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Show /. Clill. NClIn1-tlphthtlil,1t1/. 5: 37-40, 19R5. Reversible Optic Neuropathy Due to Carotid-Cavernous Fistula THOMAS R. HEDGES, III GERARD DEBRUN SAMUEL SOKOL Abstract Optic nerve dysfunction occurred several weeks after traumatic carotid-cavernous fistula developed in a 21-year-old man. Vision was completely restored after the fistula was dosed with an intraarterial detachable balloon. By carefully monitoring visual function in patients with traumatic carotid- cavernous fistulas, delayed optic neuropathy can be recognized and treated successfully. Introduction Lpss lli \'isipn as a complication of carotidca\, ernL'US iistula may result from ocular ischemia. Sl)metimes accompanied by vitreous hemllrrhage and retinal detachment, 1 and several diiierent iorms of pptic neuropathy. The optic nen'e ma\, be infarcted when there is severe ocular ischemia, C it may be damaged at the same time the carotid artery is injured if trauma is the cause of the fistula,l and, when glaucoma results from increased orbital venous pressure, the nerve head may become progressively atrophic. 4 Rarely, the optic nerve may degenerate in long-standing fistulas, presumably from compression of the nerve bv distention of the cavernous sinus or because' of retrobulbar ischemic optic neuropath v' 'We recently observed another form of optic nerve dysfunction which occurred following traumatic carotid-cavernous fistula. Unlike other previously reported cases with optic neuropathy, our patient's vision deteriorated weeks after his injury, and it was completely restored by occluding the fistula with intra-arterial balloon placement. Case Report A 21-year-old soldier in the Bermudan army was riding on the back uf a motor bike when it Frum tht: [)l'partmt:nt, (If Ophth,llm"l"gy (TRII, SS) and eurul"g\' (TRH), 't:w England M"dlC,11 Ct:nll'r, Tuft- Uni· ve"it\'; and tht' [)l'Partmt:nt "f Nl'urm,ldi"l"g\' (CD), M,,,· sachusdts General fl,,'pita!. Ilarv",d Uni""r,it\', H,,,t,,n, Massachusetts. March 1985 struck a telephune pole. He was thrown a considerable distance and regained consciousness 15 minutes later as he was being taken to the hospital in an ambulance. Ilis mandible was fractured, and the right eye protruded with limitation of all extraocular muvement, especially abductiun. Vision was 20/15 on the right and 20/20 on the left. He was aware of the sound of "heavy breathing" in his right ear. One month following the injury vision remained nurmal. However, 7 weeks after the injury the patient became aware of decreased vision in the right eye. Visual acuity in the right eye had declined to 20/40, and rightsided orbital congestion was worse. He was referred to us for further treatment. He was able to identify most of the letters on the 20/40 line of the Snellen acuity chart with the right eye, and read the 20/20 line easilv with the left eye. He could recognize only the brightest of AOHRR color plates with the right eve, but correctly sawall of them with the left. When the maculae were exposed to bright light for 10 seconds, it took 40 seconds to recover normal visual acuity with the right eye and 30 seconds for normal vision to return with the left (/1 < 40 seconds). There was bilateral proptosis, 3 mm greater on the right side. A loud bruit was audible over most of the skull, more so on the right. Veins were dilated in the skin of the lids on the right and in the episclera bilaterally. There was no right lateral rectus iunction, but eve movements were otherwise normal (Fig. 1). A 'relative ,1fferent pupillary detect was nllted when a penlight was swung from one eye to the other. Intraocular pressures were 19 mm Hg on the right and 20 mm Hg on the left. There was minimal retinal venous dilatation, two patches oi pigment epithehal thinning were seen in the retina belllw the right macula (Fig. 2), but no other significant abnormalities were noted in either fundus. Diastolic ophthalmodynamometry reLldings were 30 on the right and 35 on the left with the Bailliart instrument. The right visual field showed irregular constrictIOn and ,1 peripheral temporal scotoma. The Idt visual field was normal. Visual-evoked potential amplitudes were 37 Optic Nl'lIWp,llhv/CCr Figure 1. I'hologr,lph of the patll'nt H Wl'l'''' following Inlury ~howlng n~ht latt,ral r",etus dvsfunclion and l'piscll'ral Vl'n"u~ l'ngorgt'ml'nl Figure 2. I'hotogr.lph of tht' pdtil>n!"s nght rt'lina Sh'l\\"Ing ,In unrt'n1.1rk,lbll' l,~'ti( nt'rn' .lnd nl'rrnal rt'tinal l'ds(uldlurt' markedly reduced, and P-100 latencies were abnormally prolonged when the right eye was tested with large and small pattern reversal checks. The left visual-evoked potential was normal. Cerebral angiography showed a high-flow, right, carotid-cavernous fistula, assllCiated with swelling of the cavernous sinus and distention of the ophthalmic artery (Fig 3/1) Nine weeks following the injury, a detachable balloon was placl'd into the right CJvernllUS sinus by way of the right internal carotid arten'. There was immediall' improvement in the patient's .lp- 38 pearance, and he claimed that vision had returned to ntlrmal. HllWe\'er, his bruit recurred the next d,n', and 7 days later a second balloon was placed in the ca\'t'rnllUS sinus next to the first one. This p,utiall\' occluded the cavernous portion of the carotid arten', and additional balloons were placed abl)\'e'and below the large opening in the carotid ,uter\', allowing for closure of the cavernous carotid artery (Fig. 3b). Six days after the second procedure, vision was 20/15 when the right eye was tested, and 20/20 on the left. The patient could recognize all Journal of Clinical Neuro-ophthalmology Figure 3". Ri"ht CMlltid ,In!,I,'!,ram lAP. ,·iew). shllwing I""n" "1th,' n"ht cavernllUS sinus and llphthalmic wins. Figure 3b. Left cdrl\tid anK"'gr.lm afler dl'l.lchment 1\1 the ballolln (arrlllY) llceluding the (i,tula and the right intern,ll carotid arterv. March 1985 Hedges, Debrun, Sokol AOIIRR color plates with both eyes. Pupillary re,Ktivity had rl'turned to normal. There was no proptosis and no bruit. Right lateral rectus dysfunction persisted. The retinal veins were of normal caliber, ,md diastolic ophthalmodynamometry readings were 45 on the right and 45 on the left. Visual fields were normal. Visual-evoked potL'ntial amplitudes and latencies were now norm, ll for the right eye, with only minur asymmetry lwtween thl' right and left eyes. Discussion The loss of normal culor perception, the affert> nt pupillary defect, the type uf visual field loss, and the visual-evokt>d potential findings, in the face of only minimal retinal venous engorgement and normal retinal rt>covery from bright light exposure, strongly suggest that the cause of our patient's visual impairment was optic nerve dysfunction. We fet'! that it is most probable that the markedly enlarged cavernous sinus seen on angiography compressed the optic nerve just before it entered the optic canal. Optic nerve compression was demonstrated pathologically in one of the cases of carotidcavernous fistula described by Dandy in 1944.' He found "enlargement of the cavernous sinuses had elevated both optic nerves at the optic foramina to such a degree that a decided angulation resulted," and histologic examination of the nerves showed focal atrophy where they entered the optic canals. Additional evidence of optic nerve compression in our case is the rapid and complete return of vision experienced when the fistula was closed. A less likely mechanism explaining our patient's visual loss is chronic hypoxia involving either the optic nerve or the retina due to hemodynamic changes such as venous stasis or diversion of arterial blood from the eye to the fistula. The rapid and complete therape~tic response our patient experienced is n1llre suggestive llf neural comprl'ssion rathl'r than ischl'mia, and thl'rt, was no l'vidl'nce llf significant retinal dysfunctilln, although this may cause rl'versibll' visual loss in other cases. h It was critical that our patient's visual function was monitored carefully enough to demonstrate that it was nllrmal after the injury and deteriorated several weeks later. Had this nllt bel'n dllne, our patient's llptiC nerve abnormality might have been erronl'ously ascribed to the irreversible type of nerve damage which can occur directly from trauma. However, loss of vision W,lS recognized to occur after thl' injury It>ading to urgent treatment which was successful in restoring normal visual function. The frl'quency with which the kind of visual impairment observed in our case occurs is un- 39 Optir Nl'Urup.lthy/CCF known. To our knowll'dgl', this has nut bl'l'n n'portl'd in thl' litl'r.ltun' bdon', and it may uccur mon' commonly in p.ltil'nts with largl' fistulas n'lluiring tn'.ltnll'nt bdon' thl'y loan bl' l'valuatl'd c.udull\' by .mophtll.llmulogist. It is also possibll' th.lt sonll' p.ltil'nts who .Ul' thought tu h.wl' irrl'\' l'rsibll' tr.llIm.ltil" optil" nl'rVl' Il'siuns associatl'd with fistul.1S instl'.ld m.1Y h.wl' l"umprl'ssiw uptic Ill'urup.lthy sl'cond.uy tu l".Wl'rnous sinus swl'lling.• md thl' rewrsibility uf this typl' uf visual dysfunction may go unn'cugnizl'd. Thl' cllmplete resulutiun uf our patient's visual loss afforded by the currently successful ml'thud of intr.l-arterial balluun placl'ment,7 indicates that careful munitoring of visual function in patients with carotid-cavernuus fistulas should be perfurmed. Dl'Iayed optic nl'uropathy, once recognized, shuuld be considered a strong indication for therapeutic intervention. References 1. Sand~rs. M.D., and Hoyt. W.F.: Hypoxic ocular s~quda~ of carotid-cavernous fistula~. Br. ,. O"IJ'IJallllll/. 53: 82-97, 1969. 40 2. Spencer, H.W., Thompson, H.S., and Hoyt, W.F.: Ischaemic ocular necrosis from carotid-cavernous fistula. Br. /. O,I1l"lalmol. 57: 145-152, 1973. 3. Walker, A.E., and Allegre, G.E.: Carotid-cavernous fistulas. SlIr:.:ay 39: 411-422, 1956. 4. Ifl'ndl'rsun, j.W., and Schneider, R.C.: The ocular findings in carotid-cavernous fistula in a series of 17 cases. Alii. /. Op"'"almol. 48: 585-597,1959. 5. Dandy, W.F., and Follis, R.H.: On the pathology of carotid-caVl'rnous aneurysm (pulsating exophthalmos). Am. /. O'l"'"almol. 24: 365-385, 1941. h. Ifostuvskv, M., Wirtschafter, J.D., Tubman, D.E., et al.: Reductiun of retinal venous tortuosity after detachable balloon ucclusion of carotid-cavernous fistulae. Am. /. Op"'"almol. 95: 841-843, 1983. 7. Debrun, G., Lacour, P., Vinuela, F., et al.: Treatment uf 54 traumatic carotid-cavernous fistulas. J. Nl'urll~lIr.l(. 55: "78-692, 1981. Acknowledgment The pati~nt was initially evaluated and then referred to us by Raymond Smith. M.D.. of B~rmuda. Journal of Clinical Neuro-ophthalmology |
