68 Reports Investiuativc Ophthalmology

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68 Reports Investiuativc Ophthalmology January 1975 Aphakic macular edema: incidence and pathogenesis. 0 R. A. HITCHINCS, I. H. CHISHOLM, AND A. C. BIRD.

1 68 Reports Investiuativc Ophthalmology January 1975 Aphakic macular edema: incidence and pathogenesis. 0 R. A. HITCHINCS, I. H. CHISHOLM, AND A. C. BIRD. In a prospective study, the incidence of cystoid macular edema for two groups of patients was found at six weeks following surgery. The first group who underwent cataract extraction had a 50 per cent incidence. The second group who underwent elective glaucoma surgery had no patient with cystoid macular edema. At six weeks, 16 per cent of those patients who had originally developed cystoid. edema, had a visual acuity of 6/12 or less, with no other cause for the poor visual result. The two major differences between these two groups of patients were the actual cataract extraction, and the presence of postoperative vitreous inflammation. No factors were noted to cause persistence of the aphakic macular edema although the technique of cataract extraction and vascular disease were implicated. The aim of this paper is fourfold: (1) to report the results or a prospective study on the incidence of aphakic macular edema, (2) to assess the visual outcome of those cases developing aphakic macular edema, (3) to compare this incidence with a series ot phakic patients undergoing glaucoma surgery, and (4) to discuss possible predisposing and peipetuating factors of this condition. The incidence of aphakic cystoid macular edema has been variously reported on as ranging Irom 1 per cent (on biomicroscopical studies 1 ' 1 -') to 40 per cent (on a prospective fluorescein study'), and 60 per cent. 1 To test the validity of this high incidence of aphakic cystoid macular edema, a prospective study was carried out on all the cataract patients cared for by two of us (RAH and IHC) from October 1972 until June Materials and methods. All patients cared for were asked if they would undergo Huorescein angiography at six to seven weeks following their cataract extraction. All agreed; however, not all attended for the angiogram. Those that did attend had a refraction, examination, and Huorescein angiogram. The angiographic technique used was the standard one employed by the retinal diagnostic unit at Moorfields Eye Hospital, City Road/ 1 and the angiograms were interpreted by members of that unit. At approximately six months after the initial angiogram those patients whose eyes showed leakage of fluorescein at the time of the initial angiogram were invited to attend for a follow-up examination and further angiogram. The clinical course of all these aphakic: patients was analyzed for possible predisposing factors. To assess the incidence of cystoid macular edema following intraocular glaucoma surgery, Huorescein angiography was carried out at six to seven weeks postoperatively on twenty-two eyes of nineteen phakic patients who had undergone glaucoma surgery. Again, the pie- and postoperative courses were analyzed for possible predisposing and differentiating factors. Results. The results were analyzed from four aspects: (1) the incidence of cystoid edema at the time of the initial angiogram for the aphakic patients, (2) the incidence of cystoid edema for the aphakic patients at the time of their repeat angiogram, (3) the glaucoma patients, and (4) an analysis of factors predisposing to aphakic macular edema. Section I. One hundred and one consecutive patients were asked to participate. Thirty patients either lailed to attend their appointments or had unsatisfactory photographs. Therefore, seventy-one patients, giving angiograms on seventy-five aphakic eyes, were analyzed. Thirty-eight eyes (50.6 per cent) showed cystoid macular edema six to seven weeks postoperatively. The range of leakage varied from the classical petaloid appearance to perifoveal cystoid pools of Huorescein which did not coalesce to give this petaloid appearance. There were five patients in the group which did not show cystoid edema with a visual acuity of 6/18 or less, each of whom had pre-existing ocular disease (two eyes with chorioretinal degeneration and one with retinoschisis, each with the macula involved; one with severe macular degeneration; and one amblyopic eye). Cystoid edema was the only cause of the poor visual results in the group showing leaking of Huorescein. The mean visual acuity was 6/6 in the nonleaking group, discounting the five patients with preexisting ocular disease, compared with 6/9 in the leaking group ( Fig. 1). Section II. Twenty-eight patients (twenty-nine eyes) who had shown aphakic macular edema at six to seven weeks after the operation returned lor a follow-up angiogram. Of these, sixteen eyes did not show leakage of Huorescein, eight eyes now showed minimal leakage, two eyes showed little change from the initial angiogram, while three eyes were now apparently worse. The mean visual acuity of this group was now 6/7.5 (Fig. 2). Four patients had a visual deterioration of two or more lines. Six patients still had a visual acuity of 6/12 or less and although four still showed a typical petaloid pattern of Huorescein leakage, two no longer showed leakage of Huorescein. No patient had developed any other apparent cause for this poor visual acuity. Section III. GLAUCOMA PATIENTS. Nineteen patients, twenty-two eyes, had elective intraocular glaucoma surgery. A filtering procedure was carried out on all but one case, where a peripheral iridectomy was performed. All except two of these patients were white. The age range and sex

2 Volume N Number 1 Reports 69 NONLEAKERS NONLEAKERS 15 Mean V A = 6/6 Mean V.A = 6/6 6/5 6/6 6/9 6/12 6/5 6/6 6/9 6/12 LEAKERS AT 6 WEEKS 15 LEAKERS AT 6 MOS. H Mean V A : = 6/9.ll... 6/5 6/6 Visual 6/9 Acuity 6/12 6/18 <6/l8 Fig. I. Comparison of visual acuity in patients showing leakage of fluorescein at six weeks postoperatively and those who do not leak fluorescein. A, nonleakers. /3, leakers at six weeks. incidence approximated to that of the aphakic patients. Marked postoperative hypotony was seen with every case except the peripheral iridectoiny procedure. All the patients had postoperative uveitis. There was, however, no more than a minimal vitritis present in any case. Analysis of the angiograms carried out at six to seven weeks lollowing the glaucoma procedure showed that m> patient had evidence of cystoid maciilar edema. Section IV. riu-:msi'o.sin<: KACITOHS. Predisposing factors can he conveniently grouped according to preoperative, operative, and postoperative factors. 5 Mean V A --6/7 5 6/5 6/6 6/9 6/12 6/18 <6/l8 Fig. 2. Comparison of visual acuity in patients not leaking fluorescent at six weeks postoperatively with the visual acuity of the patients at six months who originally leaked Hunrescein at six weeks postoperatively. A, nonleakers. B, Leakers at six months. ( 1 ) Prcopcrcitwc factors: There was no age; or sex difference between the two groups. All of our patients were white. Those diseases, ocular and systemic, which could be expected to affect the visual result were noted as pail of the pre-operative assessment. All systemic diseases severe enough to merit treatment were included. Table I shows the visual outcome of those patients with pre-existent ocular disease. Table II shows a visual outcome of those patients with co-existent systemic disease. (2) Operative factors: (A) technique; all cases had a limbus-based conjunctival Hap. Cryoextraetion was used in nearly every case. AJphachymotrypsin had been used in 97 per cent of the cases,

3 70 Reports Investigative Ophthalmology Jonuanj 1975 Table I. Co-existent ocular disease and visual Ocular diseasenoiileakers Ocular disease leakers 1. Subluxed lens 6/6 Heterochromic uveitis 6/6 2. Advanced chronic Heterochromic open-angle glau- uveitis 6/9 coma " 6/12 3. Senile macular degeneration 6/18 4. Myopic chorioretinal degeneration affecting macula 6/18 5. Retinoschisis affecting macula 6/24 6. Amblyopic eye 6/24 7. Myopic chorioretinal degeneration affecting macula 6/24 Table IT. Co-existent systemic disease and visual Systemic disease nonleakers Rheumatoid arthritis 6/6 (on systemic Hypertension <^ X steroids) 6/6 6/9 Rheumatoid arthritis Diabetes mellitus 6/6 (on systemic Diabetes mellitus 6/18 steroids) 6/24 Table III. Operative complications and visual Complications nonleakers Systemic diseaseleakers Complicationsleakers Vitreous loss 6/6 Vitreous loss 6/9 Vitreous loss 6/18 Vitreous loss 6/9 ( high myope with Massive hyphaema 6/9 chorioretinal de- Lens capsule rupgeneration affect- ture 6/6 ing the macula) Persistent flat anterior chamber 6/18 Lens capsule rupture 6/6 36 out of 38 eyes, which leaked fluorescein, but in only 81 per cent of the cases, 30 out of 37 eyes, not showing leakage of fluorescein. (B) complications, Table III shows the operative complications occurring in the two groups of patients, those that did and did not leak Huorescein at six weeks. These are grouped together with visual acuity attained at that time. (3) Postoperative factors: (A) postoperative intraocular pressure. There were 16 eyes which had an intraocular pressure of 8 mm. Hg or less lasting for one or more days. Eight of these eyes showed leakage of fluorescein at six weeks. Nine eyes had an intraocular pressure greater than 25 mm. Hg for one or more days; four of these showed leakage of fluorescein. (B) postoperative vitreous factors. AIJ cases had postoperative anterior uveitis together with inflammatory cells in the vitreous. In most cases, these cells could be seen in the posterior vitreous as well. In no case were vitreous strands incarcerated in the corneoscleral section, nor was vitreomacular traction seen. There was one case of late rupture of the anterior hyaloid face. Posterior vitreous detachment was very common in both groups. (C) postoperative medication. Topical mydriatics and antibiotics were used routinely in all patients. Topical steroids were used in 54 eyes, of which 22 (40 per cent) developed aphakic macular edema; compared with 12 out of the 21 eyes (57 per cent) not treated with topical steroids. No patient had had topical adrenergic medications in the postoperative period. Discussion. This study shows that cystoid macular edema is a common sequel to cataract extraction and confirms the results obtained by Irvine and co-workers* and Yoshioka and Kawashima. 1 The study period was limited to the sixth and seventh postoperative weeks, this being the peak incidence time shown by Irvine and co-workers. 1 Any patient 1 who developed transient cystoid edema outside this time would not have been detected, and the overall incidence could have been even higher. (i To be certain that these figures represent the incidence of cystoid edema occurring after extraction, angiograms should be performed preoperatively. In our series, most patients had cataracts of sufficient density to preclude any preoperative fundal view. To perform preoperative angiograms on those patients in whom a view of the fundus could be obtained would be artificially selective, and not representative of the group as a whole. No patient had a macular hole, which would have suggested long-standing cystoid edema 7 existing preoperatively. Ten of the glaucoma patients had had preoperative angiography, and no cystoid edema was noted. The degree of leakage did not correlate perfectly with the amount of visual loss. A few patients could achieve 6/5 despite gross petaloid edema. However, all patients who had a fall in their visual acuity between the time of the first and second examination of two or more lines showed an increase in the extent of their cystoid edema. Furthermore, those patients whose visual acuity had improved by two or more lines by the time of the follow-up visit showed a marked reduction in the degree of fluorescein leakage. Of those six patients with visual acuity

Volume M Number 1 Reports 71 of 6/12 or less at the time ol the h)ll<>w-up examination, four still showed evidence of gross leakage but two did not now leak.

4 Volume M Number 1 Reports 71 of 6/12 or less at the time ol the h)ll<>w-up examination, four still showed evidence of gross leakage but two did not now leak. The poor acuity obtained by two patients at the time of the follow-up angiograni despite no Hiiorescein leakage may rellect permanent structural damage, or pre-existing inacular hypofunction. There was a reduction in the mean visual acuity of those patients with cystoid edema at the six-week period, 6/9 compared to 6'/6. At the time of the follow-up examination this visual acuity had improved to fi/7.5, but was still below that of patients who did not leak Hiiorescein at the time of the original angiogiam. Many factors have been implicated in the causation of aphakic cystoid macular edema. The positive factors present in our series were systemic vascular disease severe enough to require treatment, and ocular inflammatory disease. All five patients with these two complications developed cystoid edema. We had a low incidence of vitreous complications, suggesting that while vitreous loss, incarceration, or late rupture of the anterior hyaloid lace may be important in persistence ol eystokl edema in our patients, they were not instrumental in its inception. Hypotony was not a lactor. There was an equal incidence of hypotony in both the group who did and did not leak Hiiorescein; similarly, hypotony was a constant feature in all the h'stulizing glaucoma procedures. There was no real evidence that topical steroids in the postoperative period inlliienced the incidence of cystoid inacular edema. A comparison of the cataract and glaucoma patients was made to see what factors might account for the disparity in the incidence of cystoid edema. Intraocular surgery with resultant anterior uveitis and/or hypotony was not enough to precipitate the condition. The factors of lens removal and the absence of postoperative vitritis in the glaucoma patients appeared as major dilferences between these two groups. Ryan, s too, noted that cystoid edema in association with a marked vitiitis developed following buckling procedures in two phakic patients. On accepting that after extraction, cystoid inacular edema is an exceedingly common and usually transient condition. It behooves us to try and search for lactors which may determine its persistence. For it is in those few patients with persisting cystoid inacular edema that permanent visual loss may develop. Thirteen aphakic patients in our series showed persistent leakage at the six-month period and those patients with the poorest visual results were in this group. On looking for factors which might account for this persistence, we could see no evidence that age, sex, operative complications, postoperative medications, vitreous disturbance, or hypotony played any part. We were unable to assess the degree of postoperative vitreous inflammation, the degree of operative trauma, or to correlate these factors with the existence of ocular or systemic vascular disease. It may well be that the actual traumatic episode of lens extraction varies from eye to eye and that this eflect is, in some cases, exceedingly long-lasting. It is interesting that Kelniiin" noted a very low incidence of cystoid inacular edema following phaco-emulsification. The significance of this is difficult to assess as many of his patients may be younger than those in this series. 1 " The trauma of lens removal, in combination with the existence of ocular or systemic vascular disease may be sufficient cause to determine the duration of the condition of postoperative cystoid macular edema. We would like to thank the members of the retina service at Moorfields Eye Hospital for analyzing the angiograms. Similarly, the consultants who allowed us to use their cases. We thank Dr. C. L. Spaeth for permission to use his patients and for facilities in the glaucoma service at Wills Eye Hospital for Hiiorescein angiography of his glaucoma patients. From the Glaucoma Service, Wills Eye Hospital, Philadelphia, Pa. Submitted for publication July 2, Reprint requests: Dr. Roger A. Hitchings, Research Associate, Glaucoma Service, Wills Eye Hospital, 1601 Spring Garden St., Philadelphia, Pa "This paper was presented in part at the Association for Research in Vision in Ophthalmology (ARVO) meeting at Sarasota, Flu., April, Key words: cystoid edema, aphakics, glaucoma surgery, Hiiorescein, predisposing factors. REFERENCES 1. N'laumenee, A. E.: Further advances in the study of the macula, Arch. Ophthalmol. 78: 151, Tolentino, F. 1., and Schepens, C. L.: Edema of the posterior role after cataract extraction, Arch. Ophthalmol. 74: 781, Irvine, S. R., Bresky, R., Crowder, B. M., et al.: Macular edema after cataract extraction, Ann. Ophthalmol. 3: 1234, Yoshioka, H., and Kawashima, K.: Macular edema following cataract extraction, Acta. Soc. Ophthalmol. ap. 75: 2269, Teeters, V. W., aiid Bird, A. C.: The development of neovascularization of senile disciform inacular degeneration, Am.. Ophthalmol. 7G: 1, West, C. E., Fitzgerald, C. R., and Sewell,. S.: Cystoid macular edema following aphakic keratoplasty, Am. J. Ophthalmol. 75: 77, Aaberg, T. M.: Macular Holes, a review, Surv. "Ophthalmol. 15: 139, 1970.

5 72 Reports Investigative Ophthalmology January Ryan, S. J.: Cystoid maeulopathv in phakie retinal detachment procedures, Am. J. Ophthalmol. 76: 519, Kelman, E. D.: Summary of personal experience. Symposium: phacoemulsification, Trans. Am. Acad. Ophthalmol. Otol. 78: 33, Ryan, E.: Presented at San Francisco residents and fellows meeting May, Ultrasonic transmission holography of the eye. EDWIN E. BOLDREY, DAVID R. HOL- BROOKE, AND VICTOR RICHARDS. Ocular ultrasonic transmission holography of the eye using equipment capable of real-time imaging has not previously been described. A method using pulsed, ultrasound focused on an air/liquid interface is used to demonstrate normal ocular structures including lens, optic nerve, and sclcra. Intraocular foreign bodies imaged include radiopaque and nonradiopaque materials. A limit of resolution of at least I mm. is demonstrated. Holography is a method of recording and reproducing life-like images of an object. A hologram is formed when light or other energy illuminating a scene is combined with the energy of a second identical but unaffected energy field. The combination of these two beams the illuminating and reference beams forms an interference pattern which can be recorded on film. When this film is illuminated with the reference beam, the interference pattern formed by the combination of the original two beams is interrogated, resulting in an image of the original illuminated field. This image is identical in all respects to the original field, containing both amplitude and phase information. Unlike ordinary photography, which records only amplitude information, a hologram is a true perspective image allowing true threedimensional viewing. 1 The basic principles of holography were first described by Cabor in 1948,-' but the first laser optical holograms were not reported until : Optical holographic imaging of a model eye was first done in 1966,' but not until 1970 did Calkins LENS LASER LIQUID SURFACE HOLOGRAM OBJECT OBJECT TRANSDUCER ACOUSTIC LENSES REFERENCE TRANSDUCER Fig. 1. Functional schematic diagram of immersion-type surface levitation holographic imaging system.

NEW YORK UNIVERSITY SCHOOL OF MEDICINE DEPARTMENT OF OPHTHALMOLOGY EDUCATIONAL OBJECTIVES AND GOALS

NEW YORK UNIVERSITY SCHOOL OF MEDICINE DEPARTMENT OF OPHTHALMOLOGY EDUCATIONAL OBJECTIVES AND GOALS Revision Date: 6/30/06 Distribution Date: 7/6/06 The Department of Ophthalmology at the NYU Medical Center