocystinuria, and syphilis.

    
    
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    Patients may present with unilateral headache, cranial nerve palsy (from mechanical compression or neurapraxia from the expanded artery or transient impairment of blood supply), Horner′s syndrome, and/or focal cerebral ischemia.

  
  
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  Aneurysm

  
  
  
  
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    Traumatic aneurysms account for < 1% of all intracranial aneurysms in adults, but comprise about one-third of pediatric aneurysms. ¹³

    
    
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    Aneurysms in this setting result from rapid deceleration, which causes sudden brain movement and arterial wall injury from stationary structures such as the skull base or falx cerebri.

    
    
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    Pericallosal branch (anterior communicating artery [ACA]) aneurysms, resulting from collision between the artery and the edge of the falx, are most common.

    
    
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    Basilar artery and petrocavernous segment aneurysms often are associated with skull base fractures.

  
  
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  Arteriovenous fistula

  
  
  
  
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    Arteriovenous fistulas—arising from either the carotid or vertebral circulation—are present in 4% of all patients with blunt TCVI. ¹⁴

    
    
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    The most common intracranial traumatic fistula is a direct carotid-cavernous fistula (CCF).

    
    
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    Seventy-five percent of direct CCFs occur secondary to trauma.

    
    
    
    
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      Most are associated with facial or skull base fractures.

      
      
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      Iatrogenic injury—due to transsphenoidal surgery, skull base surgery, or percutaneous lesioning of the trigeminal ganglion—also accounts for a significant number of traumatic fistulas.

    
    
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    Patients typically present with cavernous sinus syndrome (see box on next page).

    
    
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    Indications for urgent treatment include:

    
    
    
    
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      Increased intracranial pressure or the presence of cerebral cortical venous hypertension

      
      
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      Progressive visual deficit

      
      
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      Increased intraocular pressure

      
      
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      Worsening proptosis

Penetrating intracranial injury may result in dissection, occlusion, traumatic aneurysm, or arteriovenous fistula. All have been discussed previously. However, the formation of traumatic intracranial aneurysms secondary to penetrating injury warrants further consideration.

Traumatic intracranial aneurysms can result from direct injury by missile, bullet, or bone fragments. Aneurysms are present in:

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  2.7% of patients with missile injuries to the head. ¹⁶

  
  
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  12% of patients with stab wounds to the head. ¹⁷

Aneurysms may appear as soon as 2 hours after the injury and are most commonly found along branches of the middle cerebral artery (MCA) (as opposed to intracranial aneurysms due to blunt trauma, which are most often identified on branches of the ACA).

Factors that should raise suspicion for a traumatic aneurysm include:

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  Missile or bone fragments close to the skull base

  
  
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  Large hematoma at the missile entrance wound

Though aneurysms occurring secondary to trauma are believed to carry a high risk of rupture, one study found that 19.4% of these lesions healed spontaneously and shrank or disappeared altogether on subsequent angiograms. ¹⁸