Cli~.RadioL (1979) 30, 111-116
Ernbolisation of the External Carotid Artery in the Treatment of Carotid Cavernous Sinus Fistulae A.J. GERLOCK, JR
From the Department of Radiology and Radiological Sciences, Vanderbilt University School of Medicine, Nashville, Tennessee 37232 A review of treatment methods used to control carotid cavernous sinus fistulae is presented. Three cases are described in which embolisation of the external carotid artery was done along with intracranial vascular procedures in the management of carotid cavernous fistulae.
Numerous treatment methods have been used in the management of carotid cavernous sinus fistulae over the years with success or failure reported by various writers (Arutinunou et al., 1968; Black et al., 1971; Brooks, 1930; Dandy, 1935; Echols and Jackson, 1959; Gindi and Andrew, 1967; Gurdjian, 1938; Hamby and Gardner, 1933; Hamby, 1964; Hayes, 1958; Ismat et al., 1970; Ishimori et al., 1967; Jaeger, 1959; Kosary et al., 1968; Lang and Bucy, 1965; Parkinson, 1967; Sedzimir et al., 1967). The radiologist, in the performance of angiography or the performance of therapeutic embolisation catheter procedures, may enter into the management of these patients after several surgical procedures or others forms of treatment have failed. For this reason, the following review is necessary to acquaint the radiologist with some of the standard treatment methods so that the diagnostic angiography or therapeutic embolisation procedures can be planned and evaluated. This will also point out the reason for complete angiographic documentation of all vessels feeding the carotid cavernous sinus fistula. A direct approach to the fistula is difficult and a dangerous undertaking (Parkinson, 1965; Sedzimir and Occleshaw, 1967; Stern et al., 1967). Treatment is generally directed at reducing the blood flow through the fistula so that thrombosis can occur in the intracavernous portion of the internal carotid artery. The flow of blood through the fistula will then be completely shut off. Early methods to cut down on blood flow through the fistula began with intermittent carotid artery compression for seven days, which is reported to have a cure rate of 16% (Dandy, 1935). Later methods consisted of single ligation of the carotid artery in the neck, either the common or internal carotid artery, with a device allowing a slow gradual occhision to occur. The Selverstone clamp has been widely used for this purpose (Fig. la). Cure or improvement rates with this procedure are varied. Locke reported a 68%
cure or improvement with common carotid artery ligation with a mortality rate of 7%. When the internal carotid artery was ligated, he reported a cure rate of 87.5% with a mortality rate of 9.4% (Locke, 1924). Success after internal carotid artery ligation in the neck alone has been reported by others to be 50% or less (Lang and Bucy, 1965). Tonnis (1960) states that ligation of the common and internal carotid arteries in the neck produced a satisfactory result in only 3 5 - 4 0 % of cases. Neck ligation of the internal carotid artery alone is undesirable because it not only deprives the fistula and brain of blood supplied by this artery, but the opposite hemisphere as well. Since only the ipsilateral internal carotid artery has been occluded, blood from the opposite carotid circulation will be sucked across the circle of Willis and down into the fistula opening. The trapping procedure is another surgical technique used in the treatment of these fistulae. This consists of ligating vessels intracranially in an attempt to isolate the fistula from arterial blood flow. One such method consists of ligating the supraclinoid segment of the internal carotid artery proximal to the posterior communicating artery and neck ligation of the internal carotid artery (Fig. lb). This procedure has a cure rate of 56.7% (Hayes, 1963). 'Complete trapping' occurs when there is intracranial occlusion of the supraclinoid carotid segment and ophthalmic artery, followed by neck ligation of the internal and external carotid arteries (Fig. lc). This procedure has a cure rate of approximately 78.8% (Hayes, 1963). Failure of these types of surgical procedures seem to be the result of numerous anastomotic channels particularly concerning the intracavemous portion of the internal carotid artery (Hayes, 1958, 1963; Margolis and Newton, 1969; Parkinson, 1964). In order more effectively to occlude these rich anastomotic channels, as well as the fistula itself, intraluminal embolisation of the internal carotid artery has been attempted. This has been done alone and in
112
CLINICAL RADIOLOGY S.C.C.
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Fig. 1 - (a) Selverstone clamp neck occlusion of either the common carotid (CC) or internal carotid (IC). This decreased the blood flow through the fistular opening (arrow) of the intracavernous portion of the IC into the cavernous sinus (CS). (b) Ligation of the supraclinoid carotid (SCC) proximal to the posterior communicating artery (PC) and neck ligation of the IC. (c) 'Complete trapping" combines ligation of the ophthalmic artery (opth) and SCC with neck ligation of the external carotid artery (EC) and IC. (d)
Occlusion of the fistular opening by intraluminal muscle embolisation of the IC and ligation of the CC. (e) Ligation of the opth and SCC is performed first followed by obliteration of the collaterals to the intracavernous portion of the IC by embolisation. This is then followed by ligating the EC, IC and CC. (f) Occlusion of the fistular opening by embolising a piece of muscle attached to a nylon thread followed by ligation of the CC.
combination with other surgical procedures (Fig. l d - f ) (Brooks, 1930; Gindi and Andrew, 1967; Gurdjian, 1938; Hamby and Gardner, 1933; Hamby, 1964; Ismat eta/., 1970; Ishimori et al., 1967; Jaeger, 1959; Kosary et al., 1968; Lang and Bucy, 1965; Parkinson, 1965). Brooks (1930) successfully a t t e m p t e d treatment o f a carotid cavernous fistula by muscle embolisation o f the intracavernous portion o f the carotid artery and ligation of the common carotid artery (Fig. l d). Complications of this pro-
cedure prevented its wide use. These complications consist o f possible obstruction of the distal segments of the middle or anterior cerebral arteries with loose fragments of the embolised material. The possibility of such complications led to the combination of intracranially ligating the supraclinoid segment of the internal carotid artery first, before performing the embolisation procedure. This is done especially when the carotid angiogram fails to show the major flow of blood from the internfil carotid artery into the ~istula.
EMBOLISATION OF THE EXTERNAL CAROTID ARTERY ThiS is also done when the intracranial vessels fdl mainly from the internal carotid artery on the s~ae side as the fistula. Such a procedure is the definitive one stage attack described by Hamby (1964)- In this procedure, the supraclinoid segment. of the internal carotid artery between the posterior communicating artery and cavernous sinus is clipped first. This is done along with the ophthalmic artery, if possible. The collaterals to the intracavernous carotid artery are then attacked by obliteration of this entire segment with intraluminal muscle enabolisation. Tying and severing the common, interhal and external carotid arteries completes the procedure (Fig. le). Ligation of the internal cartid artery ha the neck facilitates thrombosis and prevents the enabolised muscle from passing through the fistula. In the event that it is considered unwise to obstruct the carotid artery on the side of the fistula, a guided embolisation procedure has been used (Black et aL, 1971). A piece of muscle is introduced into the carotid artery to which is attached a nylon thread to control the embolus until it .is in place (Fig. l f). This method has the advantage that, if the embolus fails to occlude the fistula, it can be removed and not be allowed to pass distally into the intracranial vessels. A potential hazard of this technique concerns permanent presence of a long thread in the carotid lumen, with the possibility of thrombus formation on the thread. Other cases have been reported using various embolisation materials, such as gelfoam wrapped in a gold film as an X-ray marker (Ishimori e t al., 1967),
Fig. 2 - Shows branches of the internal maxillary artery supplyingthe fistula (unlabelled arrows).
113
5 m m porcelain beads (Kosary e t al., 1968) and acrylic materials (Gindi and Andrew, 1967). To this we would like to add our experience in three patients with gelfoam embolisation of the external carotid circulation. The indications and reasons for its use will also be discussed.
REPORT OF CASES Case 1. A 17-year-old male sustained a gunshot wound to the face and subsequently developed a left carotid cavernous fistula. Initial debrediment of the left facial wound resulted in neck ligation of the lacerated left internal carotid artery. Postoperative angiographic evaluation revealed a left carotid cavernous fistula and confirmed obstruction of the left internal carotid artery. The carotid cavernous fistula was fed througja the intracavernous portion of the left internal carotid. This segment was supplied blood by the left posterior communicating as demonstrated on the vertebral angiogram. A right internal carotid angiogram showed blood flow to the left cerebral hemisphere and carotid cavernous fistula across a patent anterior communicating artery. No branches of the right external carotid were found to supply the carotid cavernous fistula. Subselective angiography of the left external carotid showed numerous branches from the internal maxillary artery feeding the carotid cavernous fistula (F~g. 2). Fig. 3 shows obstruction of the internal maxillary and its branches following embolisation with 32 gelfoam particles expressed through a Red Kifa 5.4 French catheter wedged in the internal maxillary artery. No filling of the carotid cavernous fistula from the external carotid was present following the embolisation procedure. Approximately 16h following embolisation of the external carotid, this patient experienced a mild temperature elevation and discomfort in the region of the angle of the mandible. This subsided within 24 h, and no further discomfort was noted.
Fig_ 3 - Shows obstruction of the internal maxillary artery and its branches following embolisation (arrows). Note absence of filling of the fistula.
114
CLINICAL RADIOLOGY
Fig. 4 - Shows filling o f the fistula from branches of t h e proximal portion o f the o p h t h a l m i c artery (arrow).
Intracranial clipping o f the supraclinoid s e g m e n t of t h e left internal carotid artery and o p h t h a l m i c artery was carried out. This resulted in a m o d e r a t e d decrease o f proptosis and obliteration of t h e intracranial bruit. A one year follow-up shows no evidence of recurrence of t h e carotid cavernous fistula. Case 2. This 28-year-old male developed proptosis of t h e left eye following impalement o f t h e left orbit u p o n t h e sharp point of a pencil. Bilateral selective angiography of t h e internal carotid and external carotid were performed. A cavernous sinus fistula was seen to fill from the proximal portion of the left ophthalmic, artery on the internal carotid angiogram (Fig- 4) and from vascular c o m m u n i c a t i o n s from the internal maxillary artery on the external angiograrn (Fig. 5). No direct c o m m u n i c a t i o n b e t w e e n the intracavernous p o r t i o n of the internal carotid and cavernous sinus were d e m o n s t r a t e d (Fig. 4). Embolisation of the left external carotid was done, followed by intracranial clipping of the left ophthalmic artery. This resulted in a transient decrease in the patient's intracranial bruit and proptosis. Repeat external carotid angiography was done following the recurrence of s y m p t o m s and an incomplete o b s t r u c t i o n of the branches o f the external carotid feeding t h e fistula was f o u n d to be present (Fig_ 6). A second embolisation procedure of the external carotid was performed resulting in occlusion of these branches. This patient also experienced a mild temperature elevation and pain around t h e angle of the mandible following t h e procedure. This subsided within 24 h w i t h o u t further discomfort. A 13-month follow-up of this patient shows no evidence of progression or recurrence of the fistula. Case 3. This 52-year-old male presented with failing vision, progressive proptosis of the right eye, distended facial veins, and an intracranial bruit. Past history revealed that a Selverstone clamp occlusion of t h e right internal carotid h a d been done 15 years earlier for t r e a t m e n t of a carotid cavernous fistula obtained following orbital t r a u m a (Fig. 7). Angiography for evaluation of this progressive recurrent
Fig. 5 - Left external carotid artery angiogram shows branches of the internal maxillary artery supplying the carotid cavernous fistula (arrows). A dilated superior op. thalmic vein is seen draining the fistula (vertical unlabeUed arrow).
carotid cavernous fistula, showed it to be fed from left internal carotid, right external carotid and vertebral basllar system. T r e a t m e n t of this chronic fistula consisted ofintracranial clipping of the supracllnoid portion o f the right internal
Fig. 6 - Shows external carotid angiogram following fi~st embolisation. Two large black arrows point to the ascending pharyngeal artery which supplies the fistula. The small arrows shows persistent small collaterals from the inter ~al maxillary artery.
E M B O L I S A T I O N O F THE E X T E R N A L C A R O T I D A R T E R Y
115
carotid, which obstructed the flow of blood to the fistula from the left interfial carotid and vertebral basflar circulation. The extensive collateral bxanches from the right external carotid to the carotid cavernous fistula (Fig. 8) were obliterated by gelfoam embolisation of the right external carotid (Fig. 9). Because of the large well-established collaterals between the external carotid and carotid cavernous fistula, 103 gelfoam emboli were required to obstruct completely the external carotid and its branches to the carotid cavernous fistula. The carotid cavernous fistula was controlled but the embolisation of these rich well-formed collaterals resulted in tissue necrosis of the right temporalis muscle, pterygoid muscles, parotid gland and overlying skin. Osteonecrosis of the temporal bone also developed with the sequelae of loss of function of the right middle ear and non-healing of the temporal craniotomy site. A portion of the angle o f the mandible was also devitalised and became necrotic, but no loss of function of the mandible occurred. Paralysis of the seventh cranial nerve developed shortly after the embolisation procedure, its aetiology possibly resulting from reflux of the emboli from the external carotid into the vertebral basilar system. A one-year follow-up of this patient shows the carotid cavernous fistula is controlled, but the loss of hearing and seventh cranial paralysis remain permanent. The cosmetic appearance of the area of tissue necrosis is fair as a result of skin grafting procedures of the upper cervical and temporal regions. DISCUSSION
Fig. 7 - The middle arrow points to the Selverstone clamp occlusion of the internal carotid. The common carotid is shown, lower arrow, and the upper arrow points to the enlarged external carotid.
Fig. 8 - Selective external carotid angiogram showing numerous large collaterals from the internal maxillary artery to the carotid cavernous fistula (arrows).
E m b o l i s a t i o n o f the e x t e r n a l carotid can b e perf o r m e d either p r i o r to surgery or after surgery, and s h o u l d be d o n e even w h e n t h e subselective e x t e r n a l c a r o t i d angiograms fail t o s h o w its b r a n c h e s f e e d i n g
Fig. 9 - Post-embolisation angiogram showing occlusion of the external carotid and its branches (upper arrow). No filling of the fistula is present. The lower arrows point to the Selverstone clamp occluding the internal carotid.
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CLINICAL RADIOLOGY
the carotid cavernous fistula. This type of embolisation is done t o prevent any collateral pathways from the external carotid from opening up and resulting in a failure of the intracranial surgical clipping procedures. Complications of embolising the external carotid can occur, as shown in Case 3. The reasons for these complications are not clearly understood in this patient. Contamination of the embolised particles or to extensive embolisation o f the external carotid circulation may explain, in part, the resultant tissue necrosis and infection. The internal carotid had been occluded for five years prior to embolisation of the external carotid in this patient. Multiple large collateral pathways between the external carotid and intracavernous portion of the internal carotid had now formed involving the meningeal branches of the infra-orbital artery, accessory meningeal artery, accessory meningeal o f the pterygoid artery and ascending pharyngeal artery. This extensive n e tw o r k of long-standing coUaterals required numerous gelfoam emboli to occlude them. Cranial nerve damage can only be assumed to have occurred as a result o f reflux of embolised particles either intra- or extracranially into the vertebral basilar circulation. To prevent these complications in the future, patients with long-standing widely patent collaterals from the external carotid to the intracavernous portion of the internal carotid should be carefully evaluated and the procedure abandoned when small numbers o f embolised particles are found inefficient at occluding these collaterals. Cases 1 and 2, 2 4 h after the embolisation procedure, were found to have only mild temperature elevations and mild discomfort in the region of the angle of the ipsilateral mandible. These symptoms subsided within 48 h after their onset, 8 - 2 4 h following embolisation of the external carotid, and no further discomfort was noted. A one-year follow-up of all cases shows the fistulae have remained controlled. Acknowledgements. The author wishes to express appreciation,to Mrs Linda Bland, Research Technician, and Mrs Dorothy Gutekunst, BA, Research Technician, for their technical and photographic assistance. REFERENCES
Arutinunou, A. I. et al. (1968)- Surgical treatment of carotidcavernous fistulas. Progressive Brain Research, 3 0 , 4 4 1 444. Black, P. et al. (1971). Carotid-cavernous fistula: a technique for occlusion of fistula with preservation of carotid blood flow. Transactions of the American Neurological Association, 96,205-208. Brooks, B. (1930). The treatment of traumatic arteriovenous fistula. Southern Medical Journal, 23, 100-106. Dandy, W. E. (1935). The treatment of carotid-cavernous
arteriovenous aneurysm. Annals of Surgery, 102, 916~ 926. Echols, D. H. & Jackson, J. D. (1959). Carotid-cavernous fistula: a-perplexing surgical problem. Journal o f Neuro, surgery, 16,619-627. Gindi, S. E_ & Andrew, J. (1967). Successful closure of carotid-cavernous fistula by the use of acrylic, case report. Journal of Neurosurgery, 27,- 153 - 156. Gurdjian, E_ S. (1938). Packing of internal carotid artery with muscle in treatment of carotid-cavernous arteri0, venous aneurysm. Archives of Ophthalmology, 19, 936~ 904Harnby, W. 13. & Gardner, W. J. (1933). Treatment of put, sating exophthalmos with report of two cases. Archives of Surgery, 27,676-685. Hamby, W. B. (1964), Carotid-cavernous fistula. Report of thirty-two surgically treated cases and suggestions for definitive operation. Journal o f Neurosrugery, 21,859_ 866. Hayes, G. J. (1958). Carotid-cavernous fistulas: diagnosis and surgical management. American Surgery, 24,839. Hayes, G. I. (1963). External carotid-cavernous sinus fistulas. Journal of Neurosurgery, 20, 692-700. Ismat, F., Salleras, U. et al. (1970). Artificial embolisation of carotid-cavernous fistula with post-operative patency of the internal carotid artery. Journal of Neurology, Neuro, surgery and Psychiatry, 33,674-678. Ishimori, S., Hattori, M. et al. (1967). Treatment of carotid, cavernous fistula by geffoam embolisation. Journal of Neurosurgery, 27, 315-319. Jaeger, R. (1959). In discussion of paper by D. H. Echols and J. D. Jackson. Carotid-cavernous fistula: a perplexing surgical problem. Journal of.Neurosurgery, 16, 626. Kosary, I. Z., Lerner, M. A., Mozes, M. & Lazar, M. (1968), Artificial embolic occlusion of the terminal internal carotid-cavernous fistula. Journal of Neurosurgery, 28, 605 -608. Lang. E. R. &Bucy, P. C. (1965). Treatment of carotid. cavernous fistula by muscle embolisation alone, the Brooks method_ Journal of Neurosurgery, 22, 387-392. -Locke, C. E., Jr (1924). Intracranial arteriovenous aneurysm or pulsating exophthalmus. Annals of Surgery. 80, 1 24. 272-285. Margolis, M. T. & Newton, T. H. (1969). Collateral pathways between the cavernous portion of the internal carotid and external carotid arteries, Radiology, 93,834-836. Parkinson, D. (1964). Collateral circulation of the cavernous carotid artery: anatomy. Canadian Journal of Surgery, 7, 251-268. Parkinson, D. (1965). Surgical approach to the cavernous portion of the carotid artery. Anatomical studies and case report. Journal of Neurosurgery, 23,474-483. Parkinson, D. (1967). Transcavernous repair of carotidcavernous fistula_ Case report. Journal of Neurosurgery, 23,474-483. Sedizimir, C. B. & Occleshaw, J. U. (1967). Treatment of carotid-cavernous fistula by muscle embolisation and Jaeger's manoeuvre. Journal o f Neurosurgery, 27, 309314. Stern, W. E., Brown, W. J. et al. (1967). The surgical challenge of carotid-cavernous fistula: the critical role of intracranial circulatory dynamics. Journal of Neurosurgery, 27,298-308. Tonnis, W. (1960). Zur entshehung der rezidire bei der behandlung tier carotis-sinus-cavernous-anerurysmen und ihre verhtitung. Archiv fiir klinische Chirurgie, 295, 186-191.
Ernbolisation of the External Carotid Artery in the Treatment of Carotid Cavernous Sinus Fistulae A.J. GERLOCK, JR
From the Department of Radiology and Radiological Sciences, Vanderbilt University School of Medicine, Nashville, Tennessee 37232 A review of treatment methods used to control carotid cavernous sinus fistulae is presented. Three cases are described in which embolisation of the external carotid artery was done along with intracranial vascular procedures in the management of carotid cavernous fistulae.
Numerous treatment methods have been used in the management of carotid cavernous sinus fistulae over the years with success or failure reported by various writers (Arutinunou et al., 1968; Black et al., 1971; Brooks, 1930; Dandy, 1935; Echols and Jackson, 1959; Gindi and Andrew, 1967; Gurdjian, 1938; Hamby and Gardner, 1933; Hamby, 1964; Hayes, 1958; Ismat et al., 1970; Ishimori et al., 1967; Jaeger, 1959; Kosary et al., 1968; Lang and Bucy, 1965; Parkinson, 1967; Sedzimir et al., 1967). The radiologist, in the performance of angiography or the performance of therapeutic embolisation catheter procedures, may enter into the management of these patients after several surgical procedures or others forms of treatment have failed. For this reason, the following review is necessary to acquaint the radiologist with some of the standard treatment methods so that the diagnostic angiography or therapeutic embolisation procedures can be planned and evaluated. This will also point out the reason for complete angiographic documentation of all vessels feeding the carotid cavernous sinus fistula. A direct approach to the fistula is difficult and a dangerous undertaking (Parkinson, 1965; Sedzimir and Occleshaw, 1967; Stern et al., 1967). Treatment is generally directed at reducing the blood flow through the fistula so that thrombosis can occur in the intracavernous portion of the internal carotid artery. The flow of blood through the fistula will then be completely shut off. Early methods to cut down on blood flow through the fistula began with intermittent carotid artery compression for seven days, which is reported to have a cure rate of 16% (Dandy, 1935). Later methods consisted of single ligation of the carotid artery in the neck, either the common or internal carotid artery, with a device allowing a slow gradual occhision to occur. The Selverstone clamp has been widely used for this purpose (Fig. la). Cure or improvement rates with this procedure are varied. Locke reported a 68%
cure or improvement with common carotid artery ligation with a mortality rate of 7%. When the internal carotid artery was ligated, he reported a cure rate of 87.5% with a mortality rate of 9.4% (Locke, 1924). Success after internal carotid artery ligation in the neck alone has been reported by others to be 50% or less (Lang and Bucy, 1965). Tonnis (1960) states that ligation of the common and internal carotid arteries in the neck produced a satisfactory result in only 3 5 - 4 0 % of cases. Neck ligation of the internal carotid artery alone is undesirable because it not only deprives the fistula and brain of blood supplied by this artery, but the opposite hemisphere as well. Since only the ipsilateral internal carotid artery has been occluded, blood from the opposite carotid circulation will be sucked across the circle of Willis and down into the fistula opening. The trapping procedure is another surgical technique used in the treatment of these fistulae. This consists of ligating vessels intracranially in an attempt to isolate the fistula from arterial blood flow. One such method consists of ligating the supraclinoid segment of the internal carotid artery proximal to the posterior communicating artery and neck ligation of the internal carotid artery (Fig. lb). This procedure has a cure rate of 56.7% (Hayes, 1963). 'Complete trapping' occurs when there is intracranial occlusion of the supraclinoid carotid segment and ophthalmic artery, followed by neck ligation of the internal and external carotid arteries (Fig. lc). This procedure has a cure rate of approximately 78.8% (Hayes, 1963). Failure of these types of surgical procedures seem to be the result of numerous anastomotic channels particularly concerning the intracavemous portion of the internal carotid artery (Hayes, 1958, 1963; Margolis and Newton, 1969; Parkinson, 1964). In order more effectively to occlude these rich anastomotic channels, as well as the fistula itself, intraluminal embolisation of the internal carotid artery has been attempted. This has been done alone and in
112
CLINICAL RADIOLOGY S.C.C.
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.
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Fig. 1 - (a) Selverstone clamp neck occlusion of either the common carotid (CC) or internal carotid (IC). This decreased the blood flow through the fistular opening (arrow) of the intracavernous portion of the IC into the cavernous sinus (CS). (b) Ligation of the supraclinoid carotid (SCC) proximal to the posterior communicating artery (PC) and neck ligation of the IC. (c) 'Complete trapping" combines ligation of the ophthalmic artery (opth) and SCC with neck ligation of the external carotid artery (EC) and IC. (d)
Occlusion of the fistular opening by intraluminal muscle embolisation of the IC and ligation of the CC. (e) Ligation of the opth and SCC is performed first followed by obliteration of the collaterals to the intracavernous portion of the IC by embolisation. This is then followed by ligating the EC, IC and CC. (f) Occlusion of the fistular opening by embolising a piece of muscle attached to a nylon thread followed by ligation of the CC.
combination with other surgical procedures (Fig. l d - f ) (Brooks, 1930; Gindi and Andrew, 1967; Gurdjian, 1938; Hamby and Gardner, 1933; Hamby, 1964; Ismat eta/., 1970; Ishimori et al., 1967; Jaeger, 1959; Kosary et al., 1968; Lang and Bucy, 1965; Parkinson, 1965). Brooks (1930) successfully a t t e m p t e d treatment o f a carotid cavernous fistula by muscle embolisation o f the intracavernous portion o f the carotid artery and ligation of the common carotid artery (Fig. l d). Complications of this pro-
cedure prevented its wide use. These complications consist o f possible obstruction of the distal segments of the middle or anterior cerebral arteries with loose fragments of the embolised material. The possibility of such complications led to the combination of intracranially ligating the supraclinoid segment of the internal carotid artery first, before performing the embolisation procedure. This is done especially when the carotid angiogram fails to show the major flow of blood from the internfil carotid artery into the ~istula.
EMBOLISATION OF THE EXTERNAL CAROTID ARTERY ThiS is also done when the intracranial vessels fdl mainly from the internal carotid artery on the s~ae side as the fistula. Such a procedure is the definitive one stage attack described by Hamby (1964)- In this procedure, the supraclinoid segment. of the internal carotid artery between the posterior communicating artery and cavernous sinus is clipped first. This is done along with the ophthalmic artery, if possible. The collaterals to the intracavernous carotid artery are then attacked by obliteration of this entire segment with intraluminal muscle enabolisation. Tying and severing the common, interhal and external carotid arteries completes the procedure (Fig. le). Ligation of the internal cartid artery ha the neck facilitates thrombosis and prevents the enabolised muscle from passing through the fistula. In the event that it is considered unwise to obstruct the carotid artery on the side of the fistula, a guided embolisation procedure has been used (Black et aL, 1971). A piece of muscle is introduced into the carotid artery to which is attached a nylon thread to control the embolus until it .is in place (Fig. l f). This method has the advantage that, if the embolus fails to occlude the fistula, it can be removed and not be allowed to pass distally into the intracranial vessels. A potential hazard of this technique concerns permanent presence of a long thread in the carotid lumen, with the possibility of thrombus formation on the thread. Other cases have been reported using various embolisation materials, such as gelfoam wrapped in a gold film as an X-ray marker (Ishimori e t al., 1967),
Fig. 2 - Shows branches of the internal maxillary artery supplyingthe fistula (unlabelled arrows).
113
5 m m porcelain beads (Kosary e t al., 1968) and acrylic materials (Gindi and Andrew, 1967). To this we would like to add our experience in three patients with gelfoam embolisation of the external carotid circulation. The indications and reasons for its use will also be discussed.
REPORT OF CASES Case 1. A 17-year-old male sustained a gunshot wound to the face and subsequently developed a left carotid cavernous fistula. Initial debrediment of the left facial wound resulted in neck ligation of the lacerated left internal carotid artery. Postoperative angiographic evaluation revealed a left carotid cavernous fistula and confirmed obstruction of the left internal carotid artery. The carotid cavernous fistula was fed througja the intracavernous portion of the left internal carotid. This segment was supplied blood by the left posterior communicating as demonstrated on the vertebral angiogram. A right internal carotid angiogram showed blood flow to the left cerebral hemisphere and carotid cavernous fistula across a patent anterior communicating artery. No branches of the right external carotid were found to supply the carotid cavernous fistula. Subselective angiography of the left external carotid showed numerous branches from the internal maxillary artery feeding the carotid cavernous fistula (F~g. 2). Fig. 3 shows obstruction of the internal maxillary and its branches following embolisation with 32 gelfoam particles expressed through a Red Kifa 5.4 French catheter wedged in the internal maxillary artery. No filling of the carotid cavernous fistula from the external carotid was present following the embolisation procedure. Approximately 16h following embolisation of the external carotid, this patient experienced a mild temperature elevation and discomfort in the region of the angle of the mandible. This subsided within 24 h, and no further discomfort was noted.
Fig_ 3 - Shows obstruction of the internal maxillary artery and its branches following embolisation (arrows). Note absence of filling of the fistula.
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Fig. 4 - Shows filling o f the fistula from branches of t h e proximal portion o f the o p h t h a l m i c artery (arrow).
Intracranial clipping o f the supraclinoid s e g m e n t of t h e left internal carotid artery and o p h t h a l m i c artery was carried out. This resulted in a m o d e r a t e d decrease o f proptosis and obliteration of t h e intracranial bruit. A one year follow-up shows no evidence of recurrence of t h e carotid cavernous fistula. Case 2. This 28-year-old male developed proptosis of t h e left eye following impalement o f t h e left orbit u p o n t h e sharp point of a pencil. Bilateral selective angiography of t h e internal carotid and external carotid were performed. A cavernous sinus fistula was seen to fill from the proximal portion of the left ophthalmic, artery on the internal carotid angiogram (Fig- 4) and from vascular c o m m u n i c a t i o n s from the internal maxillary artery on the external angiograrn (Fig. 5). No direct c o m m u n i c a t i o n b e t w e e n the intracavernous p o r t i o n of the internal carotid and cavernous sinus were d e m o n s t r a t e d (Fig. 4). Embolisation of the left external carotid was done, followed by intracranial clipping of the left ophthalmic artery. This resulted in a transient decrease in the patient's intracranial bruit and proptosis. Repeat external carotid angiography was done following the recurrence of s y m p t o m s and an incomplete o b s t r u c t i o n of the branches o f the external carotid feeding t h e fistula was f o u n d to be present (Fig_ 6). A second embolisation procedure of the external carotid was performed resulting in occlusion of these branches. This patient also experienced a mild temperature elevation and pain around t h e angle of the mandible following t h e procedure. This subsided within 24 h w i t h o u t further discomfort. A 13-month follow-up of this patient shows no evidence of progression or recurrence of the fistula. Case 3. This 52-year-old male presented with failing vision, progressive proptosis of the right eye, distended facial veins, and an intracranial bruit. Past history revealed that a Selverstone clamp occlusion of t h e right internal carotid h a d been done 15 years earlier for t r e a t m e n t of a carotid cavernous fistula obtained following orbital t r a u m a (Fig. 7). Angiography for evaluation of this progressive recurrent
Fig. 5 - Left external carotid artery angiogram shows branches of the internal maxillary artery supplying the carotid cavernous fistula (arrows). A dilated superior op. thalmic vein is seen draining the fistula (vertical unlabeUed arrow).
carotid cavernous fistula, showed it to be fed from left internal carotid, right external carotid and vertebral basllar system. T r e a t m e n t of this chronic fistula consisted ofintracranial clipping of the supracllnoid portion o f the right internal
Fig. 6 - Shows external carotid angiogram following fi~st embolisation. Two large black arrows point to the ascending pharyngeal artery which supplies the fistula. The small arrows shows persistent small collaterals from the inter ~al maxillary artery.
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carotid, which obstructed the flow of blood to the fistula from the left interfial carotid and vertebral basflar circulation. The extensive collateral bxanches from the right external carotid to the carotid cavernous fistula (Fig. 8) were obliterated by gelfoam embolisation of the right external carotid (Fig. 9). Because of the large well-established collaterals between the external carotid and carotid cavernous fistula, 103 gelfoam emboli were required to obstruct completely the external carotid and its branches to the carotid cavernous fistula. The carotid cavernous fistula was controlled but the embolisation of these rich well-formed collaterals resulted in tissue necrosis of the right temporalis muscle, pterygoid muscles, parotid gland and overlying skin. Osteonecrosis of the temporal bone also developed with the sequelae of loss of function of the right middle ear and non-healing of the temporal craniotomy site. A portion of the angle o f the mandible was also devitalised and became necrotic, but no loss of function of the mandible occurred. Paralysis of the seventh cranial nerve developed shortly after the embolisation procedure, its aetiology possibly resulting from reflux of the emboli from the external carotid into the vertebral basilar system. A one-year follow-up of this patient shows the carotid cavernous fistula is controlled, but the loss of hearing and seventh cranial paralysis remain permanent. The cosmetic appearance of the area of tissue necrosis is fair as a result of skin grafting procedures of the upper cervical and temporal regions. DISCUSSION
Fig. 7 - The middle arrow points to the Selverstone clamp occlusion of the internal carotid. The common carotid is shown, lower arrow, and the upper arrow points to the enlarged external carotid.
Fig. 8 - Selective external carotid angiogram showing numerous large collaterals from the internal maxillary artery to the carotid cavernous fistula (arrows).
E m b o l i s a t i o n o f the e x t e r n a l carotid can b e perf o r m e d either p r i o r to surgery or after surgery, and s h o u l d be d o n e even w h e n t h e subselective e x t e r n a l c a r o t i d angiograms fail t o s h o w its b r a n c h e s f e e d i n g
Fig. 9 - Post-embolisation angiogram showing occlusion of the external carotid and its branches (upper arrow). No filling of the fistula is present. The lower arrows point to the Selverstone clamp occluding the internal carotid.
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the carotid cavernous fistula. This type of embolisation is done t o prevent any collateral pathways from the external carotid from opening up and resulting in a failure of the intracranial surgical clipping procedures. Complications of embolising the external carotid can occur, as shown in Case 3. The reasons for these complications are not clearly understood in this patient. Contamination of the embolised particles or to extensive embolisation o f the external carotid circulation may explain, in part, the resultant tissue necrosis and infection. The internal carotid had been occluded for five years prior to embolisation of the external carotid in this patient. Multiple large collateral pathways between the external carotid and intracavernous portion of the internal carotid had now formed involving the meningeal branches of the infra-orbital artery, accessory meningeal artery, accessory meningeal o f the pterygoid artery and ascending pharyngeal artery. This extensive n e tw o r k of long-standing coUaterals required numerous gelfoam emboli to occlude them. Cranial nerve damage can only be assumed to have occurred as a result o f reflux of embolised particles either intra- or extracranially into the vertebral basilar circulation. To prevent these complications in the future, patients with long-standing widely patent collaterals from the external carotid to the intracavernous portion of the internal carotid should be carefully evaluated and the procedure abandoned when small numbers o f embolised particles are found inefficient at occluding these collaterals. Cases 1 and 2, 2 4 h after the embolisation procedure, were found to have only mild temperature elevations and mild discomfort in the region of the angle of the ipsilateral mandible. These symptoms subsided within 48 h after their onset, 8 - 2 4 h following embolisation of the external carotid, and no further discomfort was noted. A one-year follow-up of all cases shows the fistulae have remained controlled. Acknowledgements. The author wishes to express appreciation,to Mrs Linda Bland, Research Technician, and Mrs Dorothy Gutekunst, BA, Research Technician, for their technical and photographic assistance. REFERENCES
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