Endovascular Treatment of Head and Neck Bleeding

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Chapter 92 Endovascular Treatment of Head and Neck Bleeding

Alexandros D. Zouzias, Paul Schmitt, Chirag D. Gandhi, Charles J. Prestigiacomo

The role of endovascular therapy in the treatment of neurologic disease has had a relatively short history. Since its initial introduction by Luessenhop and Spence in 1960, the technological improvements and subsequent indications for the use of endovascular techniques have evolved dramatically.¹ The advances in polymer science, device design, and technique development have resulted in the maturation of this specialty and its integration into neurosurgical management. Indeed, the last 20 years have demonstrated endovascular surgical neuroradiology’s complementary role in several vascular disorders. One of the areas where this complementary relationship exists is in the treatment of traumatic injury to the vessels of the head and neck.

Though the incidence of blunt traumatic vascular injury is relatively rare—variably reported between 0.1% and 0.45% in trauma centers treating carotid injury—such injuries can be associated with high morbidity and mortality that have been reported from 20% to 40%.² Intracranial injury secondary to blunt trauma or penetrating trauma can range from subintimal dissection with possible ischemia, or pseudoaneurysm formation with potential rupture, to acute or delayed traumatic aneurysm formation and frank transection with subsequent hemorrhage or arteriovenous fistula formation. The role of endovascular therapy in the setting of these pathologic entities not only has grown but also has expanded into areas where previous treatment options were very high risk or unavailable. This chapter thus discusses the role of endovascular therapy as it relates to the multidisciplinary treatment of acute vascular injury of the head and neck.

Evaluating Effects of Ischemia

Basic principles of surgical management should be followed prior to advancing to therapeutic interventions. Control of airway and breathing, along with establishment of venous access for appropriate fluid resuscitation, are a priority.³ The patient is usually under minimum sedation, allowing accurate neurologic assessment. If complete internal carotid artery (ICA) occlusion is necessary, collateral supply should be measured prior to occlusion to determine the effects of ischemia at the distal ICA segment. The standard procedure for assessing collateral sufficiency in the stable patient is balloon test occlusion (BTO), as introduced by Serbinenko.⁴^–⁷ BTO of the ICA is designed to identify patients who are at risk for ischemic events following permanent ICA occlusion and to minimize the associated rates of complication.⁸ The location of the balloon at the time of inflation depends on the location of the ICA lesion and the type of balloon, but the procedure should always be performed under road map guidance. Modern BTO implies simultaneous anatomic and physiologic assessment before and after inflation.

Anatomic testing consists of visualization of collateral circulation through the circle of Willis. Collateral circulation may be assessed in a number of ways, including transcranial Doppler sonography, electroencephalography, quantitative cerebral blood flow (CBF) analyses, and qualitative CBF analyses. Any of these studies represent an attempt to identify those patients with compromised hemodynamics despite a normal examination.^5,⁶ There has also been success with use of delayed venous phase protocols in assessing collateral adequacy.⁸ A negative test occlusion, according to venous phase protocol, is when the delay of venous drainage between the territory of the injected artery and the occluded hemisphere is 2 to 3 seconds or less. The major advantages of relying on venous phase criteria are that the neurologic assessment is unnecessary and the patient may be placed under general anesthesia.

Physiologic testing traditionally includes a neurologic assessment (standard Wada) with or without electroencephalogram (EEG) monitoring.^5,⁹ EEG monitoring is primarily used for patients in whom the neurologic assessment may not be accurate. The addition of physiologic stressors—such as a hypotensive challenge, acetazolamide, or carbon dioxide challenge—represent an effort to identify patients who have a deficient circulatory reserve that would not be elucidated in a normal physical exam. A hypotensive challenge is performed with agents such as nitroprusside or labetalol, and blood pressure is brought down to 75% to 66% of baseline for 20 minutes. Confounding factors such as tumor-related deficits, hemorrhage- or vasospasm-related infarction, and embolic infarction have brought the predictive value of these challenges into question.⁴ In patients who tolerate BTO, the surgeon can proceed to carotid occlusion. If technical problems occur, or if the patient demonstrates evidence of ischemic deficits, patency of the carotid artery must be maintained.¹⁰

Blunt and Penetrating Injuries of the Head

Blunt and penetrating trauma of the head can result in acute or delayed vascular injuries ranging from life-threatening hemorrhage, to infarction secondary to occlusion, to delayed hemorrhage from ruptured traumatic aneurysms. Because of this extreme variation in presentation, understanding the mechanisms of injury and anticipating and assessing for these injuries, whether acute or delayed, are critical in mitigating the potentially lethal sequelae.

Penetrating injuries of the head can result in a spectrum of vascular lesions, which partly depend on the anatomic structures involved, as well as the mechanism of injury. Laceration of an intracranial artery, such as the supraclinoid carotid artery, can be a fatal event, whereas a similar laceration of the cavernous portion of the ICA may result in a high-flow carotid–cavernous fistula (CCF) that is not uniformly fatal. Penetrating injuries to the more posterior regions of the skull or to the anterior portions of the face may result not only in exsanguinations but also in arteriovenous fistulas. Blast or cavitation injury from a gunshot wound can result in an occlusive dissection and subsequent cerebral infarction or in delayed formation of traumatic aneurysms. A keen awareness of the potential for these sequelae of trauma is important in determining the assessment and subsequent treatment paradigm.

Carotid–Cavernous Fistulas

CCF or caroticocavernous fistula is the result of a tear of the ICA that allows it to form a high-flow, low-resistance fistula with the venous system of the cavernous sinus.^4,¹¹ A CCF can be either direct or indirect. In a direct carotid–cavernous fistula (DCCF), blood is shunted from the ICA into the sinus; in an indirect carotid–cavernous fistula (ICCF), there is a dural arteriovenous communication and a slower flow rate. Barrow et al.¹² classified direct, trauma-induced, high-flow shunts between the ICA and the cavernous sinus as a type A fistula. In contrast to dural-based fistulas, spontaneous cure of a type A CCF is rare.^13,¹⁴ However, rare cases of spontaneous DCCF are found in cases of ruptured intracavernous ICA aneurysms and in patients with collagen vascular disease.¹⁵ A comprehensive description of the dural CCF is beyond the scope of this chapter.

The pressure gradient in a DCCF results in reversal of flow into the superior ophthalmic vein and superficial middle cerebral vein, with concomitant rapid shunting to the inferior petrosal sinus and the pterygoid vein.^16,¹⁷ Classical presentation of DCCF is a pulsating exophthalmos with orbital bruit. Other symptoms may include visual changes, orbital pain, and proptosis. It is evident that most symptoms are a direct result of arterialization of the cavernous sinus and draining orbital veins.¹⁸^–²⁰ Some common sequelae encountered include venous congestion, hemorrhage, headache, tinnitus, vertigo, and cranial nerve palsies.²¹ In patients showing evidence of arterial steal phenomenon, such as cerebral hypoperfusion with subsequent focal neurologic deficits, urgent intervention is indicated.

Management of CCF depends on the stability of the patient, the anatomy of the fistula, and the hemodynamics involved in the system. Ideally, the focus of management should be on repair or obliteration of the tear or communication while preserving flow through the ICA.⁵ Sometimes, complete occlusion of the artery may be necessary. In 1973, Parkinson described a direct surgical repair of a traumatic CCF with preservation of the ICA. While any procedure in this anatomic region is delicate, open repair in the acute setting amid potential polytrauma carries a significant risk of morbidity, so endovascular repair, if tolerated by the patient, is the method of choice.²²

Approach of the CCF may be performed via transarterial or transvenous routes.^11,¹⁸ The transvenous approach consists of retrograde catheterization and embolization of the venous structure draining the fistula. A venous route is only appropriate if the diseased, venous portion of the system is permanently occluded—and only if occlusion of this venous outflow does not compromise the drainage of the surrounding neural structures. Transarterial routes are more selective. Using a microcatheter, access to the fistula is provided by the arterial branches supplying it, and these pedicles are selectively occluded.²³ The number of vessels occluded, and the route chosen to occlude them, are necessarily linked to the choice of embolic material. Today, the primary methods for endovascular embolization employ detachable coils or liquid embolic agents (Fig. 92-1).

FIGURE 92-1 A 36-year-old man presenting 2 weeks after being struck in the head with a bat and with a proptotic, injected right eye; a pulse-synchronous bruit; and a right abducens palsy. A and B, A right ICA, anteroposterior (AP), and lateral angiogram demonstrating a type A CCF with opacification of both cavernous sinuses. There is also an associated 7-mm cavernous ICA aneurysm. C, A 4×10 mm Hyperglide (ev3 Neurovascular) is placed across the fistula site, and an Excelsior SL-10 microcatheter (Boston Scientific) is within the right cavernous sinus. D and E, A right ICA, AP, and lateral angiogram after the placement of coils into the cavernous sinus, showing no further filling of the fistula and no early venous phase. Symptoms resolved within 3 weeks of treatment.

Transarterial versus Transvenous Approach

Transvenous embolization is possible via the femoral vein or jugular vein and inferior petrosal sinus, or it may be possible by directly accessing the ophthalmic vein.²⁴ The goal of treatment is to thrombose the cavernous sinus, with the assumption that spontaneous resolution of fistula will follow. If the draining sinus is occluded but the upstream fistula is neglected, the high flow system forces drainage through other veins, potentially draining into the cortical venous system.^17,²⁴^–²⁶ Cortical venous drainage in the setting of these shunts may result in potentially fatal intracranial hemorrhage.²⁷

The transvenous approach for embolization, reported by Debrun in 1981, has become the treatment of choice for ICCF ²⁸ and for some traumatic dural arteriovenous fistulas. However, for reasons already discussed, it is not ideal in the management of DCCF.²⁰ For instance, when treating traumatic dural fistulas of the cavernous sinus, the inferior petrosal sinus is the simplest and shortest venous route to the cavernous sinus. A guiding catheter is introduced via a femoral sheath and resides in the internal jugular vein near the inferior petrosal sinus. In cases of fistulas with feeders from the ICA, another guiding catheter is run through the ICA containing a balloon for BTO and a microcatheter for injection of the embolic.²⁹ The balloon may also be inflated during embolization to prevent inadvertent reflux of the embolic agent into the ICA. Alternative access points are the basilar plexus, the pterygoid plexus, or the facial and angular veins.²⁰ In cases of high-flow fistulas, coils may be placed at the confluence of the draining veins and within the cavernous sinus to act as a mesh, thus slowing the flow through the fistula and decreasing the efflux of embolic material through the veins.²⁰

A transarterial approach allows the selective obliteration of individual pedicles feeding the CCF and makes the problem of venous rerouting less threatening.^5,²³ Problems with a transarterial approach may include several feeding arteries, anastomotic connections to cortical or nervous arterial supplies, or tortuous vessels that limit microcatheter access. For instance, catheterization of the small-caliber meningeal branches of ICCFs can be difficult or may supply several cranial nerves, thus limiting the success of this technique.^20,³⁰

In Barrow type A CCFs, a guide catheter is maneuvered into the ICA, followed by selective catheterization of feeding vessels. A microcatheter is navigated through the fistulous point into the cavernous sinus, and embolization is conducted. It may be necessary to simultaneously inflate a balloon in the cavernous ICA to prevent reflux into the parent artery.²⁰ Again, an angiogram should be performed to assess progress and screen for dangerous anastomoses.

In some instances, a combination of arterial and venous approaches may be used.^25,²⁶ The transarterial component of therapy in this case decreases blood flow through the system, thus providing a less turbulent environment when deploying coils and allowing more precise targeting of the fistula from the venous side. During the procedure, the injection should be performed at a pace that allows the surgeon to monitor the evolving shape of the embolic. If a balloon is used, it should be deflated and any abnormal reflux should be noted prior to retrieval. Finally, a reference microguidewire should always be anchored in place to allow intraoperative navigation of the artery.²⁹

Regardless of the route of approach, several principles apply: reflux of embolics into the parent vessel must be avoided. The ICA and the fistula have to be completely occluded, and the occlusion should be visually confirmed immediately after the procedure via angiography of the primary vascular tree, as well as potential collateral pathways.

Embolic Agents for Endovascular Occlusion

In choosing an embolic agent for CCF occlusion, consider what the desired properties of an ideal agent would be. The occlusion should be complete and permanent, and the delivery should be highly controllable. Radiopacity allows assessment of progress and precision of the occlusion. Finally, while some degree of proinflammatory properties may facilitate vessel occlusion, the material should not be antigenic. Modern embolics all attempt to strike a balance between these general themes, and some are more successful than others, depending on the task for which they were designed. Regardless of which embolic is chosen, all have inherent risks, including vessel rupture, vein occlusion, and embolization to normal parenchymal branches.^23,³¹

The three broad categories of embolics are mechanical devices, such as balloons and detachable coils; particles; and liquids. Liquid embolics can further be divided into cyanoacrylates and polymers.³² Coils are principally used in the occlusion of larger vessels and aneurysms. Liquid embolic agents include n-butyl-2-cyanoacrylate (n-BCA) and ethylene–vinyl alcohol copolymer (Onyx, ev3 Neurovascular, Irvine, CA).

Balloons

For almost 30 years, the procedure of choice for the management and repair of type A CCFs was detachable balloon occlusion. While detachable balloons are no longer available in the United States, their description by Serbinenko in 1974 helped stimulate the growth of balloon technology in endovascular therapy.⁶ The balloon had many advantages, including low cost, easy navigability to the fistula, and the ability to intermittently inflate and deflate the balloon, which allowed constant reassessment of fistula anatomy. However, some difficulties encountered with permanent balloon occlusion were early detachment or deflation, rupture by bone fragments, and iatrogenic dilation of the ostium of the fistula or the cavernous sinus proper, causing a delayed recurrence of the fistula.³³ If large balloons were used, or multiple balloons were deployed, de novo cranial nerve palsies sometimes resulted, or the resolution of preexisting palsies were sometimes hindered due to mass effect from the balloons.¹³

Particles

While particle embolic agents had been used for embolization of arteriovenous malformations,¹ the first use of a permanent particle for CCF embolization was by Kosary et al. in 1968.³⁴ Kosary et al. combined a porcelain bead with a Gelfoam technique described by Speakman in 1964.³⁵ The Gelfoam—used to quicken the clotting process in the sinus and prevent “downward displacement” of the bead—would herald the use of balloons in preventing reflux of liquid and particle embolics in later years. Gelfoam can be used as either a macro- or a microparticle, depending on how it is prepared, but in both cases it is a temporary embolic agent.³⁶ The choice of a porcelain bead was an important advancement, because it represented a rational choice of embolic particle size based on direct angiographic findings. Calibrated microparticles, such as Embospheres (BioSphere Medical, Rockland, MA) or polyvinyl alcohol particles of various sizes, now allow the physician to select a size based on the diameter of the vessels to be occluded, thus facilitating more accurate delivery of the embolics to the target vessel.

In the setting of high-flow CCF or trauma, where larger caliber vessels are directly involved, particle embolization would not be a consideration for treatment and is currently of historical interest only.

Coils

Detachable coils are easy to retrieve, reposition, or exchange when necessary, making them an appealing embolic agent. Endovascular treatment of CCF with coils is one of primary modes of treatment, with excellent results. In the setting of traumatic CCF, where the site of the fistula may be quite large, the coils may migrate or protrude into the ICA, thus risking carotid occlusion. Balloon-assist embolization, whereby the ICA is “protected” from coil migration and occlusion by the presence of a balloon that is inflated during coil delivery, has been quite efficacious in reducing this risk. Alternatively, similar to the principle of balloon assist, combining the use of coils with stents can prevent or mitigate such a risk.³⁷ Complete obliteration of the fistula may be difficult, and there is a risk of impingement on the parent vessel and subsequent mass effects when excessive amounts of coil are packed.^13,³⁷ However, certain coated coils, such as Hydrocoils, the coating of which expands when placed in contact with blood, seem to require fewer coils to achieve occlusion than others.

n-Butyl-Cyanoacrylate

The first description of n-BCA as an embolic material was by Brothers et al. in 1989.³⁸ This adhesive cyanoacrylate derivative polymerizes in the presence of anionic substances (e.g., blood) to form a solid cast that molds into the shape of the embolized region. The polymerization of n-BCA is immediate but can be prolonged by adding hydrophobic contrast agents (e.g., Ethiodol) or glacial acetic acid,³⁸ rendering this embolic agent more controllable when depositing it into the intravascular system. During long injection times, great care must be taken to avoid microcatheter retention, which may result from the polymerization of the n-BCA along the outer wall of the microcatheter.

Onyx

Onyx is an ethylene–vinyl alcohol copolymer suspended in dimethyl sulfoxide with tantalum added for radiopacity.^20,^39,⁴⁰ The first reported case of CCF embolization using Onyx was a type D fistula described by Arat et al. in 2004.³⁹ In contrast to n-BCA, which rapidly polymerizes, this cohesive embolic agent precipitates slowly from its outer surface as the dimethyl sulfoxide slowly diffuses into the circulation and the Onyx precipitates. The result is the formation of a cast in the embolized vessel. The slow speed of precipitation allows deep penetration of Onyx with a slow, controlled injection.^20,⁴⁰ Because of these properties, Onyx permits the embolization of a venous sinus by a transarterial approach.²³ Unique to this liquid embolic agent, it is possible to interrupt the injection during the procedure to allow assessment of the degree of embolization and occlusion. In this way, the endovascular surgeon can recognize the presence of dangerous anastomoses and avoid occlusion of normal vascular anatomy.

In contrast to n-BCA, Onyx’s nonadhesive characteristics allow a greater degree of reflux to be tolerated during embolization, leading to a reduced risk of catheter retention.^20,⁴⁰ Some limitations exist with the use of Onyx. The current microcatheter technology is somewhat limited in provided access to very distal vasculature secondary to the inherent stiffness of the microcatheters approved for use with Onyx. Furthermore, the solvent, dimethyl sulfoxide, may cause painful necrosis in the vasculature if rapidly infused. Like n-BCA, occlusion of the vasa nervorum can result in cranial neuropathies.

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