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Show J. Clin. Neuro-ophthalmol. 4: 255-257, 1984. Ischemic Optic Neuropathy Following Secondary Intraocular Lens Implantation MICHAEL ]. SPEDICK, M.D. ROBERT L. TOMSAK, M.D., Ph.D. Abstract Ischemic optic neuropathy occurred 10 days after secondary implantation of an intraocular lens in an otherwise healthy 50-year-old man who had undergone two other previously successful cataract operations. General anesthesia was used and postoperative intraocular pressures were normal. Postcataract extraction ischemic optic neuropathy is compared and contrasted to nonarteritic ischemic optic neuropathy occurring in phakic patients. Introduction Ischemic optic neuropathy (ION), as defined by Boghen and Glaser,l is "infarction of the optic nerve in the absence of identifiable inflammation, demyelination, compression by mass lesion or hypoperfusion in the extracranial carotid system." This condition is not exclusive to phakic eyes and may thwart the beneficial effects of cataract surgery. We report the unusual occurrence of ION following secondary implantation of an intraocular lens and discuss the relationship between phakic and aphakic ION. Case Report A 50-year-old white man underwent extracapsular cataract extraction in the left eye in December 1980. A similar procedure was performed on the right eye, but with implantation of a posterior chamber intraocular lens in July 1982. Because of the good postoperative result in the right eye and because of contact lens problems, a secondary intraocular lens implantation was performed on the left eye under general anesthesia on May 4, 1984. Visual acuity was 20/30 on the fifth postoperative day and applanation tension was 14 mm Hg. On the sixth postoperative day, he ex- From the Department of Ophthalmology, Cleveland Clinic Foundation, Cleveland, Ohio. December 1984 perienced a flashbulb-like effect in the left eye that lasted about 1 hour. On the same day, he experienced a shade-like orange-brown barrier arising in the inferior one-third of the visual field of the left eye which gradually disappeared over 5-10 minutes. On the 10th postoperative day, he was examined because of sudden visual loss which persisted. Examination disclosed left eye vision of counting fingers at 2 ft. and the left optic disc was swollen inferiorly with some peripapillary retinal edema. He was treated with aspirin, topical steroids, and oral Prednisone. On July 1, 1983, he was hospitalized and had a complete medical evaluation including bilateral carotid angiography and two-dimensional electrocardiography, both of which were normal. No evidence of diabetes, hypertension, hyperlipidemia, or vasculitis was detected. On August 5 1983, he was seen by us for a second opinion. Right eye vision was 20/20 and ]1+. left eye vision was 8/200. A 4+ afferent pupillary defect was present in the left eye. Slit lamp examination showed well-positioned posterior chamber lenses in both eyes. Applanation tensions were 17 mm Hg bilaterally. Fundus examination was normal on the right, but showed diffuse optic atrophy on the left. There were no emboli seen. Goldmann visual fields were normal on the right, but showed only a temporal island of vision remaining on the left. Blood pressure was 140/95. Comment This patient had two successful cataract surgeries without complication. Ten days following reoperation for a secondary implant he developed ischemic optic neuropathy. No rise in intraocular pressure was noted in the postoperative period and retrobulbar anesthesia was not used. Aside from borderline hypertension, no predisposing cause for ischemic optic neuropathy was uncovered. 255 TABLE 3. Postcataract Extraction ION"13 Our case is of interest for three reasons: 1) ION occurred within days of surgery yet the intraocular pressure was never found to elevated; 2) this patient's problem is unusual in that he underwent successful cataract surgery in both eyes without complication until secondary implantation of a pseudophakos was performed; and 3) to our knowledge, only one other instance of postcataract extraction ION occurring after secondary implant has been documented.? TABLE 1. Proposed Mechanisms of Postcataract Extraction ION Ref. No Mechanism 3 4 8 10 11 12 16 17 1. Hypotony + + + + 2. Sympathetic tone + 3. Capillary perme- + ability 4. Vitamin C defi- + ciency 5. Posterior vitreous + + + detachment 6 Rupture of ante- + + + rior hyaloid 7. Optic nerve + + + + trauma 8. Infection + 9. Optic neuritis 2° + + to uveitis 10. Vascular occlu- + + + + sive disease 11 Postretrobulbar + pressure 12. Systemic hypo- + + tension ---- Ischemic Optic Neuropathy Discussion In 1946, Vila-Coro1? described optic atrophy as a consequence of cataract surgery. The subjects of his report lost vision weeks to months after surgery without apparent cause. The incidence of this condition was approximately 0.2% in his series. Townes et al. 1S reported four cases of "optic neuritis" from a series of 565 cataract procedures. In two of these patients, visual loss did not occur until 4 and 15 months after surgery. Reese and Carroll13 presented a series of patients who developed"optic neuritis" 6-12 weeks after cataract surgery. The pertinent findings were: 1) optic disc edema with flame hemorrhages, 2) narrowing of peripapillary arterioles, 3) visual acuties in the 20/70-20/200 range, 4) central scotomas 5-20° in size,S) normal intraocular pressures, 6) a mean age of 69 years (range 49-82), and 7) the occurrence of a similar event in the fellow eye in 30-50% of patients." Debate has arisen over whether ischemic optic neuropathy following cataract surgery is truly a separate entity. Maumenee9 raised the question of coincidence, but Carroll 13 pointed to his series of 450 cases of optic neuritis of diverse causes and stated that he had not seen papillitis develop in the untreated eye of a monocular aphake, whereas five patients who were bilateral aphakes developed papillitis after both surgeries. Others~U.10.ht::,.1.j.1R have reported ION as a delayed event following cataract surgery in support of Carroll's observations. Another form of postcataract extraction ION that occurs in the early postoperative period has also been recognized. s 19 HayrehSspeculated that this form of ION is mainly related to elevated intraocular pressure postoperatively. Numerous other mechanisms have also been proposed (Table 1). More recently, attention has been turned to structural factors in the pathogenesis of ION. Feit et al?' found that the average cup to disc ratios of uninvolved eyes of phakic patients with nonarteritic ION were smaller than the average cup to disc ratios of age-matched controls. They speculated that crowding ofaxons might lead to mechanical compromise ofaxoplasmic flow or to subsequent small vessel alterations which would ultimately result in ION. It is not yet known if this trend towards small optic cups is also present in the aphakic variants of ION. However, when nonarteritic ION is compared with postcataract extraction ION, many other similarities exist (Tables 2 and 3). The age of the affected patients is roughly the same, the occurrence of ION in the fellow eye is about as often, the sedimentation rate is not elevated, and both respond poorly to medical treatment. TABLE 2. Idiopathic ION' Age Onset ESR Bilaterality Therapy Age Onset ESR Bilateralitv Therapv 55-70 Spontaneous <40 Second eye involved in 40% of cases after months to years Poor response to steroids or anticoagulants 49-82 Follows cataract surgery 4 wks. to 15 mos. Normal Up to 30-50c" have involvement of second eye if cataract surgery performed !oor resp~nse_t(j.steroids or anti~oagulants 256 Journal of Clinical Neuro-ophtha)mo)ogy We agree with Hayreh~ that ION which occurs weeks or months after cataract surgery is most likely the same disease as nonarteritic ION which occurs in phakic patients. As such, there is significant risk of involvement of the fellow eye. Comment Postcataract extraction ION which occurs in the early postoperative period needs further study. Careful monitoring of intraocular pressure postoperatively seems warranted. Further observations on the structure of the optic disc in the fellow eye of patients with postcataract extraction ION may also lead tomore information on the pathogenesis of this condition. It seems prudent to avoid systemic hypotension in patients undergoing cataract surgery~'~ 12 and especially in those who have suffered postcataract extraction ION in the other eye. Agents like the calcium channel blockers may be useful in preventing arteriolar vasospasm in the perioperative period, although at present, this is purely speculative. References 1. Boghen, D.R., and Glaser, J.5.: Ischemic optic neuropathy: The clinical profile and natural history. Braill 98: 689-708, 1975. 2. Carroll, F. D.: Optic nerve complications of cataract extraction. TrailS. Am. Acad. Ophthamol. Otolal1/ll-gol. 77: 623-629,1973. . 3. Gartner, S.: Optic neuritis and macular edema following cataract extraction. file far Nose Throat MOllth. 43: 45-49,1964. . 4. Gass, J.D.M.: Ischemic optic neuropathy in aphakia (and phakia), In TIle New Report 011 Cataract Surgery, R. C Welsh and J. Welsh, Eds. Miami Education Press, Miami, 1969, pp. 84-86. 5. Hayreh, S.5.: Anterior ischemic optic neuropathy IV. Occurrence after cataract extraction. Arch. Ophthamol. 98: 1410-1416, 1980. 6, Hayreh, S.5.: Post cataract extraction ischemic optic neuropathy. (Letter.) Arch. Ophthamol. 100: 853-854,1982 7. Kraff, M.D., Sanders, D.R., Lieberman, H.L., and December 1984 Spedick, Tomsak Kraff, J.: Secondary intraocular lens implantation. Ophthalmology 90: 323-326, 1983. 8. Lavy, S., and Neuman, E.: Changes of the optic nerve after cataract extraction simulating the Foster Kennedy syndrome. COllfill. Neurol. 19: 383-389, 1950. 9. Maumenee, AE,: In discussion of Reese and Carroll, TrailS. Am. Acad. Ophthalmol. Otolaryllgol. 62: 769-770,1958. 10. Michaels, D.O., and Zugsmith, G.5.: Optic neuropathy following cataract extraction. AIlIl. Ophthal1/ 101. 5: 303-306, 1973. 11. O'Keefe, D., and Choudhury, K.C: Bilateral optic neuritis following cataract extraction. Br. f. Ophthalmol. 50: 608-609, 1966. 12. Oliver, M.: Posterior pole changes after cataract extraction in elderly subjects. Am. f. Ophthalmol. 62: 1145-1148,1966. 13. Reese, AB., and Carroll, F.D.: Optic neuritis following cataract extraction. TrailS. Am. Acad. Ophthalmol. Otolanillgol. 62: 765-768, 1958. 14. Serrano, L.A, Behrens, M.M., and Carroll, F.D.: Post cataract extraction ischemic optic neuropathy. (Letter.) Arch. Ophthalmol. 100: 1177-1178,1982. 15 Townes, D., Moran, CT., and Pfingst, H.A.: Complications of cataract surgery. Trails. Am. Ophthalmol. Soc. 49: 91-107,1952. 16. Townes, C.D.: In discussion of Reese and Carroll. TrailS. Am. Acad. Ophthalmol. Otolaryllgol. 62: 768769,1958. 17. Vila-Coro, A: Atrofia del nervio optico despues de la operacion de cataracta. Arch. Soc. Oftalmol. 6: 901-904, 1946. 18. Welch, R.B., and Cooper, J.C: Macular edema, papilledema, and optic atrophy after cataract extraction. Arch. Ophthalmol. 59: 665-675, 1958. 19. Garvin, CG., and Weber, P.A.: Intermediate post cataract extraction ischemic optic neuropathy associated with an intraocular lens implant. Am. 111traocular Soc. Implallt. f. 8: 144-146, 1982. 20, Feit, R., Tomsak, R.L., and Ellenberger, C, Jr.: Structural factors in the pathogenesis of ischemic optic neuropathy. Am. f. Ophthalmol. (111 press.) Write for reprillts to: Robert L. Tomsak, M.D., Ph.D., Head, Section of Neuro-ophthalmology, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, Ohio 44106 257 |
