Traumatic Injury of the Carotid and Vertebral Arteries and their Neurointerventional Treatment

Abstract

Traumatic injuries of the carotid and vertebral arteries include direct carotid-cavernous fistula, intracranial pseudoaneurysm and arterial dissection, which cause a series of symptoms and may be life threatening. Computed tomographic angiography is the most common modality for initial screening and diagnosis. The subsequent management of any identified vessel injury, however, is not clearly defined. With the development of neurointerventional materials and technology, endovascular therapy is playing an important role in treatment of these neurovascular injuries. Balloon, coil, liquid embolic materials, covered stent and flow diversion have been effectively used in clinical practice. This chapter reviews the epidemiology, injury mechanism, clinical manifestations, classification system, diagnostic imaging and endovascular treatment of traumatic neurovascular injuries.

1. Introduction

Distribution of traumatic neurovascular injuries by location was 42% intracranial, 39% cervical, and 19% extracranial [1]. For the early recognition of lesions in different locations, imaging and clinical manifestations are the key to diagnosis. With regard to the treatment of these traumatic neurovascular diseases, the paradigm of treatment has shift from the destructive modality of carotid artery ligation or trapping to reconstructive modality of neurointerventional treatment. Endovascular treatment has been the first line treatment for traumatic injuries of the carotid and vertebral arteries including direct carotid-cavernous fistula, intracranial pseudoaneurysm and arterial dissection [1].

2. Traumatic carotid-cavernous fistula

Traumatic carotid-cavernous fistula (TCCF) represents abnormal vascular communications in the skull base between the carotid artery system and the adjacent cavernous sinus [2]. TCCF is the most common type of CCF [3, 4]. Within the cavernous sinus, the internal carotid artery (ICA) is bound by strong dural filaments and attachments, especially at its entrance and exit by its inferior and superior ascending segments [5]. Trauma can cause an intima-to-adventitia tearing in the ICA, leading to high-flow shunt between the cavernous sinus portion of the ICA and the cavernous sinus (Figure 1) [6]. TCCF also can be caused by iatrogenic injury from neurointerventional therapy, percutaneous treatment of trigeminal neuralgia, or transsphenoidal resection of pituitary tumor [6]. Endovascular recanalization of symptomatic chronic internal carotid artery occlusion (ICAOS) may cause CCF, because during the operation there may be severe ICA dissection with intimal inlet at the proximal end of ICA and adventitial outlet in ICA [6, 7]. In 1985, Barrow and his colleagues developed the classification system after extensive angiographic studies (Table 1) [8]. TCCF is of type A in Barrow’s classification system. A recent grading system of dural arteriovenous fistulas (DAVFs) was proposed by Zipfel GJ from Washington University in 2009 covering CCFs (Table 2) [9]. The Zipfel’s classification can stratify clinical status of cerebral and spinal DAVFs according to understanding of natural history in order to guide the appropriate evaluation and therapies of lesions [10].

Figure 1.

A woman presented a traumatic CCF treated with detachable coils. A: Lateral view of the left internal carotid artery angiogram showing a direct CCF of Zipfel’s type II with ophthalmic vein reflux (arrow). B: Lateral view of the left internal carotid artery angiogram showing complete obliteration of the CCF after coil embolization (arrow).

Type	Feeding arteries
A	the cavernous segment of the internal carotid artery
B	the branch of the internal carotid artery that supplies the dura mater
C	the branch of the external carotid artery that supplies the dura mater
D	the branch of the internal and external carotid artery that supplies the dura mater.

Table 1.

The classification system of CCF introduced by Barrow and his colleagues [8].

Type	Description
I	DAVFs are those that drain into the dural sinus with antegrade venous flow, e.g., the flow of the veins draining from the parenchyma or spinal cord into the dural sinuses or epidural veins is anterograde, a cavernous sinus fistula (CSF) without cortical or ophthalmic vein (OV) drainage.
II	DAVFs drain into dural sinus with retrograde venous flow, a CSF with OV drainage without cortical drainage. Type II DAVFs can drain into spinal perimedullary veins via dural sinuses.
III	DAVFs are those that drain into the pial veins and the spinal coronal or perimedullary veins, including CSF with cortical drainage. Type III can drain into spinal perimedullary veins and Type III spinal DAVFs can drain intracranially via pial veins.

Table 2.

The classification system of dural arteriovenous fistulas (DAVFs) introduced by Zipfel et al. in 2009 [9].

The clinical manifestations of TCCF are mainly related to venous hypertension or venous rupture. The venous drainage from the cavernous sinus to the superior and inferior ophthalmic veins causes prominent ocular symptoms, such as progressive pulsatile exophthalmos, conjunctival congestion or edema, in 90% patients [5]. In up to 50% patients, visual loss may result from decreased ocular or retinal perfusion and papilledema because of venous stasis [11]. Cranial nerve dysfunction in III, IV, VI can cause diplopia [11]. Intracranial pulsatile tinnitus was obvious in patients with inferior petrosal sinus. The increased venous pressure caused by cortical venous drainage leads to venous rupture and bleeding.

3. Traumatic neurovascular Pseudoaneurysm

Neurovascular pseudoaneurysm formation is the result of partial to complete disruption of the cerebral arterial wall, which ultimately leads to hematoma that is contained by the adventitia of the vessel wall or the perivascular soft tissues [12]. Traumatic ICA pseudoaneurysms are rare, mostly occurring in the petrous bone segment and cavernous sinus segment, accounting for less than 1% of all aneurysms [13]. Traffic accidents, stab wounds and falling injuries cause 51%, 12% and 8% of traumatic aneurysms, respectively [14]. The risk factors related to pseudoaneurysm formation mainly include male patient, young age, skull base fracture, intracranial hemorrhage and high-energy injury mechanism [15, 16]. The pressure of arterial pulsation can form pulsatile hematoma, so pseudoaneurysm is easy to rupture. It is reported that most pseudoaneurysms will bleed again 3–7 days after injury, and the mortality rate is as high as 50% [17].

Pseudoaneurysms of carotid and vertebral arteries caused by iatrogenic arterial injury have also been reported. The injury of ICA during the operation of pituitary tumor and complex cervical hypervascular tumor can cause carotid pseudoaneurysm (Figure 2). Michael J. Alexander and his colleagues reported a case of acute petrous carotid pseudoaneurysm after myringotomy procedure [18]. Surgical treatment of craniocervical junction lesions may lead to the vertebral artery pseudoaneurysm.

Figure 2.

A 59-year-old woman presented decreased vision in both eyes. A: Axial MR imaging, T2-weighted, showing an invasive pituitary tumor involving bilateral internal carotid arteries (arrows). During transnasal endoscopic pituitary tumor resection, the left internal carotid artery was injured. After hemostasis by tamponade, cerebral angiography was performed for endovascular intervention. B: Frontal view of the left carotid artery angiogram showing a giant pseudoaneurysm of the cavernous segment of the internal carotid artery (arrow). C: Lateral view of the unsubtracted image showing the Willis covered stent was released (arrow). D: Lateral view of the left internal carotid artery angiogram showing complete obliteration of the giant pseudoaneurysm (arrow). E: the histological examination confirmed pituitary adenoma (H-E staining).

Rupture of intracranial pseudoaneurysm will lead to subarachnoid hemorrhage, and the patient is characterized by severe headache, nausea, vomiting and meningeal irritation [19]. Giant hematoma can compress and damage adjacent nerves and blood vessels, resulting in ischemic symptoms of distal cerebral tissues. Moreover, pseudoaneurysm changes the blood flow, and easily forms thrombus in the aneurysm sac. When the thrombus falls off, it will cause the embolism of the distal artery leading to symptoms of stroke.

4. Traumatic arterial dissection

Dissections of the carotid and vertebral arteries are due to laceration that occur in the intimal layer, which leads to blood under arterial pressure to enter the wall of the vessel and form an intramural hematoma [20]. The incidence of traumatic dissection of the carotid and vertebral arteries has been reported to be 0.08–0.4% of overall traumatic populations [21]. The most common sites of traumatic carotid and vertebral arterial dissections are 2–3 cm from the distal end of the bifurcations of the carotid artery and at C1–2 level, respectively [22]. Iatrogenic neurovascular dissection is a common complication, which is mainly attributed to damage of intimal layer caused by manipulation of guide wire and catheters [23].

Headaches are often the first symptom in adults [24]. Children usually present with symptoms of cerebral ischemia and most commonly hemiparesis [21, 25]. Because children’s blood vessel is particularly vulnerable to stretching, and distorting forces. Trauma leads to a traumatic endothelial intimal lesion, followed by fibrin accumulation, leucocyte reaction, and the formation of thrombus to occlude the vascular lumen [26]. In patients presenting with sudden onset of unilateral Horner syndrome, the diagnosis of vertebral arterial dissection should be considered [27].

Early diagnosis of traumatic neurovascular dissection is necessary. Transcranial Doppler, computed tomography (CT), computed tomography angiography (CTA), and magnetic resonance imaging (MRI) can diagnose traumatic neurovascular diseases. Neurovascular dissection can be seen on T1 and T2 weighted images [28, 29]. According to a new study on the diagnosis of dissection, simultaneous non-contrast angiography and intraplaque hemorrhage (SNAP) sequence and T1-weighted volumetric isotropic turbo spin echo acquisition (T1-w VISTA) sequences in MRI can recognize intramural hematoma, intimal flap, and double lumen but SNAP images had significantly higher intramural hematoma wall contrast than T1-w VISTA images. Therefore, SNAP sequence can early diagnose the neurovascular arterial dissection [29]. Cerebral angiography is not only a diagnostic tool, but also the basis of endovascular therapy of cerebrospinal vascular disorders.

5. Neurointerventional treatment

5.1 Traumatic carotid cavernous fistula

With the development of endovascular neurosurgery, neurovascular therapy has become the main treatment of TCCFs [30, 31, 32, 33]. In the 1960s and early 1970s, it is known that Serbinenko had developed a detachable, flow-directed balloon that was used to treat TCCF while preserving the carotid artery [33]. In China, detachable balloon was used to treat TCCF since the late of 1980s (Figures 3 and 4). Coil embolization may be considered in case of the small fistula (Figure 1). Temporary balloon or neurostent can be placed in the parent artery to prevent the coil from falling off and occluding the distal intracranial circulation [31]. But, balloon or coil embolization might cause cranial nerve palsy [32]. The detachable balloon or the application of the coil can occlude the fistula, which can maintain the patency of the ICA of the affected side in 70–90% cases (Figure 5) [33]. Transarterial embolization of TCCFs using detachable balloons or coils was considered to be a feasible, effective, and safe method for the treatment [34].

Figure 3.

Molds used by Prof. Zhongxue Wu for making detachabel latex balloons in the year of 1988.

Figure 4.

A 40-year-old man presented a traumatic CCF treated with detachable balloon in the year of 1988. A: Lateral view of internal carotid artery angiogram showing a direct CCF of Zipfel’s type III with cortical veins reflux (arrow). B: Lateral view of internal carotid artery angiogram showing complete obliteration of the CCF after balloon embolization (arrow).

Figure 5.

A 27-year-old man presented a traumatic CCF treated with Willis covered stent. A: Lateral view of the right internal carotid artery angiogram, early arterial phase. B: Lateral view of the right internal carotid artery angiogram, late arterial phase. Showing a direct CCF of Zipfel’s type III with pial veins reflux (arrow). C: Lateral view of the unsubtracted image showing the inflation of the balloon(arrow). D, lateral view of the unsubtracted image showing the Willis covered stent was released (arrow). E: Lateral view of the right internal carotid artery angiogram showing complete obliteration of the CCF after treatment (arrow).

Two liquid embolic agents, n-butyl cyanoacrylate (nBCA) (Codman Neurovascular, Raynham, Massachusetts) and ethylene-vinyl alcohol copolymer (EVOH) (Onyx, ev3, Irvine, California) have become good choices. TCCF can be cured by transvenous catheterization of the cavernous sinus and embolization using Onyx assisted with transient balloon occlusion of the ICA at the fistula site. The Willis covered stent (Micro-Port, Shanghai, China) can protect the parent artery and the mid- and long-term occlusion rate is reported to be 95.7% (Figure 6) [35]. Flow diversion is also an effective treatment. Its principle is that a flow diversion in the parent artery can reduce and disturb blood flow in the aneurismal sac causing blood stagnation and thrombosis [36].

Figure 6.

A 27-year-old woman presented a traumatic CCF treated with detachable balloon. A: Lateral view of the left internal carotid artery angiogram showing a direct CCF of Zipfel’s type II with ophthalmic vein reflux. B: Lateral view of the left internal carotid artery angiogram showing complete obliteration of the CCF after detachable balloon embolization.

5.2 Neurovascular Pseudoaneurysm

Endovascular treatment for neurovascular pseudoaneurysm mainly includes liquid embolic agent, balloon or stent assisted coil embolization, Willis covered stent and flow diversion. The Onyx can be injected into the pseudoaneurysm cavity until the aneurysm cavity is completely closed [37]. Balloon or stent can assist coil embolization to prevent the coil from falling out. Willis covered stent can be a curative option and is placed in the parent artery to occlude the neck of pseudoaneurysm. When there are important arterial branches in the lesional area, the application of Willis covered stent may sacrifice the functional branches and cause symptoms of cerebral ischemia. Therefore, its use is limited to the area where no functional branches are found [38].

5.3 Arterial dissection

Coil occlusion of the parent artery is sufficient to prevent subsequent rupture of arterial dissection [39]. This procedure can be performed in the ICA with an open circle of Willis or a vertebral artery with adequate contralateral flow [40]. If the collateral circulation is insufficient, endovascular reconstruction therapy, such as covered stent or flow diversion, may be helpful to preserve the luminal patency and prevent further rupture of the arterial dissection [39].

6. Conclusion

Traumatic injury of internal carotid and vertebral arteries mainly include TCCF, pseudoaneurysm and arterial dissection, which can cause pain, bleeding, edema, diplopia, visual impairment, and death. Cerebral angiography is the gold standard of diagnosis and endovascular treatment is the main method for traumatic neurovascular disease. This chapter helps to understand how endovascular treatments are slowly becoming the norm.