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Clinical factors relating to cystoid macular edema after lens implantation
clinical factors relating to cystoid macular edema after lens implantation Piers Percival, F.R.C.S. Scarborough, England
ABSTRACT Of 232 eyes undergoing intraeapsular or extracapsular cataract extraction with implantation of a Binkhorst-style 2-loop lens, 46 (20%) developed persistent or transient clinical cystoid macular cdema. The incidence of cystoid macular edema was lowest when the posterior capsule and vitreous face were intact, and was unaffected by administration of prophylactic oral indomethacin. Key words: cystoid macular edema, cataract extraction, intraocular lens implantation, indomethacin
There is angiographic evidence of cystoid macular edema (CME) after approximately 50% of all cataract operations, 1-3 but its reported incidence as a clinical complication of intracapsular cataract surgery varies between 3% and 20%.4-7 Part of the reason for this variation is the difficulty in establishing agreed-upon criteria for normal vision. This paper discusses several factors which relate to the development of postoperative CME. For the purposes of this discussion, 20/30 is used as the standard for normal visual acuity.
SUBJECTS AND METHODS Between 1972 and 1978, 268 primary lens implantations were performed after intracapsular cataract extraction (ICCE) or extracapsular cataract extraction (ECCE). Patients received Binkhorst-style 2-100p, 3-100p* or 4-loop intraocular lenses manufactured by Rayner in England. Fourteen eyes were excluded from this study because of preoperative visual defects, eight were excluded because of visual complications occurring during the first postoperative year which were unrelated to CME, and 14 were lost to followup. The remaining 232 eyes were followed from one to seven years. All intracapsular cases performed between November 1976 and May 1978 received 75 to 100 mg of oral indomethacin daily, starting the day before surgery and continuing through the second postoperative week. Applanation tonometry was routinely performed on the third, sixth and fifteenth postoperative days; any reading over 24 mm Hg was considered an elevated pressure.
CME was diagnosed as a postoperative drop in visual acuity of at least 1.5 Snellen lines, to less than 20/30, associated with either a macular scotoma on the Amsler recording chart or an ophthalmoscopic abnormality of the macula. The diagnosis was based on clinical observations alone; angiography was not performed. A search was made for factors which could have influenced the development of CME: method of surgery, age and sex of patient, rupture of the vitreous face, use of indomethacin, presence of systemic vascular disease, elevated intraocular pressure or use of epinephrine.
RESULTS There were 46 (20%) cases of clinical CME in this series. Of these, 42 (92%) developed CME before the ninth postoperative month (Table 1). The incidence of persistent or transient CME was 23% after ICCE and 15% after ECCE (Table 2). In the extracapsular group, the incidence of CME was 13% for cases with an intact posterior capsule and 27% for cases with a ruptured capsule. A persistent visual acuity ofless than 20/30 occurred in 9% of the intracapsular group, compared to 1 % of the extracapsular group with intact capsules. Table 1. Time of onset and duration of CME. Number of Cases (%)
< 3 months
3-9 months
> 9 months
Onset
26 (57)
16 (35)
4 (8)
Duration
17 (37)
12 (26)
17 (37)
*The Binkhorst-style 3-loop lens is a 4-loop iris clip lens without the anteroinferior loop. From the Department of Ophthalmology, Scarborough General Hospital, Scarborough, England. Read in part to a meeting of the International Intraocular Implant Club in Cannes, May 3, 1979. Reprint requests to Dr. Percival, Scarborough Hospital, Scarborough, North Yorkshire.Y012 6QL. AM INTRA-OCULAR IMPLANT SOC J-VOL. 7, JANUARY 1981
43
Table 2. Incidence of clinical CME. Cases with Cystoid Macular Edema
Type of Cataract Surgery
No. of Eyes
Intracapsular
Persistent Transient* (%) (%)
128
11 (9)
Total (%)
19 (14)
30 (23)
Extracapsular, with posterior capsule rupture
15
2 (13)
2 (14)
4 (27)
Extracapsular, with intact posterior capsule
89
1 (1)
11 (12)
12 (13)
232
14 (6)
32 (14)
46 (20)
*Cases of transient CME cleared within ten months.
The incidence of persistent CME increased slightly in patients over the age of 76 (Table 3). The incidence of CME was approximately 20% for both male (22/112 cases) and female (24/120 cases) patients. Table 3. Incidence of persistent CME according to patient age and type of surgery.
Patient Age (Years)
Cases of CYlE after Intracapsular Surgery
Cases of CME after Extracapsular Surgery
< 66
3 in 26 (12%)
o in
23
3 in 49 (6%)
66-76
3 in 62 (5%)
2 in 46 (4%)
5 in 108 (5%)
> 76
5 in 40 (13%)
1 in 35 (3%)
6 in 75 (8%)
Total
Slitlamp evidence of vitreous in the anterior chamber postoperatively indicated rupture of the vitreous face in 30 (13%) eyes, 18 after ICCE and 12 following ECCK Ten (33%) patients in this group had CMK In six (20%) cases CME caused a persistent visual defect. None of the 30 eyes had had vitreous loss, vitrectomy or vitreous adherence to the wound. Indomethacin, a prostaglandin synthetase inhibitor, was given to 50 patients undergoing planned intracapsular surgery. Eleven (22%) patients in this group developed CME; persistent visual loss occurred in four (8%) cases. Six patients taking indomethacin experienced nausea and/or gastric distress, and one patient developed thrombocytopenic purpura with aplastic anemia. Forty-five patients in this study had systemic vascular disease, as evidenced by known coronary artery insufRciency or cerebrovascular insufRciency. Seven of these patients developed CMK In the 21 intracapsular eyes the incidence of CME was 19%; three (14%) of the four intracapsular cases had permanent visual defects. In the 24 extracapsular eyes the incidence of CME was 12%; all of these had an intact posterior cap44
sule and none had a permanent visual defect. None of the nine diabetic patients developed CMK Elevated intraocular pressure during the first two postoperative weeks was noted in 27 (21 %) eyes in the intracapsular group. This transient complication was attributed mainly to the use of alpha chymotrypsin (routine for all intracapsular surgery) and subconjunctival and topical steroids (routine for all surgeries). Six (22%) of these intracapsular eyes developed CME, two (8%) with a persistent visual defect. Elevated lOP was noted in seven eyes with intact posterior capsules; one of these eyes developed transient CMK Five of the 15 extracapsular cases with a ruptured posterior capsule had elevated lOP; three developed transient CMK Of the 12 intracapsular patients receiving topical epinephrine postoperatively, four (33%) developed CME, one (8%) with a persistent visual defect. These eyes also had a complicated postoperative course.
DISCUSSION This study supports the conclusions of others 4 ,8 that an intact posterior capsule reduces the severity and duration of CMK The most significant factor increasing the incidence of CME was rupture of the vitreous face (Table 4). Systemic vascular disease and advancing age were also associated with an increased incidence of persistent CME, although numbers were not large enough to be of statistical significance. There was no correlation between CME and elevated lOP. Oral indomethacin was not found to alter either the incidence or severity of CME or the incidence of elevated intraocular pressure. Table 4. Significance of factors relating to CME after planned IeCE.
Eyes
CYlE*
Persistent Visual Defect
Systemic indomethacin
50
11 (22%)
4 (8%)
(N.S.)
Age over 76
40
11 (27%)
5 (12%)
(N.S.)
Svstemic vascular disease
21
4 (19%)
3 (14%)
(N.S.)
Elevated lOP
27
6 (22%)
2 (8%)
(N.S.)
Topical adrenaline
12
4 (33%)
1 (8%)
(N.S.)
Ruptured vitreous face
30t
10 (33%)
6 (20%)
(p
Intact posterior capsule
89
12 (13%)
1 (1%)
(p<0.02)
No. of Cases of
* Includes
transient cases t Includes 12 cases of ECCE
AM INTRA-OCULAR IMPLANT SOC J-VOL. 7, JANUARY 1981
Significance (chi-square)
SUMMARY Of 143 primary implantations after either intracapsular cataract extraction or extracapsular extraction with a ruptured posterior capsule, cystoid macular edema caused a persistent loss of vision in 13 (9%) cases which had no other visual defect. A milder form of clinical CME was detected in 21 (15%) cases. The use of indomethacin at the time of surgery did not significantly reduce the incidence or severity of clinical CME in intracapsular cases, nor did it alter the incidence of postoperative ocular hypertension as measured on the third, sixth and fifteenth postoperative days. Of 89 extracapsular primary implantations with an intact posterior capsule, only one case had a pennanent visual defect caused by persistent CME.
REFERENCES 1. Hitchings RA, Chisholm IH, Bird AC: Aphakic macular edema: incidence and pathogenesis. Invest Ophthalmol Visual Sci 14:68, 1975 2. Irvine SR, Bresky R, Crowder BM et al: Macular edema after cataract extraction. Ann Ophthalmol 3:1234, 1971 3. Yoshioka H, Kawashima K: Macular edema following cataract extraction. Acta Soc Ophthalmol Jap 75:2269, 1971 4. Binkhorst CD: The iridocapsular (two-loop) lens and the iris clip (four-loop) lens in pseudophakia. Trans Am Acad Ophthalmol Otolaryngol 77:589, 1973 5. Gills JP: Intraocular lens in perspective. Contact and Intraocular Lens Med J 1(3):39, 1975 6. Shepard DD: Intraocular lens implantation - analysis of 500 consecutive cases. Ophthalmic Surg 8:,57, 1977 7. Snider NL, McReynolds WU: Analysis of our first 500 implantations. Am Intra-Ocular Implant Soc J 3:':10, 1977 8. The Miami Study Group: Cystoid macular edema in aphakic and pseudophakic eyes. Am] Ophthalmol 88:45, 1979
AM INTRA-OCULAR IMPLANT SOC J-VOL. 7, JANUARY 1981
45
ABSTRACT Of 232 eyes undergoing intraeapsular or extracapsular cataract extraction with implantation of a Binkhorst-style 2-loop lens, 46 (20%) developed persistent or transient clinical cystoid macular cdema. The incidence of cystoid macular edema was lowest when the posterior capsule and vitreous face were intact, and was unaffected by administration of prophylactic oral indomethacin. Key words: cystoid macular edema, cataract extraction, intraocular lens implantation, indomethacin
There is angiographic evidence of cystoid macular edema (CME) after approximately 50% of all cataract operations, 1-3 but its reported incidence as a clinical complication of intracapsular cataract surgery varies between 3% and 20%.4-7 Part of the reason for this variation is the difficulty in establishing agreed-upon criteria for normal vision. This paper discusses several factors which relate to the development of postoperative CME. For the purposes of this discussion, 20/30 is used as the standard for normal visual acuity.
SUBJECTS AND METHODS Between 1972 and 1978, 268 primary lens implantations were performed after intracapsular cataract extraction (ICCE) or extracapsular cataract extraction (ECCE). Patients received Binkhorst-style 2-100p, 3-100p* or 4-loop intraocular lenses manufactured by Rayner in England. Fourteen eyes were excluded from this study because of preoperative visual defects, eight were excluded because of visual complications occurring during the first postoperative year which were unrelated to CME, and 14 were lost to followup. The remaining 232 eyes were followed from one to seven years. All intracapsular cases performed between November 1976 and May 1978 received 75 to 100 mg of oral indomethacin daily, starting the day before surgery and continuing through the second postoperative week. Applanation tonometry was routinely performed on the third, sixth and fifteenth postoperative days; any reading over 24 mm Hg was considered an elevated pressure.
CME was diagnosed as a postoperative drop in visual acuity of at least 1.5 Snellen lines, to less than 20/30, associated with either a macular scotoma on the Amsler recording chart or an ophthalmoscopic abnormality of the macula. The diagnosis was based on clinical observations alone; angiography was not performed. A search was made for factors which could have influenced the development of CME: method of surgery, age and sex of patient, rupture of the vitreous face, use of indomethacin, presence of systemic vascular disease, elevated intraocular pressure or use of epinephrine.
RESULTS There were 46 (20%) cases of clinical CME in this series. Of these, 42 (92%) developed CME before the ninth postoperative month (Table 1). The incidence of persistent or transient CME was 23% after ICCE and 15% after ECCE (Table 2). In the extracapsular group, the incidence of CME was 13% for cases with an intact posterior capsule and 27% for cases with a ruptured capsule. A persistent visual acuity ofless than 20/30 occurred in 9% of the intracapsular group, compared to 1 % of the extracapsular group with intact capsules. Table 1. Time of onset and duration of CME. Number of Cases (%)
< 3 months
3-9 months
> 9 months
Onset
26 (57)
16 (35)
4 (8)
Duration
17 (37)
12 (26)
17 (37)
*The Binkhorst-style 3-loop lens is a 4-loop iris clip lens without the anteroinferior loop. From the Department of Ophthalmology, Scarborough General Hospital, Scarborough, England. Read in part to a meeting of the International Intraocular Implant Club in Cannes, May 3, 1979. Reprint requests to Dr. Percival, Scarborough Hospital, Scarborough, North Yorkshire.Y012 6QL. AM INTRA-OCULAR IMPLANT SOC J-VOL. 7, JANUARY 1981
43
Table 2. Incidence of clinical CME. Cases with Cystoid Macular Edema
Type of Cataract Surgery
No. of Eyes
Intracapsular
Persistent Transient* (%) (%)
128
11 (9)
Total (%)
19 (14)
30 (23)
Extracapsular, with posterior capsule rupture
15
2 (13)
2 (14)
4 (27)
Extracapsular, with intact posterior capsule
89
1 (1)
11 (12)
12 (13)
232
14 (6)
32 (14)
46 (20)
*Cases of transient CME cleared within ten months.
The incidence of persistent CME increased slightly in patients over the age of 76 (Table 3). The incidence of CME was approximately 20% for both male (22/112 cases) and female (24/120 cases) patients. Table 3. Incidence of persistent CME according to patient age and type of surgery.
Patient Age (Years)
Cases of CYlE after Intracapsular Surgery
Cases of CME after Extracapsular Surgery
< 66
3 in 26 (12%)
o in
23
3 in 49 (6%)
66-76
3 in 62 (5%)
2 in 46 (4%)
5 in 108 (5%)
> 76
5 in 40 (13%)
1 in 35 (3%)
6 in 75 (8%)
Total
Slitlamp evidence of vitreous in the anterior chamber postoperatively indicated rupture of the vitreous face in 30 (13%) eyes, 18 after ICCE and 12 following ECCK Ten (33%) patients in this group had CMK In six (20%) cases CME caused a persistent visual defect. None of the 30 eyes had had vitreous loss, vitrectomy or vitreous adherence to the wound. Indomethacin, a prostaglandin synthetase inhibitor, was given to 50 patients undergoing planned intracapsular surgery. Eleven (22%) patients in this group developed CME; persistent visual loss occurred in four (8%) cases. Six patients taking indomethacin experienced nausea and/or gastric distress, and one patient developed thrombocytopenic purpura with aplastic anemia. Forty-five patients in this study had systemic vascular disease, as evidenced by known coronary artery insufRciency or cerebrovascular insufRciency. Seven of these patients developed CMK In the 21 intracapsular eyes the incidence of CME was 19%; three (14%) of the four intracapsular cases had permanent visual defects. In the 24 extracapsular eyes the incidence of CME was 12%; all of these had an intact posterior cap44
sule and none had a permanent visual defect. None of the nine diabetic patients developed CMK Elevated intraocular pressure during the first two postoperative weeks was noted in 27 (21 %) eyes in the intracapsular group. This transient complication was attributed mainly to the use of alpha chymotrypsin (routine for all intracapsular surgery) and subconjunctival and topical steroids (routine for all surgeries). Six (22%) of these intracapsular eyes developed CME, two (8%) with a persistent visual defect. Elevated lOP was noted in seven eyes with intact posterior capsules; one of these eyes developed transient CMK Five of the 15 extracapsular cases with a ruptured posterior capsule had elevated lOP; three developed transient CMK Of the 12 intracapsular patients receiving topical epinephrine postoperatively, four (33%) developed CME, one (8%) with a persistent visual defect. These eyes also had a complicated postoperative course.
DISCUSSION This study supports the conclusions of others 4 ,8 that an intact posterior capsule reduces the severity and duration of CMK The most significant factor increasing the incidence of CME was rupture of the vitreous face (Table 4). Systemic vascular disease and advancing age were also associated with an increased incidence of persistent CME, although numbers were not large enough to be of statistical significance. There was no correlation between CME and elevated lOP. Oral indomethacin was not found to alter either the incidence or severity of CME or the incidence of elevated intraocular pressure. Table 4. Significance of factors relating to CME after planned IeCE.
Eyes
CYlE*
Persistent Visual Defect
Systemic indomethacin
50
11 (22%)
4 (8%)
(N.S.)
Age over 76
40
11 (27%)
5 (12%)
(N.S.)
Svstemic vascular disease
21
4 (19%)
3 (14%)
(N.S.)
Elevated lOP
27
6 (22%)
2 (8%)
(N.S.)
Topical adrenaline
12
4 (33%)
1 (8%)
(N.S.)
Ruptured vitreous face
30t
10 (33%)
6 (20%)
(p
Intact posterior capsule
89
12 (13%)
1 (1%)
(p<0.02)
No. of Cases of
* Includes
transient cases t Includes 12 cases of ECCE
AM INTRA-OCULAR IMPLANT SOC J-VOL. 7, JANUARY 1981
Significance (chi-square)
SUMMARY Of 143 primary implantations after either intracapsular cataract extraction or extracapsular extraction with a ruptured posterior capsule, cystoid macular edema caused a persistent loss of vision in 13 (9%) cases which had no other visual defect. A milder form of clinical CME was detected in 21 (15%) cases. The use of indomethacin at the time of surgery did not significantly reduce the incidence or severity of clinical CME in intracapsular cases, nor did it alter the incidence of postoperative ocular hypertension as measured on the third, sixth and fifteenth postoperative days. Of 89 extracapsular primary implantations with an intact posterior capsule, only one case had a pennanent visual defect caused by persistent CME.
REFERENCES 1. Hitchings RA, Chisholm IH, Bird AC: Aphakic macular edema: incidence and pathogenesis. Invest Ophthalmol Visual Sci 14:68, 1975 2. Irvine SR, Bresky R, Crowder BM et al: Macular edema after cataract extraction. Ann Ophthalmol 3:1234, 1971 3. Yoshioka H, Kawashima K: Macular edema following cataract extraction. Acta Soc Ophthalmol Jap 75:2269, 1971 4. Binkhorst CD: The iridocapsular (two-loop) lens and the iris clip (four-loop) lens in pseudophakia. Trans Am Acad Ophthalmol Otolaryngol 77:589, 1973 5. Gills JP: Intraocular lens in perspective. Contact and Intraocular Lens Med J 1(3):39, 1975 6. Shepard DD: Intraocular lens implantation - analysis of 500 consecutive cases. Ophthalmic Surg 8:,57, 1977 7. Snider NL, McReynolds WU: Analysis of our first 500 implantations. Am Intra-Ocular Implant Soc J 3:':10, 1977 8. The Miami Study Group: Cystoid macular edema in aphakic and pseudophakic eyes. Am] Ophthalmol 88:45, 1979
AM INTRA-OCULAR IMPLANT SOC J-VOL. 7, JANUARY 1981
45