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Endovascular Treatment of Head and Neck Bleeding
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. 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.
The incidence of blunt cerebrovascular injury (BCVI) has increased over the past two decades secondary to technical improvements in computed tomography angiography (CTA) and the advent of more comprehensive screening protocols in asymptomatic patients after trauma. While traditionally considered rare, in more recent series, BCVI is present in 0.5% to 1% of trauma admissions. Such injuries can be associated with high morbidity and mortality that have been reported from 20% to 40%. 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 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. The patient is usually kept under minimal sedation, allowing accurate neurologic assessment. Based on the severity of the vascular injury, 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. 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. 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. Neurophysiologic monitoring with electroencephalography (EEG), somatosensory evoked potentials, and motor evoked potentials may be performed in patients who require general anesthesia or whose level of injury precludes intermittent neurologic evaluation during the procedure.
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, EEG, 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. , There has also been success with use of delayed venous phase protocols in assessing collateral adequacy. 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 EEG monitoring. , 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, TBI, hemorrhage- or vasospasm-related infarction, and embolic infarction have brought the predictive value of these challenges into question. 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.
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 or embolization, to delayed hemorrhage from ruptured traumatic aneurysms. Because of the wide 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) with completely different presenting symptoms. Penetrating injuries to the posterior regions of the skull or to the anterior portions of the face may result not only in significant blood loss 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. In addition, posttraumatic vasospasm, poorly understood until recently described after conflicts in Afghanistan and Iraq, may occur up to 3-4 weeks after injury. A keen awareness of the potential for these sequelae of trauma is important in determining the assessment and subsequent treatment paradigm.
Carotid-Cavernous Fistulas
CCFs are the result of an aberrant connection between the (arterial) carotid system and the (venous) cavernous sinus. The Barrow classification scheme subdivides CCFs into high-flow, direct (type A) fistulas, and low flow, indirect (types B to D) fistulas ( Fig. 66.1 ). Type A CCFs are a direct connection between the cavernous segment of the ICA and the cavernous sinus—usually of traumatic etiology. These are also a rare but well described risk of sinus or transsphenoidal surgery. Type B is the result of a fistulous connection between arterial branches of the ICA and the cavernous sinus. Type C CCFs are characterized by arterial feeders originating from the external carotid artery. Type D CCFs are a combination of types B and C, in which feeders originating from both the ICA and ECA result in communication with the cavernous sinus. In contrast to dural-based fistulas, spontaneous cure of a type A CCF is rare. , However, rare cases of spontaneous DCCF are found in cases of ruptured cavernous ICA aneurysms and in patients with collagen vascular disease. 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. , Classical presentation of DCCF is pulsating exophthalmos with orbital bruit. Other symptoms may include visual changes, chemosis, orbital pain, and proptosis. Symptoms are a direct result of arterialization of the cavernous sinus and draining orbital veins. Common sequelae encountered include venous congestion, hemorrhage, headache, tinnitus, vertigo, and cranial nerve palsies. 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. Sometimes, complete occlusion of the artery may be necessary. First described by Benjamin Travers in 1809, surgical ligation of the common carotid artery was the treatment of choice for CCFs. 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.
Endovascular approaches for CCFs may be performed via transarterial or transvenous routes, with cure rates cited to be upward of 80%. , , The transvenous approach consists of retrograde catheterization and embolization of the venous structure draining the fistula. Similar to other intracranial fistulas, obliteration of the point of fistulous connection is curative. 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. In Type A direct CCF, it may be possible to microcatheterize the fistulous connection point and obliterate the draining vein (cavernous sinus) via embolization with coils. Depending on the extent of the injury to the carotid artery, temporary balloon assistance may be helpful to prevent prolapse of coils back into the ICA, allowing the coils to fill the cavernous sinus and “spot weld” the hole in the artery. 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 (see Fig. 66.1 ).
Transarterial Versus Transvenous Approach
Venous embolization is typically performed via transcutaneous femoral vein access and catheterization of the jugular vein and inferior petrosal sinus. In cases where venous hypertension has led to thrombosis of the petrosal sinus, or in patients with anomalous cavernous sinus anatomy, another option is to directly access the ophthalmic vein. This may be accomplished via direct puncture using road map angiography or ultrasound, or with the assistance of an ophthalmologist comfortable with performing a cut-down through the upper lid. As above, the goal of treatment is to thrombose the cavernous sinus to the point of the actual fistulous connection. If the venous outflow is occluded distal to the fistulous connection, the high arterial inflow will either be diverted through collateral veins, leading to residual/recurrent fistula, or hemorrhage will occur if there is insufficient outflow. The collateral outflow may be in the form of cortical veins , and in the setting of these vascular shunts, this may result in significant intracranial hemorrhage.
The transvenous approach for embolization, reported by Debrun in 1981, has become the treatment of choice for indirect CCF, due to the difficulty of microcatheter navigation into small caliber feeding vessels and the increased risk of reflux of embolic material into the ICA. However, it may not be ideal in the management of direct CCF. Every CCF requires careful angiographic evaluation to determine the optimal endovascular approach. A guide catheter is introduced after placement of a venous femoral sheath and resides in the internal jugular vein near the inferior petrosal sinus. Placement of an arterial catheter in the carotid is also required to provide road map images for transvenous catherization as well as to assess the fistula as it is treated. Balloon assistance via the arterial catheter may be performed in order to protect the carotid circulation during embolization, or to perform BTO if embolization is unsuccessful. Alternative venous access points are the basilar plexus, the pterygoid plexus, or the facial and angular veins.
The transarterial approach allows for selective obliteration of individual vascular pedicles feeding the CCF and makes the problem of venous rerouting less threatening. , Problems with the transarterial approach may include several feeding arteries, anastomotic connections to cortical or nervous arterial supplies, or tortuous vessels that limit microcatheter access. For example, catheterization of the small-caliber meningeal branches of indirect CCFs can be difficult or may supply several cranial nerves, thus limiting the success of this technique. , Also, in cases with rapid arteriovenous shunting, high flow across the fistula may make microcatheterization challenging. In cases of high-flow fistulas, coils may be placed at the confluence of the draining veins (via either transarterial or transvenous routes) and within the cavernous sinus to act as a mesh, thus slowing the flow through the fistula and decreasing the efflux of liquid embolic material through the veins. In transarterial treatment of Barrow type A CCFs, a guide catheter is maneuvered into the ICA, followed by selective catheterization of the fistula via microcatheter, which is navigated through the fistulous point into the cavernous sinus and embolization proceeds. Follow-up angiography should be performed intermittently to assess progress and screen for dangerous anastomoses.
In some instances, a combination of arterial and venous approaches may be used. , 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. When using liquid embolics, the injection should be performed at a pace that allows the surgeon to monitor the evolving shape of the embolic material. If a balloon is used, it should be deflated and any abnormal reflux should be noted prior to retrieval.
Regardless of the route of approach, several principles apply: reflux of embolics into the parent vessel must be avoided. The fistula must 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. Without complete obliteration of the fistula, even if flow across the fistula is reduced, recurrence is expected.
Embolic Agents for Endovascular Occlusion
When choosing an embolic agent for CCF occlusion, it is important to 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. ,
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. Coils are principally used in the occlusion of larger vessels and aneurysms. Liquid embolic agents include n -butyl-2-cyanoacrylate ( n -BCA [Cordis Neurovascular, Miami, FL) 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. 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. 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.
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