Embolization Therapy: Principles and Clinical Applications, 1 Ed.

Head and Neck Trauma

Goetz Benndor

Injuries to the vasculature of the head and neck can be caused by blunt trauma during motor vehicle accidents, falls, assaults, hanging, or sporting injuries1 and may be associated with significant morbidity and mortality.29 Whereas carotid injuries are associated with 8% to 18 % mortality, injuries to the vertebral arteries can be associated with 17% to 38% mortality.10 Penetrating vascular trauma is usually caused by sharp objects or instruments, such as knives,1117 nail guns,18 broken glass, arrows,19 or by bullets from gunshot injuries (GSIs).2024 Whereas in Western Europe and Canada, low-velocity stab injuries are the most frequently seen, high-velocity gunshot injuries are by far the dominant cause of penetrating vascular trauma in the United States.21

Iatrogenic injuries to the carotid, vertebral, and facial arteries by medical tools or instruments are generally rare but may occur during both diagnostic and therapeutic percutaneous procedures or during open surgical procedures. These include injuries of the carotid during central vein catheter placement,25,26 inadvertent puncture of the vertebral arteries during cervical epidural steroid injection,27,28 or injuries to the facial and maxillary arteries during orthognathic surgery.2933

Clustered location of several major arteries, some of which difficult to reach and to control by surgical exposure, is characteristic for the head and neck area. Vascular injuries can result in various lesions with different clinical sequelae ranging from cerebrovascular insults (CVIs) to active extravasation with critical blood loss. Exsanguination and ischemic stroke are the main causal factors of morbidity and mortality for penetrating arterial injury in the head and neck area. Mortality rate is highest in the first 24 hours after presentation, with primary and secondary cerebral ischemic injury accounting for the leading causes of death, followed by exsanguination.34,35

Because blunt trauma may result in CVI, and if left untreated can lead to stroke in 30% to 50% of all patients, with severe permanent neurologic deficits in 48% to 58%,36 early screening and intervention is important to improve clinical outcome.6

Nonfatal GSI to the head and neck can be devastating, with mortality in civilian patients ranging from 2% to 29%.22,37,38 Vascular injury to the carotid or vertebral arteries occurs in 15% to 25% of patients with penetrating injuries to the neck,39,40 and the stroke rate in patients with arterial injury ranges is reported to be as high as 15%.9

Immediate therapeutic measures include hemodynamic control and preventing or decreasing morbidity associated with cerebrovascular insufficiency or embolic phenomena.20,41

Iatrogenic vascular trauma can present with local symptoms, stroke, or as acute massive bleeding requiring early therapeutic management.42 Subacute and chronic lesions such as pseudoaneurysms (PAs) or arteriovenous fistulas (AVFs) can be initially occult and may present with delay from weeks to months.43 Endovascular treatment (EVT) of vascular lesions following iatrogenic trauma is identical to those caused by penetrating or blunt trauma. Biffl et al.4 have correlated the degree of blunt injury with clinical outcome (Table 21.1). This grading system may be used to some degree also for penetrating trauma of the carotid and vertebral arteries. However, it is of limited value external carotid artery (ECA) injuries, where luminal narrowing is of no clinical importance, and does not include management of AVFs. The distal internal maxillary artery (IMA) is a relatively frequent location for gunshot-related injuries with massive extravasation that often require emergent endovascular management. Traumatic AVFs in the ECA territory are clinically relatively benign but can cause chronic headaches, bruits, or significant cosmetic problems when involving facial veins.44 They can usually be electively treated.

TYPES OF INJURIES

Trauma in the head and neck can result in a range of arterial and venous injuries. Although venous injuries can also lead to hematomas and drop in hemoglobin, their clinical presentation is often less dramatic and angiographic detection difficult. They are usually self-limiting and rarely require endovascular or surgical management. Arterial trauma on the other hand can lead to rapid critical blood loss or ischemic deficits due to downstream compromise of the cerebral circulation. The spectrum of vascular injuries is wide and ranges from minor wall irregularities and vasospasm caused by blast effects to the surrounding tissue to partial or complete disruption of arterial blood flow to the central nervous system and rupture or transection with massive extravasation and critical blood loss.

Vessel Injuries without Blood Loss

Minor Wall Irregularities (Grade I)

This most frequently observed injury (~50%) can be seen as simple vasospasm or subtle, minimal luminal irregularities (<25%) that represent minor intimal damages. These small lesions, sometimes only detectable on digital subtraction angiography (DSA), do not notably narrow the arterial lumen or compromise blood flow. Because they can be nevertheless thrombogenic, anticoagulation or antiplatelet therapy becomes necessary when carotid or vertebral arteries are involved. Conservative management with warfarin, heparin, low-molecular-weight heparin (Lovenox), or antiplatelet drugs (acetylsalicylic acid [ASA], clopidogrel) and in some cases follow up imaging is advisable7,8,45 Because grade I lesion can be associated with strokes in up to 7%,46 routine screening ideally with four-vessel angiography (DSA) is strongly recommended.

Major Wall Irregularities and Dissections (Grade II)

These injuries can present with angiographic findings identical to spontaneous dissections, including luminal narrowing (>25%) and associated intimal flaps. They may be complicated by rapid intraluminal thrombus formation and thus require a more rigorous anticoagulation regime to prevent thromboembolism.8 Of note, studies have failed to demonstrate superiority of anticoagulation over antiplatelet therapy in the prevention of stroke,46,47 which can impact management in trauma patients in whom antiplatelet therapy is generally preferred by surgeons. In select cases, endovascular management such as stent placement may be required.24,48,49 Routine angiographic follow-up has been recommended, as up to 61% of patients with grade I to II injuries will require change in management. Both, dissections and the formation of PAs are dynamic processes, and thus show morphologic changes over time that influence therapeutic decision making.46 An early 7 to 10 days FU DSA is helpful to determine the acuteness of a lesion.

Pseudoaneurysms (Grade III)

PAs are small (1 to 3 mm) or large (up to several centimeters) outpouchings of the arterial wall caused by focal arterial damage that can lead to an intramural or extramural hematoma with subsequent recanalization. Depending on the extent of the injury, the wall of the PA may be covered by tunica media, adventitia, or just thrombus material. The latter is considered the “classical pseudoaneurysm,” with an angiographic appearance identical to true saccular or fusiform aneurysms. Similar to spontaneous dissections, traumatic PAs, especially with a narrow neck, may heal spontaneously with conservative management including anticoagulation or antiplatelet therapy and follow-up computed tomography angiography (CTA) or DSA.50,51 Follow-up imaging is important to detect trends of progression or regression that impact therapeutic decision making.52 A decrease in size usually indicates healing and justifies conservative management. No signs of regression or enlarging PAs may require interventional therapy. Some authors suggest surgical repair,53 and no clear consensus when to treat asymptomatic dissections or PAs currently exist. However, most operators tend to recommend EVT, and only if there is evidence for worsening on FU imaging.8,5457 Treatment options are bare metal or covered stents with or without deployment of coils or liquids into the aneurysmal sac. Covered stents may be used in larger wide-necked lesion but can be associated with parent vessel occlusion.57 If simple stenting shows no trend of occlusion within 3 to 6 months, coils are usually safe to deploy through the stent meshes,54 or double stenting is performed.55 Alternatively, coils can be placed in jailing technique during initial stenting. Recently introduced flow diverter can be used as well but represent a rather expensive solution.58Liquids such as N-butyl cyanoacrylate ([NBCA] Trufill; DePuy Orthopaedics, Inc., Warsaw, Indiana) and Onyx (Covidien, Irvine, California) can be very efficient to achieve rapid occlusions43 but have a clearly higher (unnecessary) risk of distal migration into the cerebral circulation.

Depending on availability, both CTA and DSA can be used for screening and follow-up studies. Because detection of minor vascular injuries and visualization of small changes during follow-up can be obscured especially in patients with GSIs and bullet fragments that cause metallic artifacts,59 the author has a strong preference for DSA. Especially, patients with penetrating trauma are oftentimes of relatively young age without significant underlying vascular diseases, which minimizes the risk of neurologic deficit posed by supra-aortic or cerebral angiography that is less than 1% in experienced hands. In our institution, a protocol with at least one short-term angiogram within 7 to 10 days followed by 4 weeks and 3 months is in place.

Occlusions (Grade IV)

Similar to spontaneous dissections, severe arterial injury may lead to an enlarging hematoma in the vessel wall or in the surrounding tissue and to occlusion the arterial lumen. The consequences of interrupting the carotid blood flow on the cerebral circulation depend to a large degree on the functional status of the circle of Willis, but stroke may occur in up to 50%.46 Vertebral artery (VA) occlusion can be fully compensated by collateral supply of a contralateral VA or ipsilateral cervical anastomoses. If this collateral circulation is insufficient, cerebellar infarcts or, even worse, a devastating basilar artery occlusion may occur especially in cases with unfavorable anatomy or advanced atherosclerosis.60 Due to the dual supply to the posterior fossa, complete VA occlusions may be less dangerous than nonocclusive lesions (grades I to III).46 On the other hand, even a minimal intimal damage is potentially thrombogenic, thus early detection and anticoagulation or antiplatelet therapy can be crucial. Further, it is important to be aware that a completely occluded artery following trauma may recanalize and become a new source of thromboembolic strokes. Therefore, prophylactic anticoagulation may be indicated.

Arteriovenous Fistulas

AVFs are not included in Biffl’s grading 4 and rarely caused by blunt trauma. They are more frequently observed following penetrating vascular injuries.61 Simultaneous injury to arterial and venous vessels creates a channel for arterial blood to reenter the circulation. Traumatic AVFs are usually “single-hole” high-flow lesions that can be small or occult in the beginning, and thus not detectable during initial diagnostic screening, but develop with varying delay.43,6264 EVT of traumatic AVFs is more or less identical to the one of congenital lesions and performed using stents, coils, detachable balloons, or embolic liquids depending on location and angioarchitecture of the lesion.44,65,66 As for all arteriovenous shunting lesions, treatment is effective only when the fistula site itself is permanently occluded (either most distal arterial or most proximal venous segment, or both) and can often be performed as planned procedure (Fig. 21.1).

Injuries with Blood Loss: Rupture, Perforation, Laceration, Transection (Grade V)

Transmural arterial injury causes leakage of blood into either the surrounding structures leading to an expanding hematoma in the soft tissues or into preformed cavities. Both situations can be associated with critical, uncontrollable blood loss and can develop quickly into a life-threatening situation. Open surgery may become necessary in cases with extensive tissue damage and may allow for control of the blood loss in some locations such as common carotid artery (CCA) and proximal internal carotid artery (ICA). Endovascular techniques are more efficient in bleedings arising from the vertebral or internal maxillary arteries and are considered treatment of choice for most of these lesions. If blood leaks into large voluminous spaces, such as the mediastinum, oropharynx, or upper gastrointestinal tract, critical loss can develop very quickly, leading to shock and possible death. Therefore, rapid identification of the bleeding source and immediate occlusion of the bleeding site can become lifesaving measure. Especially, injuries of the IMA (Fig. 21.2) are frequently associated with massive bleedings that are difficult to control with packing alone and usually require multiple transfusions.3133,52,6769 In this context, it needs to be clarified that the term pseudoaneurysm is sometimes used for ruptures of the IMA or sphenopalatine artery.29,69 The aneurysm-like appearance is largely caused by a highly unstable hematoma, only supported by nasal or intraoral packing and extremely fragile. Any aggressive manipulation with catheters or guidewires or even the deployment of coils can lead to rerupture. Similarly, transmural injuries of the vertebral or carotid arteries are prone to additional injury or rerupture during intravascular manipulation with tools or occlusive devices if only temporarily occluded by clot.24 Further, it should be noted that also injuries to small arteries could cause enlarging hematomas of significant size and critical blood loss (Fig. 21.3). For all vessels difficult to reach by surgery, EVT is nowadays the method of choice, employing detachable balloons (currently not available in the United States) or vascular plug devices70 in larger vessels such as ICA or VA. Embolic liquids such as Onyx or NBCA are preferably used in smaller arteries (e.g., ECA branches). Depending on location and flow conditions, combining liquids with coils as matrix is useful to prevent distal migration (Figs. 21.4 and 21.5).24 Newer occlusion devices such as the microvascular plug system (MVP) or UNO (Reverse Medical, Irvine, California), resheatable microcatheter-based occlusion systems, may be of use as well.

ENDOVASCULAR TREATMENT

Endovascular management of acute arterial injuries is continuously evolving49 and employs standard techniques used for treating nontraumatic vascular disorders in the head and neck region. Transfemoral approach with coaxial systems using 5-Fr or 6-Fr guiding catheters and microcatheter–guidewire combination is preferred. In cases with difficult access anatomy, triaxial systems can be used (e.g., 6-Fr Envoy, DePuy Orthopaedics, Inc., Warsaw, Indiana; 0.38 DAC, Concentric Medical, Fremont, California; Excelsior SL-10 microcatheter, Stryker Corporation, Kalamazoo, Michigan). In some cases, ultrasound- or road map–guided direct puncture of the lesion can facilitate access (e.g., scalp lesions).44 Pressured flushing systems, standard in neurovascular procedures to prevent clot formation and distal thromboembolism, are advisable when embolizing ECA branches. The author regularly uses 1,000 International Units heparin in 1 L saline for flushing of guiding catheters. This can be crucial because additional heparinization is often contraindicated in patients with acute bleedings or suspected additional internal injuries. Although the choice of microcatheters depends mostly on the user’s preference, it should be kept in mind that it can become necessary to combine deployment of coils with the injection of liquids (e.g., Echelon; Covidien, Plymouth, Minnesota). Carotid artery or VA stenting is generally a straightforward procedure especially in younger patients. The use of protection devices may not be necessary as the risk of dislodging plaque material from the bifurcation usually does not exist.

TIPS AND TRICKS

• Selective injections (ICA, ECA, VA >> CCA, SA) provide more accurate information than global injection when looking for vessel injuries.

• Check for vessel stumps or abrupt occlusions in cases with blood loss and negative angiogram (extravasation can be invisible due to packing).

• Secure temporary (clot) occluded arteries with additional coils, plugs, liquids, etc.

• Checking for backflow through extracranial/intracranial collaterals after proximal/antegrade occlusion is mandatory.

• Avoid heparinization if possible, but flush meticulously guide catheter and microcatheter to avoid thromboembolism.

• Have a large balloon occlusion catheter (e.g., Cello; Covidien, Plymouth, Minnesota) ready to prevent massive blood loss while gaining time to prepare microcatheters and embolic agents (coils, liquids).

• Gentle guidewire manipulation in injured arteries is mandatory to avoid rerupture (e.g., use double-angle tip Headliner [Terumo Medical Corporation, Somerset, New Jersey] or in general loop techniques).

• Be cautious with coils in ruptured arteries or PAs: Most PAs do not have a firm wall and can be easily perforated with guidewires or coils; underpacking may be sufficient and is advised. Consider first the front door–back door technique if possible.

• Glue (NBCA [Trufill])/Onyx: Both agents may be used depending on the operator’s comfort level. Glue occlusion is fast and permanent due to immediate tissue reaction (e.g., 30% NBCA–Ethiodol mixture for IMA rupture) and high thrombogenicity. Use concentration greater than 50% for high-flow AVFs; the polymerization would be faster.

• Glue (NBCA [Trufill])/Onyx: Seal the rupture site proximally and distally by withdrawing the catheter during injection (trapping). Avoid proximal occlusion only.

• Glue (NBCA [Trufill])/Onyx: Advance guiding catheter into ECA before removing a microcatheter after injection into IMA.

• Glue (NBCA [Trufill])/Onyx: Be well familiar with so-called dangerous anastomoses.

• Glue (NBCA [Trufill])/Onyx: Position the microcatheter close enough to target to avoid proximal occlusion or backflow.

• Glue (NBCA [Trufill])/Onyx: If possible and not too time consuming, block anastomoses with coils (e.g., occipital artery–VA) before injecting.

• Glue (NBCA [Trufill])/Onyx: Use flow control when injecting liquids into AVFs. Superficial veins in face or scalp can be manually compressed using a hemostat clamp.

• Circle of Willis approach: Be prepared to perform retrograde approach to a bleeding site through the circle of Willis if antegrade route is blocked, too difficult, or time consuming.

• Consider removing packings or deflating balloons for repeat angiogram if initial run is negative and there is strong clinical suspicion.

• Consider removing packings postembolization in angiography suite before sending patient to ICU.

• Use low-molecular-weight or antiplatelet (ASA/Plavix) in minor (grade I) injuries to prevent thromboembolism and stroke.

CONCLUSION

The endovascular management of traumatic vascular injuries in the head and neck is technically not more demanding than that of other vascular lesions. However, the scenarios and settings can be fast-paced and dramatic and thus may represent a particular challenge for the inexperienced interventionalist.

REFERENCES

 1. Biffl WL, Moore EE, Offner PJ, et al. Blunt carotid and vertebral arterial injuries. World J Surg. 2001;25(8):1036–1043.

 2. Biffl WL, Moore EE. Identifying the asymptomatic patient with blunt carotid arterial injury. J Trauma. 1999;47(6):1163–1164.

 3. Biffl WL, Moore EE, Mestek M. Patients with blunt carotid and vertebral artery injuries. J Trauma. 1999;47(2):438–439.

 4. Biffl WL, Moore EE, Offner PJ, et al. Blunt carotid arterial injuries: implications of a new grading scale. J Trauma. 1999;47(5):845–853.

 5. DiCocco JM, Fabian TC, Emmett KP, et al. Optimal outcomes for patients with blunt cerebrovascular injury (BCVI): tailoring treatment to the lesion. J Am Coll Surg. 2011;212(4):549–557; discussion 557–559.

 6. Emmett KP, Fabian TC, DiCocco JM, et al. Improving the screening criteria for blunt cerebrovascular injury: the appropriate role for computed tomography angiography. J Trauma. 2011;70(5):1058–1063; discussion 1063–1065.

 7. Fabian TC, Patton JH Jr, Croce MA, et al. Blunt carotid injury. Importance of early diagnosis and anticoagulant therapy. Ann Surg. 1996;223(5):513–522; discussion 522–525.

 8. Harrigan MR, Weinberg JA, Peaks YS, et al. Management of blunt extracranial traumatic cerebrovascular injury: a multidisciplinary survey of current practice. World J Emerg Surg. 2011;6:11.

 9. Ramadan F, Rutledge R, Oller D, et al. Carotid artery trauma: a review of contemporary trauma center experiences. J Vasc Surg. 1995;21(1):46–55; discussion 55–56.

10. Fusco MR, Harrigan MR. Cerebrovascular dissections: a review. Part II: blunt cerebrovascular injury. Neurosurgery. 2011;68(2):517–530; discussion 30.

11. Kabanchuk IN, Skorik VT. Knife wound of the neck with injury of the carotid artery [in Russian]. Klin Khir. 1989;(4):70.

12. Tu RK, Eskridge JM, Grady MS. Endovascular treatment of a kitchen knife pseudoaneurysm of the cervical internal carotid artery. AJR Am J Roentgenol. 1996;166(3):704.

13. Xia X, Zhang F, Lu F, et al. Stab wound with lodged knife tip causing spinal cord and vertebral artery injuries: case report and literature review. Spine. 2012;37(15):E931–E934.

14. Mehanna HM, MacGregor FB. The case of the missing carotid artery—a well aimed knife! J Laryngol Otol. 1998;112(4):387–388.

15. Sergeev VM. Ligation of the vertebral artery in partial knife wounds [in Russian]. Zh Vopr Neirokhir Im N N Burdenko. 1981;(1):53–54.

16. Petrovic P, Nastasic S, Dimkovic D. Knife wounds of the carotid arteries in their cervical segment. Apropos of 3 cases [in French]. Chirurgie. 1976;102(10):894–897.

17. Polunin AP, Volkov VG. Knife injury of the common carotid artery [in Russian]. Vestn Khir Im I I Grek. 1975;114(3):76.

18. Hiraishi T, Kawaguchi T, Kobayashi T, et al. Unstable stenosis of the internal carotid artery caused by a craniofacial nail-gun injury-case report. Neurol Med Chir (Tokyo). 2009;49(12):590–593.

19. Lubarsky M, Helmer R, Knight C, et al. Internal carotid artery dissection following wooden arrow injury to the posterior pharynx. Case report. J Neurosurg Pediat. 2008;1(4):334–336.

20. Bell RB, Osborn T, Dierks EJ, et al. Management of penetrating neck injuries: a new paradigm for civilian trauma. J Oral Maxillofac Surg. 2007;65(4):691–705.

21. Burgess CA, Dale OT, Almeyda R, et al. An evidence based review of the assessment and management of penetrating neck trauma. Clin Otolaryngol. 2012;37(1):44–52.

22. Miller RH, Duplechain JK. Penetrating wounds of the neck. Otolaryngol Clin North Am. 1991;24(1):15–29.

23. Sofianos C, Degiannis E, Van den Aardweg MS, et al. Selective surgical management of zone II gunshot injuries of the neck: a prospective study. Surgery. 1996;120(5):785–788.

24. Yevich SM, Lee SR, Scott BG, et al. Emergency endovascular management of penetrating gunshot injuries to the arteries in the face and neck: a case series and review of the literature. J Neurointerv Surg. 2014;6(1):42–46.

25. Parsons AJ, Alfa J. Carotid dissection: a complication of internal jugular vein cannulation with the use of ultrasound. Anesth Analg. 2009;109(1):135–136.

26. Forestner JE. Ipsilateral mydriasis following carotid-artery puncture during attempted cannulation of the internal jugular vein. Anesthesiology. 1980;52(5):438–439.

27. Rozin L, Rozin R, Koehler SA, et al. Death during transforaminal epidural steroid nerve root block (C7) due to perforation of the left vertebral artery. Am J Forensic Med Pathol. 2003;24(4):351–355.

28. Ziai WC, Ardelt AA, Llinas RH. Brainstem stroke following uncomplicated cervical epidural steroid injection. Arch Neurol. 2006;63(11):1643–1646.

29. Avelar RL, Goelzer JG, Becker OE, et al. Embolization of pseudoaneurysm of the internal maxillary artery after orthognathic surgery. J Craniofac Surg. 2010;21(6):1764–1768.

30. Hacein-Bey L, Blazun JM, Jackson RF. Carotid artery pseudoaneurysm after orthognathic surgery causing lower cranial nerve palsies: endovascular repair. J Oral Maxillofac Surg. 2013;71(11):1948–1955.

31. Jo HW, Kim YS, Kang DH, et al. Pseudoaneurysm of the facial artery occurred after mandibular sagittal split ramus osteotomy. J Oral Maxillofac Surg. 2013;17(2):151–154.

32. Kim YW, Baek MJ, Kim HD, et al. Massive epistaxis due to pseudoaneurysm of the sphenopalatine artery: a rare post-operative complication of orthognathic surgery. J Laryngol Otol. 2013;127(6):610–613.

33. Lanigan DT, Hey JH, West RA. Major vascular complications of orthognathic surgery: false aneurysms and arteriovenous fistulas following orthognathic surgery. J Oral Maxillofac Surg. 1991;49(6):571–577.

34. Acosta JA, Yang JC, Winchell RJ, et al. Lethal injuries and time to death in a level I trauma center. J Am Coll Surg. 1998;186(5):528–533.

35. Sauaia A, Moore FA, Moore EE, et al. Epidemiology of trauma deaths: a reassessment. J trauma. 1995;38(2):185–193.

36. Biffl WL, Moore EE, Ryu RK, et al. The unrecognized epidemic of blunt carotid arterial injuries: early diagnosis improves neurologic outcome. Ann Surg. 1998;228(4):462–470.

37. Pereira C, Boyd JB, Dickenson B, et al. Gunshot wounds to the face: level I urban trauma center: a 10-year level I urban trauma center experience. Ann Plast Surg. 2012;68(4):378–381.

38. Biffl WL, Moore EE, Rehse DH, et al. Selective management of penetrating neck trauma based on cervical level of injury. Am J Surg. 1997;174(6):678–682.

39. Asensio JA, Valenziano CP, Falcone RE, et al. Management of penetrating neck injuries. The controversy surrounding zone II injuries. Surg Clin North Am. 1991;71(2):267–296.

40. Munera F, Soto JA, Palacio DM, et al. Penetrating neck injuries: helical CT angiography for initial evaluation. Radiology. 2002;224(2):366–372.

41. Wang AC, Charters MA, Thawani JP, et al. Evaluating the use and utility of noninvasive angiography in diagnosing traumatic blunt cerebrovascular injury. J Trauma Acute Care Surg. 2012;72(6):1601–1610.

42. Benndorf G. Endovascular management of a major vascular complication after orthognatic surgery. Interv Neuroradiol. 1998;4(4):307–310.

43. Lee SR, Metwalli ZA, Yevich SM, et al. Variability in evolution and course of gunshot injuries to the neck and impact on management. A case report. Interv Neuroradiol. 2013;19(4):489–495.

44. Benndorf G, Lehmann TN, Lanksch WR. Treatment of external carotid artery fistula by percutaneous venous approach. Interv Neuroradiol. 1999;5(3):251–256.

45. Cothren CC, Biffl WL, Moore EE, et al. Treatment for blunt cerebrovascular injuries: equivalence of anticoagulation and antiplatelet agents. Arch Surg. 2009;144(7):685–690.

46. Biffl WL, Ray CE Jr, Moore EE, et al. Treatment-related outcomes from blunt cerebrovascular injuries: importance of routine follow-up arteriography. Ann Surg. 2002;235(5):699–706; discussion 706–707.

47. Kennedy F, Lanfranconi S, Hicks C, et al. Antiplatelets vs anticoagulation for dissection: CADISS nonrandomized arm and meta-analysis. Neurology. 2012;79(7):686–689.

48. Biffl WL, Moore EE, Ray C, et al. Emergent stenting of acute blunt carotid artery injuries: a cautionary note. J Trauma. 2001;50(5):969–971.

49. DuBose J, Recinos G, Teixeira PG, et al. Endovascular stenting for the treatment of traumatic internal caroid injuries: expanding experience. J Trauma. 2008;65(6):1561–1566.

50. Guillon B, Brunereau L, Biousse V, et al. Long-term follow-up of aneurysms developed during extracranial internal carotid artery dissection. Neurology. 1999;53(1):117–122.

51. Tekiner A, Gokcek C, Bayar MA, et al. Spontaneus resolution of a traumatic vertebral artery pseudoaneurysm. Turk Neurosurg. 2011;21(1):90–93.

52. Lee CY, Yim MB, Benndorf G. Traumatic pseudoaneurysm of the pharyngeal artery: an unusual cause of hematemesis and hematochezia after craniofacial trauma. Surg Neurol. 2006;66(4):444–446; discussion 446.

53. Garg K, Rockman CB, Lee V, et al. Presentation and management of carotid artery aneurysms and pseudoaneurysms. J Vasc Surg. 2012;55(6):1618–1622.

54. Phatouros CC, Sasaki TY, Higashida RT, et al. Stent-supported coil embolization: the treatment of fusiform and wide-neck aneurysms and pseudoaneurysms. Neurosurgery. 2000;47(1):107–113; discussion 113–115.

55. Benndorf G, Wellnhofer E, Schneider GH. Doubled stenting for effective occlusion of a dissecting carotid artery aneurysm. Interv Neuroradiol. 2000;6(4):343–348.

56. Berne JD, Reuland KR, Villarreal DH, et al. Internal carotid artery stenting for blunt carotid artery injuries with an associated pseudoaneurysm. J Trauma. 2008;64(2):398–405.

57. Cox MW, Whittaker DR, Martinez C, et al. Traumatic pseudoaneurysms of the head and neck: early endovascular intervention. J Vasc Surg. 2007;46(6):1227–1233.

58. Rahal JP, Dandamudi VS, Heller RS, et al. Use of concentric Solitaire stent to anchor Pipeline flow diverter constructs in treatment of shallow cervical carotid dissecting pseudoaneurysms. J Clin Neurosci. 2014;21:1024–1028.

59. DiCocco JM, Emmett KP, Fabian TC, et al. Blunt cerebrovascular injury screening with 32-channel multidetector computed tomography: more slices still don’t cut it. Ann Surg. 2011;253(3):444–450.

60. Desouza RM, Crocker MJ, Haliasos N, et al. Blunt traumatic vertebral artery injury: a clinical review. Eur Spine J. 2011;20(9):1405–1416.

61. Amirjamshidi A, Rahmat H, Abbassioun K. Traumatic aneurysms and arteriovenous fistulas of intracranial vessels associated with penetrating head injuries occurring during war: principles and pitfalls in diagnosis and management. A survey of 31 cases and review of the literature. J Neurosurg. 1996;84(5):769–780.

62. Perry MO. Complications of missed arterial injuries. J Vasc Surg. 1993;17(2):399–407.

63. Fox CJ, Gillespie DL, Weber MA, et al. Delayed evaluation of combat-related penetrating neck trauma. J Vasc Surg. 2006;44(1):86–93.

64. Johnson ON, Fox CJ, O’Donnell S, et al. Arteriography in the delayed evaluation of wartime extremity injuries. Vasc Endovascular Surg. 2007;41(3):217–224.

65. Redekop G, Marotta T, Weill A. Treatment of traumatic aneurysms and arteriovenous fistulas of the skull base by using endovascular stents. J Neurosurg. 2001;95(3):412–419.

66. Herrera DA, Vargas SA, Dublin AB. Endovascular treatment of traumatic injuries of the vertebral artery. AJNR Am J Neuroradiol. 2008;29(8):1585–1589.

67. Manafi A, Ghenaati H, Dezham F, et al. Massive repeated nose bleeding after bimaxillary osteotomy. J Craniofac Surg. 2007;18(6):1491–1493.

68. Pappa H, Richardson D, Niven S. False aneurysm of the facial artery as complication of sagittal split osteotomy. J Craniomaxillofac Surg. 2008;36(3):180–182.

69. Silva AC, O’Ryan F, Beckley ML, et al. Pseudoaneurysm of a branch of the maxillary artery following mandibular sagittal split ramus osteotomy: case report and review of the literature. J Oral Maxillofac Surg. 2007;65(9):1807–1816.

70. Ross IB, Buciuc R. The vascular plug: a new device for parent artery occlusion. AJNR Am J Neuroradiol. 2007;28(2):385–386.