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Interventional radiology in the treatment of intracranial vascular injuries and fistulae
Injury, Int. J. Care Injured (2008) 39, 1242—1248
www.elsevier.com/locate/injury
Interventional radiology in the treatment of intracranial vascular injuries and fistulae B.J. McGuinness *, M. Moriarty, J.K.A. Hope Radiology Department, Auckland City Hospital, Park Road, Grafton, Auckland, New Zealand Accepted 27 January 2008
KEYWORDS Traumatic intracranial aneurysm; Traumatic carotid cavernous fistulae; Endovascular treatment; Intracranial vascular injury
Summary Traumatic intracranial vascular injuries are uncommon. However prompt diagnosis and management is essential because of the high morbidity and mortality associated with these conditions. The imaging evaluation and potential endovascular management of traumatic intracranial aneurysms and traumatic intracranial fistulae is discussed. # 2008 Elsevier Ltd. All rights reserved.
Intracranial vascular injuries that may require emergency endovascular management can be broadly divided into intradural traumatic aneurysms, extradural arterial injury usually involving the internal carotid artery and traumatic arteriovenous fistulae most commonly related to the cavernous sinus. These may arise as the result of penetrating or more commonly blunt trauma. Prior to the widespread use of CT traumatic intracranial vascular injury was more readily identified as angiography was the main imaging modality in significant head trauma. With unenhanced CT now being the standard imaging modality in trauma the diagnosis of traumatic intracranial aneurysms and fistulae relies on clinical suspicion and the presence of certain indirect findings on unenhanced CT. * Corresponding author. Tel.: +6493074949x24504. E-mail address: [email protected] (B.J. McGuinness).
Traumatic intracranial aneurysms Less than 1% of intracranial aneurysms are traumatic in origin in adults although they account for a much larger proportion of aneurysms in children. Traumatic aneurysms can be classified based on the mechanism of injury and location of aneurysm.5 Penetrating trauma will result in a pseudoaneurysm occurring along the path of the injury. Stab wounds tend to have a higher incidence of traumatic aneurysm formation than missile wounds. In one series of 109 patients mostly with stab wounds there was an incidence of nearly 30% for major intracranial vascular injury and 10% incidence of aneurysms.14 In the case of missiles, the projectile causing a pseudoaneurysm will typically be irregular in shape and slow in velocity, hence shrapnel is much more likely to cause a traumatic aneurysm than gunshot wounds.11 In almost all cases there will not be an
0020–1383/$ — see front matter # 2008 Elsevier Ltd. All rights reserved. doi:10.1016/j.injury.2008.01.054
Interventional radiology in the treatment of intracranial vascular injuries and fistulae exit wound and the missile will be retained intracranially.11 In such cases of retained bullets the traumatic aneurysm will tend to occur along the distal aspect of its path where it has slowed. In a series of wartime penetrating injuries the angiographic incidence of traumatic aneurysms was 5.7% where patients were selected as high risk based on the path of the missile, large entry path haematoma on CT, multiple retained fragments and the surgeons’ debridement findings.1 Blunt traumatic aneurysms of the skull base will occur where the ICA is fixed either related to the petrous or cavernous portions and are often associated with basilar skull fractures. Intradural traumatic aneurysms in blunt trauma commonly occur in pericallosal and posterior cerebral artery locations as a result of impact of the artery against firm edges of the adjacent falx cerebri and tentorium cerebelli, respectively. Distal cortical aneurysms are also seen and are thought to occur as a result of transient herniation and injury within a fracture defect or through rents in surface arteries where they give small dural branches.3,5,8 Diagnosis of traumatic aneurysms relies heavily on the level of clinical suspicion. In a patient with blunt craniofacial trauma, delayed or unexplained neurological deterioration, unusual location of intracranial haemorrhage and recurrent large epistaxis all warrant further angiographic investigation. The presence of basal skull fractures on CT involving the carotid canal and particularly the petrous segment is a significant risk factor and should also result in a high clinical suspicion (up to 10% incidence of aneurysm).21 Cavernous ICA aneurysm may also present in a delayed fashion with a cavernous sinus syndrome consisting of retro orbital headache and compressive findings related to the 3rd through 6th cranial nerves. Consideration should be given to angiography in all patients with penetrating trauma given the relatively high association with vascular injury. There are several documented cases of normal initial cerebral angiograms with subsequent angiography showing a traumatic aneurysm so consideration should also be given to routine repeat angiography for those at high clinical risk or with penetrating injuries.1,3,8,23 The angiographic findings of a traumatic aneurysm includes a poorly defined neck, unusual often peripheral locations showing no relationship to arterial branch points, irregularly shaped aneurysms, and delayed filling and emptying of the aneurysm (Fig. 1). Time between trauma and aneurysm rupture ranges from 1 day to many months, with about 50% of cases likely to rupture within 3 weeks.3,5,8 There are reported cases of reduction in size and disappearance of aneurysms on angiography, in a
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series by Amirjamshidi et al. of 31 traumatic aneurysms due to missile penetrating injuries 6 (19.4%) healed spontaneously and shrank or disappeared on follow-up angiography.1,8 The mortality rates following rupture of traumatic aneurysms has been variously reported between 31% and 54%.3,5,8 In surgically treated patients the mortality rates are much lower and range between 18% and 20%.3,8,20 Surgical treatment of intradural traumatic aneurysms includes clipping, wrapping or excision and like endovascular techniques can be very challenging due to the thin and fragile walls of traumatic aneurysms often with poorly defined necks.1,5 Endovascular techniques to preserve the parent artery via coil embolisation of the aneurysm is risky in the acute phase as the wall is extremely fragile and subsequent risk of coil or microcatheter perforation high. After a period of some weeks, subacute traumatic pseudoaneurysm walls are thought more stable and at this time GDC coil embolisation can be performed with preservation of the parent vessel if anatomical features such as dome to neck ratio allow.15 Failing this endovascular occlusion of the parent vessel as close to the aneurysm as possible can be performed. If the location of the aneurysm means that parent vessel occlusion will result in devastating consequences then a conservative approach could also be considered but the patient would require intensive monitoring and regular angiographic follow-up for 6—8 weeks.1 Traumatic ICA aneurysms may be treated endovascularly either by parent vessel sacrifice via detachable balloon occlusion or by embolisation of the aneurysm sac (usually with GDC coils but detachable balloons have been used as well) with preservation of the ICA. All patients having ICA occlusion should undergo a balloon test occlusion first. Detachable balloon occlusion of the ICA is associated with neglible mortality with permanent ischaemia being the most significant complication occurring at a rate of about 5% despite clinical tolerance of balloon test occlusion.13,24 The proposed advantages over surgical ligation of the ICA more proximally in the neck include the ability to occlude immediately proximal to the aneurysm therefore reducing the risk of collateral pathways taking over supply to the aneurysm, that there is less distal stump of ICA to act as a site of embolisation while it thromboses and the fact that the patient is awake and can be monitored for neurological deterioration during occlusion. If the traumatic aneurysm has a defined neck then consideration should be given to coil embolisation of the aneurysm with preservation of the parent ICA. This technique may result in only partial occlusion of the aneurysm in up to 20% (<90% occluded) and therefore require ongoing surveillance angiography
1244
B.J. McGuinness et al.
Figure 1 Young man who sustained penetrating trauma to right frontotemporal region with a screwdriver. Noncontrast CT scan shows haematoma and some small bone fragments along the tract of injury across the midline in the inferior frontal lobes (a and b). Initial cerebral angiogram (not shown) demonstrated vasospasm but no false aneurysm. Follow-up CTangiogram (axial and sagittal) shows a small aneurysm related to the proximal A2 segment of the left anterior cerebral artery (c and d). Subsequent cerebral angiogram demonstrates the typical delayed filling and emptying of the false aneurysm. This was treated endovascularly by parent artery occlusion using liquid embolic agent (e, f, and g).
and possible retreatment. However the risk of permanent ischaemic complications is likely to be lower than for balloon occlusion of the parent ICA.15,23 Pseudoaneurysms of the ICA that are at least partially surrounded by bone are thought to be at lower risk of rupture during coil embolisation although again treatment in the subacute phase when the wall has matured should be safer.15
Traumatic carotid cavernous fistulae (TCCF) Arteriovenous fistula is an abnormal connection between an artery and vein which tends to occur when these structures are in close proximity in the setting of injury to the artery. They may not present until days or weeks after the initial injury due to the
Interventional radiology in the treatment of intracranial vascular injuries and fistulae initial protective effects of haematoma either related to the arterial false aneurysm or via local compression of the fistula site. Traumatic carotid cavernous fistula is a rare entity following blunt or penetrating craniofacial trauma but is by far the most commonly seen post-traumatic intracranial fistula. Fistula can also occur elsewhere following both penetrating and blunt trauma. The majority of these involve the middle meningeal arteries but case reports of fistulae involving intradural vessels have been described.14,20 The classic clinical presentation of TCCF includes pulsatile exophthalmos, bruit, chemosis and visual
1245
disturbance. 67—100% have associated basilar skull fractures and in one series the incidence of TCCF in patients with basilar skull fractures was 3.8%.7,18 Decreased visual acuity is common in TCFF occurring in 17—32% of cases.10,12,16 The causes of this are varied and while some may be related to associated injuries such as direct injury to the optic nerve, a proportion is due to venous hypoxic retinopathy which is potentially reversible with endovascular treatment. Most mild degrees of visual loss are reversible following treatment while complete visual loss is mostly irreversible.
Figure 2 Carotid cavernous fistula are usually well diagnosed on noninvasive angiographic imaging. CTangiogram shows early enhancement of the right cavernous sinus as well as enlargement and early enhancement of the right superior ophthalmic vein (a). Axial T2 weighted MRI and corresponding time of flight MRA of a different case shows similar characteristic enlargement of the left cavernous sinus and superior ophthalmic vein (b and c).
1246 The diagnosis of TCCF can almost always be confirmed with noninvasive angiographic imaging using CT or MR angiography (Fig. 2). The characteristic findings are enlargement and early enhancement of the cavernous sinus and superior ophthalmic vein. Conventional cerebral angiography is required to accurately localise the fistula, to look for high risk features requiring urgent treatment and to plan endovascular management (Fig. 3). Most commonly the fistula site is large and located at the anterior
B.J. McGuinness et al. wall of the ICA just beyond the foramen lacerum as it enters the cavernous sinus, less commonly it lies more distally in the cavernous ICA or arises from one of the small dural branches of the cavernous ICA, e.g. inferolateral trunk. Various angiographic techniques are useful in delineating the exact site of fistula including vertebral and contralateral carotid runs with ipsilateral carotid compression (Fig. 3b). The presence of an associated ICA pseudoaneurysm or cavernous sinus varix should be noted as this
Figure 3 Right carotid cavernous fistula. Lateral internal carotid angiogram (a) during initial work-up shows typical fistula with large draining superior ophthalmic vein anteriorly (large arrow) and inferior petrosal venous drainage posteriorly (double small thick arrows). In addition there is evidence of extensive cortical venous drainage (small thin arrows) which is an important angiographic finding indicating the need for more urgent treatment. (b) Demonstrates the usefulness of a vertebral injection while compressing the ipsilateral carotid in demonstrating the fistula site filling via the small posterior communicating artery (small arrow) and retrogradely back down the cavernous internal carotid (large arrow = fistula site). (c) Shows balloon being deployed through the fistula site with post deployment angiogram (d) demonstrating complete occlusion of the fistula and preservation of the internal carotid artery.
Interventional radiology in the treatment of intracranial vascular injuries and fistulae places the patient at higher risk for haemorrhage.12 Assessment of venous drainage from the fistula is important for both determining the potential risks of the fistula and possible endovascular access paths for treatment. While ophthalmic vein drainage is almost always present, other venous drainage is variable. The inferior petrosal sinus is a useful potential endovascular access pathway but is variably present. Superficial cortical venous drainage via the sphenoparietal sinus or otherwise means there is a small acute risk but in particular a significant longterm risk of subarachnoid and intracerebral haemorrhage. This is often preceded by formation of venous ectasia and pouches involving these draining cortical veins. It is important to assess for the presence of any significant arterial steal of the fistula in relation to the distal arterial supply of the affected ICA. The adequacy of the circle of Willis to provide collateral supply is also a consideration in case of the requirement for ICA sacrifice during treatment. The goal of endovascular treatment of TCCF is to occlude the fistula while ideally maintaining patency of the internal carotid artery. Almost all patients will require treatment as spontaneous regression of TCCFs is rare as opposed to dural AVFs. Patients should have close monitoring of visual acuity and intraocular pressures. Indications for urgent treatment include progressive visual loss, epistaxis, cortical venous drainage on angiography, sphenoid sinus ICA false aneurysm or cavernous sinus varix.12 Traditionally most fistulae can be successfully treated with transarterially deployed detachable balloons through the fistula while preserving the parent ICA (Fig. 3c and d).6,16,19,22 In approximately 75% of cases the fistula can be successfully occluded this way with preservation of the parent ICA.16 Immediate post balloon deployment angiograms need to be carefully assessed for balloon migration within the cavernous sinus and resultant disturbed venous drainage, which may make the ophthalmic venous reflux worse or more seriously divert venous drainage cortically. Occasionally the balloon deployment is unsuccessful because the fistula hole is too small, or the balloon deflates on spicules of bone or the balloons are unable to occlude the cavernous sinus. Also recently there has been an availability problem with detachable balloons. If the balloon cannot be navigated through the fistula to the cavernous sinus then transarterially deployed platinum coils can be used. The transarterial route using balloons, coils or a combination of the two can be used to successfully occlude the fistula with preservation of the parent ICA in 88—98%.10,13 Transvenous coiling is another possibility either percutaneously from the femoral
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vein and inferior petrosal sinus or via direct access of the ophthalmic vein. However this should only be considered in the subacute and chronic stages due to the risk of mechanical perforation acutely.4 Fistulae that rarely arise from cavernous branches of the ICA are best accessed from the external carotid artery. If preservation of the ICA is not possible or in the setting of a sphenoid sinus aneurysm then ICA occlusion will be necessary by trapping the fistula with balloons proximal and distal to the fistula. Immediate complications of endovascular occlusion are uncommon with permanent neurological deficits occurring in 0—4% and can be minimised by routine systemic heparinisation.6,10,13,16 Cranial neuropathy related to pressure effects from the deployed balloons is seen uncommonly and is often transient.10,16 Endovascular treatment has been shown to produce permanent radiological occlusion of the fistula and recurrence of symptoms is not seen.17 Pseudoaneurysms or venous pouches can develop at the site of fistula if a balloon deflates.17 More recently treatment with covered stents within the ICA have shown promise.2,9 The stiffness of delivery systems for these stents means that the configuration of the cavernous ICA needs to be favourable. While midterm results seem favourable, longterm patency of these stents is yet to be proven.
Summary Traumatic intracranial vascular injuries while uncommon require timely diagnosis and management due to their high associated mortality and morbidity. Diagnosis relies on having a low threshold for noninvasive and conventional angiographic investigation in patients at high clinical risk. The management of intradural false aneurysms is challenging both surgically and endovascularly. Most traumatic carotid cavernous fistula can be successfully treated with transarterial balloon deployment through the fistula site. The use of covered stents for vascular injury related to the extradural internal carotid may be seen increasingly in the future.
Conflicts of interest The authors have no conflicts of interest to disclose.
References 1. Amirjamshidi A, Rahmat H, Abbassioun K. Traumatic aneurysms and arteriovenous fistulas of intracranial vessels
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2.
3.
4.
5.
6.
7.
8. 9.
10.
11.
12.
associated with penetrating head injuries occurring during war: principles and pitfalls in diagnosis and management. J Neurosurg 1996;84:769—80. Archondakis E, Pero G, Valvassori L, et al. Angiographic follow-up of traumatic carotid cavernous fistulas treated with endovascular stent graft placement. Am J Neurorad 2007;28:342—7. Asari S, Nakamura S, Yamada O, et al. Traumatic aneurysm of the peripheral cerebral arteries. J Neurosurg 1977;46: 795—803. Berenstein A, Lasjaunias P, Ter Brugge KG. Surgical neuroangiography 2.1, second ed., Berlin Heidelberg Germany: Springer-Verlag; 2004. Buckingham M, Crone KR, Ball WS, et al. Traumatic intracranial aneurysms in childhood: two cases and a review of the literature. Neurosurgery 1988;22:398—408. Debrun GM, Lacour P, Fox AJ, et al. Traumatic carotid-cavernous fistulas: etiology, clinical presentation, diagnosis, treatment, results. Semin Interv Radiol 1987;4(4):242—8. Fabian T, Woody J, Ciraulo D. Posttraumatic carotid cavernous fistula: frequency analysis of signs, symptoms, and disability outcomes after angiographic embolization. J Trauma 1999;47(2):275—81. Fleischer AS, Patton JM, Tindall GT. Cerebral aneurysms of traumatic origin. Surg Neurol 1975;4:233—9. Gomez F, Escobar W, Gomez AM, et al. Treatment of carotid cavernous fistulas using covered stents: midterm results in seven patients. AJNR 2007;28:1762—8. Gupta AK, Purkayastha S, Krishnamoorthy T, et al. Endovascular treatment of direct carotid cavernous fistulae: a pictorial review. Neuroradiology 2006;48:831—9. Haddad FS, Haddad GF, Taha J. Traumatic intracranial aneurysms caused by missiles: their presentation and management. Neurosurgery 1991;28:1—7. Halbach VV, Hieshima GB, Higashida RT, et al. Carotid cavernous fistulae: indications for urgent therapy. AJNR 1987;8: 627—33.
B.J. McGuinness et al. 13. Higashida RT, Halbach VV, Dowd C, et al. Endovascular detachable balloon embolization therapy of cavernous carotid artery aneurysms: results in 87 cases. J Neurosurg 1990;72:857—63. 14. Kieck CF, De Villiers JC. Vascular lesions due to stab wounds. J Neurosurg 1984;60:42—6. 15. Lempert TE, Halbach VV, Higashida RT, et al. Endovascular treatment of pseudoaneurysms with electronically detachable coils. AJNR 1998;19:907—11. 16. Lewis AI, Tomsick TA, Tew Jr JM. Management of 100 consecutive direct carotid-cavernous fistulas: results of treatment using detachable balloons. Neurosurgery 1995;36:239—45. 17. Lewis AI, Tomsick TA, Tew JM, Lawless MA. Long-term results in direct carotid-cavernous fistulas after treatment with detachable balloons. J Neurosurg 1996;84:400—4. 18. Liang W, Xiaofeng Y, Weiguo L, et al. Traumatic carotid cavernous fistula accompanying basilar skull fracture: a study on the incidence of traumatic carotid cavernous fistula in the patients with basilar skull fracture and the prognostic ananlysis abourt traumatic carotid cavernous fistula. J Trauma 2007;63:1014—20. 19. Norman D, Newton TH, Edwards MS, DeCaprio V. Carotidcavernous fistula: closure with detachable silicone balloons. Radiology 1983;149:149—57. 20. Parkinson D, West M. Traumatic intracranial aneurysms. J Neurosurg 1980;52:11—20. 21. Resnick DK, Subach BR, Marion DW. The significance of carotid canal involvement in basilar cranial fracture. Neurosurgery 1997;40(6):1177—81. June. 22. Serbinenko FA. Balloon catheterization and occlusion of major cerebral vessels. J Neurosurg 1974;41:125—45. 23. Uzan M, Cantasdemir M, Sekin M. Traumatic intracranial carotid tree aneurysms. Neurosurgery 1998;43(6):1314—20. 24. Van der Schaaf IC, Brilstra EH, Buskens E, Rinkel GJE. Endovascular treatment of aneurysms in the cavernous sinus: a systematic review on balloon occlusion of the parent vessel and embolization with coils. Stroke 2002;33:313—8.
www.elsevier.com/locate/injury
Interventional radiology in the treatment of intracranial vascular injuries and fistulae B.J. McGuinness *, M. Moriarty, J.K.A. Hope Radiology Department, Auckland City Hospital, Park Road, Grafton, Auckland, New Zealand Accepted 27 January 2008
KEYWORDS Traumatic intracranial aneurysm; Traumatic carotid cavernous fistulae; Endovascular treatment; Intracranial vascular injury
Summary Traumatic intracranial vascular injuries are uncommon. However prompt diagnosis and management is essential because of the high morbidity and mortality associated with these conditions. The imaging evaluation and potential endovascular management of traumatic intracranial aneurysms and traumatic intracranial fistulae is discussed. # 2008 Elsevier Ltd. All rights reserved.
Intracranial vascular injuries that may require emergency endovascular management can be broadly divided into intradural traumatic aneurysms, extradural arterial injury usually involving the internal carotid artery and traumatic arteriovenous fistulae most commonly related to the cavernous sinus. These may arise as the result of penetrating or more commonly blunt trauma. Prior to the widespread use of CT traumatic intracranial vascular injury was more readily identified as angiography was the main imaging modality in significant head trauma. With unenhanced CT now being the standard imaging modality in trauma the diagnosis of traumatic intracranial aneurysms and fistulae relies on clinical suspicion and the presence of certain indirect findings on unenhanced CT. * Corresponding author. Tel.: +6493074949x24504. E-mail address: [email protected] (B.J. McGuinness).
Traumatic intracranial aneurysms Less than 1% of intracranial aneurysms are traumatic in origin in adults although they account for a much larger proportion of aneurysms in children. Traumatic aneurysms can be classified based on the mechanism of injury and location of aneurysm.5 Penetrating trauma will result in a pseudoaneurysm occurring along the path of the injury. Stab wounds tend to have a higher incidence of traumatic aneurysm formation than missile wounds. In one series of 109 patients mostly with stab wounds there was an incidence of nearly 30% for major intracranial vascular injury and 10% incidence of aneurysms.14 In the case of missiles, the projectile causing a pseudoaneurysm will typically be irregular in shape and slow in velocity, hence shrapnel is much more likely to cause a traumatic aneurysm than gunshot wounds.11 In almost all cases there will not be an
0020–1383/$ — see front matter # 2008 Elsevier Ltd. All rights reserved. doi:10.1016/j.injury.2008.01.054
Interventional radiology in the treatment of intracranial vascular injuries and fistulae exit wound and the missile will be retained intracranially.11 In such cases of retained bullets the traumatic aneurysm will tend to occur along the distal aspect of its path where it has slowed. In a series of wartime penetrating injuries the angiographic incidence of traumatic aneurysms was 5.7% where patients were selected as high risk based on the path of the missile, large entry path haematoma on CT, multiple retained fragments and the surgeons’ debridement findings.1 Blunt traumatic aneurysms of the skull base will occur where the ICA is fixed either related to the petrous or cavernous portions and are often associated with basilar skull fractures. Intradural traumatic aneurysms in blunt trauma commonly occur in pericallosal and posterior cerebral artery locations as a result of impact of the artery against firm edges of the adjacent falx cerebri and tentorium cerebelli, respectively. Distal cortical aneurysms are also seen and are thought to occur as a result of transient herniation and injury within a fracture defect or through rents in surface arteries where they give small dural branches.3,5,8 Diagnosis of traumatic aneurysms relies heavily on the level of clinical suspicion. In a patient with blunt craniofacial trauma, delayed or unexplained neurological deterioration, unusual location of intracranial haemorrhage and recurrent large epistaxis all warrant further angiographic investigation. The presence of basal skull fractures on CT involving the carotid canal and particularly the petrous segment is a significant risk factor and should also result in a high clinical suspicion (up to 10% incidence of aneurysm).21 Cavernous ICA aneurysm may also present in a delayed fashion with a cavernous sinus syndrome consisting of retro orbital headache and compressive findings related to the 3rd through 6th cranial nerves. Consideration should be given to angiography in all patients with penetrating trauma given the relatively high association with vascular injury. There are several documented cases of normal initial cerebral angiograms with subsequent angiography showing a traumatic aneurysm so consideration should also be given to routine repeat angiography for those at high clinical risk or with penetrating injuries.1,3,8,23 The angiographic findings of a traumatic aneurysm includes a poorly defined neck, unusual often peripheral locations showing no relationship to arterial branch points, irregularly shaped aneurysms, and delayed filling and emptying of the aneurysm (Fig. 1). Time between trauma and aneurysm rupture ranges from 1 day to many months, with about 50% of cases likely to rupture within 3 weeks.3,5,8 There are reported cases of reduction in size and disappearance of aneurysms on angiography, in a
1243
series by Amirjamshidi et al. of 31 traumatic aneurysms due to missile penetrating injuries 6 (19.4%) healed spontaneously and shrank or disappeared on follow-up angiography.1,8 The mortality rates following rupture of traumatic aneurysms has been variously reported between 31% and 54%.3,5,8 In surgically treated patients the mortality rates are much lower and range between 18% and 20%.3,8,20 Surgical treatment of intradural traumatic aneurysms includes clipping, wrapping or excision and like endovascular techniques can be very challenging due to the thin and fragile walls of traumatic aneurysms often with poorly defined necks.1,5 Endovascular techniques to preserve the parent artery via coil embolisation of the aneurysm is risky in the acute phase as the wall is extremely fragile and subsequent risk of coil or microcatheter perforation high. After a period of some weeks, subacute traumatic pseudoaneurysm walls are thought more stable and at this time GDC coil embolisation can be performed with preservation of the parent vessel if anatomical features such as dome to neck ratio allow.15 Failing this endovascular occlusion of the parent vessel as close to the aneurysm as possible can be performed. If the location of the aneurysm means that parent vessel occlusion will result in devastating consequences then a conservative approach could also be considered but the patient would require intensive monitoring and regular angiographic follow-up for 6—8 weeks.1 Traumatic ICA aneurysms may be treated endovascularly either by parent vessel sacrifice via detachable balloon occlusion or by embolisation of the aneurysm sac (usually with GDC coils but detachable balloons have been used as well) with preservation of the ICA. All patients having ICA occlusion should undergo a balloon test occlusion first. Detachable balloon occlusion of the ICA is associated with neglible mortality with permanent ischaemia being the most significant complication occurring at a rate of about 5% despite clinical tolerance of balloon test occlusion.13,24 The proposed advantages over surgical ligation of the ICA more proximally in the neck include the ability to occlude immediately proximal to the aneurysm therefore reducing the risk of collateral pathways taking over supply to the aneurysm, that there is less distal stump of ICA to act as a site of embolisation while it thromboses and the fact that the patient is awake and can be monitored for neurological deterioration during occlusion. If the traumatic aneurysm has a defined neck then consideration should be given to coil embolisation of the aneurysm with preservation of the parent ICA. This technique may result in only partial occlusion of the aneurysm in up to 20% (<90% occluded) and therefore require ongoing surveillance angiography
1244
B.J. McGuinness et al.
Figure 1 Young man who sustained penetrating trauma to right frontotemporal region with a screwdriver. Noncontrast CT scan shows haematoma and some small bone fragments along the tract of injury across the midline in the inferior frontal lobes (a and b). Initial cerebral angiogram (not shown) demonstrated vasospasm but no false aneurysm. Follow-up CTangiogram (axial and sagittal) shows a small aneurysm related to the proximal A2 segment of the left anterior cerebral artery (c and d). Subsequent cerebral angiogram demonstrates the typical delayed filling and emptying of the false aneurysm. This was treated endovascularly by parent artery occlusion using liquid embolic agent (e, f, and g).
and possible retreatment. However the risk of permanent ischaemic complications is likely to be lower than for balloon occlusion of the parent ICA.15,23 Pseudoaneurysms of the ICA that are at least partially surrounded by bone are thought to be at lower risk of rupture during coil embolisation although again treatment in the subacute phase when the wall has matured should be safer.15
Traumatic carotid cavernous fistulae (TCCF) Arteriovenous fistula is an abnormal connection between an artery and vein which tends to occur when these structures are in close proximity in the setting of injury to the artery. They may not present until days or weeks after the initial injury due to the
Interventional radiology in the treatment of intracranial vascular injuries and fistulae initial protective effects of haematoma either related to the arterial false aneurysm or via local compression of the fistula site. Traumatic carotid cavernous fistula is a rare entity following blunt or penetrating craniofacial trauma but is by far the most commonly seen post-traumatic intracranial fistula. Fistula can also occur elsewhere following both penetrating and blunt trauma. The majority of these involve the middle meningeal arteries but case reports of fistulae involving intradural vessels have been described.14,20 The classic clinical presentation of TCCF includes pulsatile exophthalmos, bruit, chemosis and visual
1245
disturbance. 67—100% have associated basilar skull fractures and in one series the incidence of TCCF in patients with basilar skull fractures was 3.8%.7,18 Decreased visual acuity is common in TCFF occurring in 17—32% of cases.10,12,16 The causes of this are varied and while some may be related to associated injuries such as direct injury to the optic nerve, a proportion is due to venous hypoxic retinopathy which is potentially reversible with endovascular treatment. Most mild degrees of visual loss are reversible following treatment while complete visual loss is mostly irreversible.
Figure 2 Carotid cavernous fistula are usually well diagnosed on noninvasive angiographic imaging. CTangiogram shows early enhancement of the right cavernous sinus as well as enlargement and early enhancement of the right superior ophthalmic vein (a). Axial T2 weighted MRI and corresponding time of flight MRA of a different case shows similar characteristic enlargement of the left cavernous sinus and superior ophthalmic vein (b and c).
1246 The diagnosis of TCCF can almost always be confirmed with noninvasive angiographic imaging using CT or MR angiography (Fig. 2). The characteristic findings are enlargement and early enhancement of the cavernous sinus and superior ophthalmic vein. Conventional cerebral angiography is required to accurately localise the fistula, to look for high risk features requiring urgent treatment and to plan endovascular management (Fig. 3). Most commonly the fistula site is large and located at the anterior
B.J. McGuinness et al. wall of the ICA just beyond the foramen lacerum as it enters the cavernous sinus, less commonly it lies more distally in the cavernous ICA or arises from one of the small dural branches of the cavernous ICA, e.g. inferolateral trunk. Various angiographic techniques are useful in delineating the exact site of fistula including vertebral and contralateral carotid runs with ipsilateral carotid compression (Fig. 3b). The presence of an associated ICA pseudoaneurysm or cavernous sinus varix should be noted as this
Figure 3 Right carotid cavernous fistula. Lateral internal carotid angiogram (a) during initial work-up shows typical fistula with large draining superior ophthalmic vein anteriorly (large arrow) and inferior petrosal venous drainage posteriorly (double small thick arrows). In addition there is evidence of extensive cortical venous drainage (small thin arrows) which is an important angiographic finding indicating the need for more urgent treatment. (b) Demonstrates the usefulness of a vertebral injection while compressing the ipsilateral carotid in demonstrating the fistula site filling via the small posterior communicating artery (small arrow) and retrogradely back down the cavernous internal carotid (large arrow = fistula site). (c) Shows balloon being deployed through the fistula site with post deployment angiogram (d) demonstrating complete occlusion of the fistula and preservation of the internal carotid artery.
Interventional radiology in the treatment of intracranial vascular injuries and fistulae places the patient at higher risk for haemorrhage.12 Assessment of venous drainage from the fistula is important for both determining the potential risks of the fistula and possible endovascular access paths for treatment. While ophthalmic vein drainage is almost always present, other venous drainage is variable. The inferior petrosal sinus is a useful potential endovascular access pathway but is variably present. Superficial cortical venous drainage via the sphenoparietal sinus or otherwise means there is a small acute risk but in particular a significant longterm risk of subarachnoid and intracerebral haemorrhage. This is often preceded by formation of venous ectasia and pouches involving these draining cortical veins. It is important to assess for the presence of any significant arterial steal of the fistula in relation to the distal arterial supply of the affected ICA. The adequacy of the circle of Willis to provide collateral supply is also a consideration in case of the requirement for ICA sacrifice during treatment. The goal of endovascular treatment of TCCF is to occlude the fistula while ideally maintaining patency of the internal carotid artery. Almost all patients will require treatment as spontaneous regression of TCCFs is rare as opposed to dural AVFs. Patients should have close monitoring of visual acuity and intraocular pressures. Indications for urgent treatment include progressive visual loss, epistaxis, cortical venous drainage on angiography, sphenoid sinus ICA false aneurysm or cavernous sinus varix.12 Traditionally most fistulae can be successfully treated with transarterially deployed detachable balloons through the fistula while preserving the parent ICA (Fig. 3c and d).6,16,19,22 In approximately 75% of cases the fistula can be successfully occluded this way with preservation of the parent ICA.16 Immediate post balloon deployment angiograms need to be carefully assessed for balloon migration within the cavernous sinus and resultant disturbed venous drainage, which may make the ophthalmic venous reflux worse or more seriously divert venous drainage cortically. Occasionally the balloon deployment is unsuccessful because the fistula hole is too small, or the balloon deflates on spicules of bone or the balloons are unable to occlude the cavernous sinus. Also recently there has been an availability problem with detachable balloons. If the balloon cannot be navigated through the fistula to the cavernous sinus then transarterially deployed platinum coils can be used. The transarterial route using balloons, coils or a combination of the two can be used to successfully occlude the fistula with preservation of the parent ICA in 88—98%.10,13 Transvenous coiling is another possibility either percutaneously from the femoral
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vein and inferior petrosal sinus or via direct access of the ophthalmic vein. However this should only be considered in the subacute and chronic stages due to the risk of mechanical perforation acutely.4 Fistulae that rarely arise from cavernous branches of the ICA are best accessed from the external carotid artery. If preservation of the ICA is not possible or in the setting of a sphenoid sinus aneurysm then ICA occlusion will be necessary by trapping the fistula with balloons proximal and distal to the fistula. Immediate complications of endovascular occlusion are uncommon with permanent neurological deficits occurring in 0—4% and can be minimised by routine systemic heparinisation.6,10,13,16 Cranial neuropathy related to pressure effects from the deployed balloons is seen uncommonly and is often transient.10,16 Endovascular treatment has been shown to produce permanent radiological occlusion of the fistula and recurrence of symptoms is not seen.17 Pseudoaneurysms or venous pouches can develop at the site of fistula if a balloon deflates.17 More recently treatment with covered stents within the ICA have shown promise.2,9 The stiffness of delivery systems for these stents means that the configuration of the cavernous ICA needs to be favourable. While midterm results seem favourable, longterm patency of these stents is yet to be proven.
Summary Traumatic intracranial vascular injuries while uncommon require timely diagnosis and management due to their high associated mortality and morbidity. Diagnosis relies on having a low threshold for noninvasive and conventional angiographic investigation in patients at high clinical risk. The management of intradural false aneurysms is challenging both surgically and endovascularly. Most traumatic carotid cavernous fistula can be successfully treated with transarterial balloon deployment through the fistula site. The use of covered stents for vascular injury related to the extradural internal carotid may be seen increasingly in the future.
Conflicts of interest The authors have no conflicts of interest to disclose.
References 1. Amirjamshidi A, Rahmat H, Abbassioun K. Traumatic aneurysms and arteriovenous fistulas of intracranial vessels
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2.
3.
4.
5.
6.
7.
8. 9.
10.
11.
12.
associated with penetrating head injuries occurring during war: principles and pitfalls in diagnosis and management. J Neurosurg 1996;84:769—80. Archondakis E, Pero G, Valvassori L, et al. Angiographic follow-up of traumatic carotid cavernous fistulas treated with endovascular stent graft placement. Am J Neurorad 2007;28:342—7. Asari S, Nakamura S, Yamada O, et al. Traumatic aneurysm of the peripheral cerebral arteries. J Neurosurg 1977;46: 795—803. Berenstein A, Lasjaunias P, Ter Brugge KG. Surgical neuroangiography 2.1, second ed., Berlin Heidelberg Germany: Springer-Verlag; 2004. Buckingham M, Crone KR, Ball WS, et al. Traumatic intracranial aneurysms in childhood: two cases and a review of the literature. Neurosurgery 1988;22:398—408. Debrun GM, Lacour P, Fox AJ, et al. Traumatic carotid-cavernous fistulas: etiology, clinical presentation, diagnosis, treatment, results. Semin Interv Radiol 1987;4(4):242—8. Fabian T, Woody J, Ciraulo D. Posttraumatic carotid cavernous fistula: frequency analysis of signs, symptoms, and disability outcomes after angiographic embolization. J Trauma 1999;47(2):275—81. Fleischer AS, Patton JM, Tindall GT. Cerebral aneurysms of traumatic origin. Surg Neurol 1975;4:233—9. Gomez F, Escobar W, Gomez AM, et al. Treatment of carotid cavernous fistulas using covered stents: midterm results in seven patients. AJNR 2007;28:1762—8. Gupta AK, Purkayastha S, Krishnamoorthy T, et al. Endovascular treatment of direct carotid cavernous fistulae: a pictorial review. Neuroradiology 2006;48:831—9. Haddad FS, Haddad GF, Taha J. Traumatic intracranial aneurysms caused by missiles: their presentation and management. Neurosurgery 1991;28:1—7. Halbach VV, Hieshima GB, Higashida RT, et al. Carotid cavernous fistulae: indications for urgent therapy. AJNR 1987;8: 627—33.
B.J. McGuinness et al. 13. Higashida RT, Halbach VV, Dowd C, et al. Endovascular detachable balloon embolization therapy of cavernous carotid artery aneurysms: results in 87 cases. J Neurosurg 1990;72:857—63. 14. Kieck CF, De Villiers JC. Vascular lesions due to stab wounds. J Neurosurg 1984;60:42—6. 15. Lempert TE, Halbach VV, Higashida RT, et al. Endovascular treatment of pseudoaneurysms with electronically detachable coils. AJNR 1998;19:907—11. 16. Lewis AI, Tomsick TA, Tew Jr JM. Management of 100 consecutive direct carotid-cavernous fistulas: results of treatment using detachable balloons. Neurosurgery 1995;36:239—45. 17. Lewis AI, Tomsick TA, Tew JM, Lawless MA. Long-term results in direct carotid-cavernous fistulas after treatment with detachable balloons. J Neurosurg 1996;84:400—4. 18. Liang W, Xiaofeng Y, Weiguo L, et al. Traumatic carotid cavernous fistula accompanying basilar skull fracture: a study on the incidence of traumatic carotid cavernous fistula in the patients with basilar skull fracture and the prognostic ananlysis abourt traumatic carotid cavernous fistula. J Trauma 2007;63:1014—20. 19. Norman D, Newton TH, Edwards MS, DeCaprio V. Carotidcavernous fistula: closure with detachable silicone balloons. Radiology 1983;149:149—57. 20. Parkinson D, West M. Traumatic intracranial aneurysms. J Neurosurg 1980;52:11—20. 21. Resnick DK, Subach BR, Marion DW. The significance of carotid canal involvement in basilar cranial fracture. Neurosurgery 1997;40(6):1177—81. June. 22. Serbinenko FA. Balloon catheterization and occlusion of major cerebral vessels. J Neurosurg 1974;41:125—45. 23. Uzan M, Cantasdemir M, Sekin M. Traumatic intracranial carotid tree aneurysms. Neurosurgery 1998;43(6):1314—20. 24. Van der Schaaf IC, Brilstra EH, Buskens E, Rinkel GJE. Endovascular treatment of aneurysms in the cavernous sinus: a systematic review on balloon occlusion of the parent vessel and embolization with coils. Stroke 2002;33:313—8.