Neodymium:YAG (Nd:YAG) laser capsulotomy is associated with retinal detachment (RD). Horseshoe-shaped retinal tears are the typical cause of pseudophakic RD, and posterior vitreous detachment (PVD) is the cause of horseshoe-shaped tears. The objective of this study was to determine whether RD after Nd:YAG laser posterior capsulotomy might be caused by a higher incidence of PVD in treated eyes than in control eyes. No study of RD after Nd:YAG capsulotomy has addressed the presence of PVD at the time of capsulotomy or its subsequent development.
Patients and Methods
All patients having Nd:YAG laser posterior capsulotomy after uneventful extracapsular cataract extraction (ECCE) with intraocular lens (IOL) implantation (treatment group) were prospectively recruited into the study. The patients' fellow eyes were used to create 2 control groups. The first comprised eyes having uneventful ECCE and IOL implantation but no laser capsulotomy (no-laser group) and the second, eyes having no cataract surgery (phakic group).
The study was performed over 5 years during the transition from ECCE to phacoemulsification. Only a small number of patients with previous phacoemulsification required Nd:YAG capsulotomy; thus, they were excluded from the study. Eyes with previous vitreoretinal surgery, proliferative diabetic retinopathy, or Nd:YAG laser capsulotomy were also excluded. Trabeculectomy, combined ECCE and trabeculectomy, and extraocular surgery were not considered grounds for exclusion.
Four hundred seventy-nine patients were recruited into the study. After exclusion of eyes because of the above criteria and loss to follow-up, the treatment group comprised 322 eyes of 302 patients; the no-laser group, 97 eyes of 97 patients; and the phakic group, 142 eyes of 142 patients. The age and sex of the 3 groups were comparable (Table 1).
The demographics, interval from ECCE with IOL implantation to baseline examination, baseline vitreous status, and Nd:YAG laser energy in patients lost to follow-up were similar to those with complete data.
A standard Nd:YAG laser posterior capsulotomy technique was used. After pupil dilation, a contact lens was inserted. A curvilinear capsulotomy was cut with a Q-switched Nd:YAG laser using the minimum possible laser energy.
Dilated fundus examination of both eyes was performed at baseline (before capsulotomy) and 1 year later. A subset of patients with attached gel at baseline was examined at 1 week and 1, 3, and 6 months to define the timing of the PVD. The diagnosis of vitreous detachment was made by the presence of a Weiss ring or the characteristic folded appearance of the posterior hyaloid membrane (Figure 1).
The chi-square test was used to assess the significance of the observed differences in proportions of patients in each group with or without PVD. The Kruskal-Wallis test was used to assess the significance of observed differences in the timing of PVD among the groups. When the results are described, the number of degrees of freedom (df) are given only if greater than 1. A P value less than 0.05 was considered significant.
The median interval between ECCE and Nd:YAG capsulotomy in the treatment group was 774 days (interquartile range 386.5 to 1159.5 days) and the median Nd:YAG laser energy used, 50 mJ (interquartile range 32.5 to 72.5 mJ). The median interval from ECCE to baseline observation in the no-laser group was 1142 days (interquartile range 419 to 1864 days).
At baseline, established PVD was observed in 199 eyes (61.8%) in the treatment group, 62 (63.9%) in the no-laser group, and 72 (50.7%) in the phakic group (P=.0488, chi square; 2 df). Partitioning the contingency table showed no significant difference in the prevalence of PVD between the treatment and no-laser groups (P=.2014, chi square). However, the prevalence of PVD in the phakic group was significantly lower than in the treatment and no-laser groups combined (P=.0151, chi square).
Of eyes with attached gel at baseline, 22 (17.9%) in the treatment group, 4 (11.4%) in the no-laser group, and 12 (17.1%) in the phakic group had PVD at 1 year (P=.6588, chi square; 2 df). At the end of the 12-monthfollow-up, 221 eyes (68.6%) in the treatment group and 66 (68.0%) in the no-laser group had PVD (P=.3038, chi square). In the phakic group, 84 eyes (59.2%) had PVD, significantly fewer than in the treatment and no-laser groups (P=.0421, chi square). The data are summarized in Table 2.
Table 3 shows the number of eyes examined at each of the intermediate time points postoperative examination. Because most patients were elderly, it was not possible to examine each one at every interval. However, 109 eyes (88.6%) in the treatment group, 31 (88.6%) in the no-laser group, and 45 (64.3%) in the phakic group had at least 1 intermediate examination.
Intermediate observations of those who developed PVD were done in 18 of 22 patients in the treatment group, 3 of 4 in the no-laser group, and 5 of 12 in the phakic group. The numbers of patients are small; however, there appeared to be no difference in the timing of the PVD among the groups (P=.807, Kruskal-Wallis; 2 df).
One eye developed an RD during the follow-up. This eye had an Nd:YAG capsulotomy, making the incidence of RD 0.31% in the treatment group.
The association between ECCE with IOL implantation and RD is well recognized, occurring in 0.7% of eyes.1 The peak risk of RD occurs in the first postoperative year but remains significantly higher than the background risk for up to 6 years.2 A further 0.8% of eyes have retinal breaks without RD.3
Our study found a significantly higher prevalence of PVD at baseline in pseudophakic eyes (61.8%, treatment group; 63.9%, no-laser group) than in phakic eyes (50.7%). It is likely that cataract extraction increases the PVD rate above normal for an undetermined time after surgery, and this accounts for the difference in the prevalence of PVD at baseline. It is likely that this relatively high PVD rate explains the reported risk of retinal tear and RD after cataract surgery.
Retrospective analysis of data based on Medicare claims in the United States suggests that Nd:YAG laser capsulotomy is associated with a significantly elevated risk for RD, although stronger associations were found for a history of RD or lattice degeneration, an axial length greater than 24.0 mm, and posterior capsule rupture during surgery.4 Several other retrospective studies confirm the higher risk of RD after capsulotomy in eyes with intraoperative complications, axial myopia, and vitreoretinal pathology5–8; however, 2 studies show no association in the absence of these risk factors.10,11
Horseshoe-shaped retinal tears are the typical cause of pseudophakic RD,12 and PVD is the cause of horseshoe-shaped tears. The mechanism by which Nd:YAG laser capsulotomy causes RD is unclear, although it has been postulated that removal or disruption of the posterior capsule predisposes to vitreous collapse and vitreous traction (ie, PVD).13 We designed our study to examine the hypothesis that the increased incidence of RD after Nd:YAG capsulotomy is caused by an increased incidence of PVD and, therefore, an increased risk for horseshoe-tear formation. We followed our patients for 12 months because 75% to 89% of RDs occur within 1 year of Nd:YAG laser capsulotomy.7,8,14
The incidence of new PVD was identical in the treatment and phakic groups (17.9% and 17.1%, respectively) but lower in the no-laser group (11.4%), although the difference was not statistically significant. There may be a real difference, but the sizes of the groups are insufficient to detect it. However, the higher PVD rate in the treatment group than in the no-laser group did not exceed the background rate of PVD in normal, phakic eyes.
If Nd:YAG laser capsulotomy causes PVD, we would expect a temporal relationship between the laser treatment and the occurrence of PVD. There was no difference in the timing of PVD among the 3 groups, and PVD after Nd:YAG capsulotomy was seen at all stages of follow-up.
If we had found a significantly higher incidence of PVD after Nd:YAG laser capsulotomy, it would support the hypothesis that the higher risk of RD after the capsulotomy is caused by laser-induced PVD. We could therefore postulate that the presence or absence of PVD at the time of capsulotomy allows patients at a higher risk for RD after capsulotomy (ie, those with attached vitreous) to be distinguished from those at lower risk (ie, those with established PVD). In this prospective study, Nd:YAG capsulotomy was not associated with an increased incidence of new PVD; therefore, the vitreous status at the time of laser treatment does not contribute to the assessment of the risk for RD in the first year after capsulotomy.
Mechanisms of RD other than the simple induction of PVD must be considered. First, Nd:YAG laser capsulotomy may increase the risk of PVD causing a retinal tear. Second, the capsulotomy may cause anterior “progression” of existing PVD with horseshoe-tear formation, which is consistent with the observation that tears causing pseudophakic detachments tend to be smaller and more anteriorly located than those causing phakic detachments.12 Third, Nd:YAG capsulotomy may cause retinal tears by a mechanism independent of PVD. Finally, Nd:YAG capsulotomy may increase the risk of RD only in certain subgroups such as in those with axial myopia. Larger prospective studies are required to test these hypotheses.
In conclusion, we found that ECCE with IOL implantation is associated with a significantly higher prevalence of PVD at baseline compared to the incidence in phakic eyes. Neodymium:YAG laser capsulotomy was not associated with a significantly higher incidence of new PVD; therefore, the presence or absence of PVD at the time of capsulotomy is not helpful in assessing the risk of RD in the first year after laser treatment.9
1. Powe NR, Schein OD, Gieser SC, et al. Synthesis of the literature on visual acuity and complications following cataract extraction with intraocular lens implantation. Arch Ophthalmol 1994; 112:239-252; erratum, 889
2. Norregaard JC, Thoning H, Andersen TF, et al. Risk of retinal detachment following cataract extraction: results from the International Cataract Surgery Outcomes Study. Br J Ophthalmol 1996; 80:689-693
3. Davison JA. Retinal tears and detachments after extracapsular cataract surgery. J Cataract Refract Surg 1988; 14:624-632
4. Tielsch JM, Legro MW, Cassard SD, et al. Risk factors for retinal detachment after cataract surgery; a population-based case-control study. Ophthalmology 1996; 103:1537-1545
5. Olsen GM, Olson RJ. Prospective study of cataract surgery, capsulotomy, and retinal detachment. J Cataract Refract Surg 1995; 21:136-139
6. Koch DD, Liu JF, Gill EP, Parke DW II. Axial myopia increases the risk of retinal complications after neodymium: YAG posterior capsulotomy. Arch Ophthalmol 1989; 107:986-990
7. Rickman-Barger L, Florine CW, Larson RS, Lindstrom RL. Retinal detachment after neodymium: YAG laser posterior capsulotomy. Am J Ophthalmol 1989; 107:531-536
8. Dardenne MU, Gerten G-J, Kokkas K, Kermani O. Retrospective study of retinal detachment following neodymium: YAG laser posterior capsulotomy. J Cataract Refract Surg 1989; 15:676-680
9. Steinert RF, Puliafito CA, Kumar SR, et al. Cystoid macular edema retinal detachment, and glaucoma after Nd:YAG laser posterior capsulotomy. Am J Ophthalmol 1991; 112:373-380
10. Nielsen NE, Naeser K. Epidemiology of retinal detachment following extracapsular cataract extraction: a follow-up study with an analysis of risk factors. J Cataract Refract Surg 1993; 19:675-680
11. Powell SK, Olson RJ. Incidence of retinal detachment after cataract surgery and neodymium: YAG laser capsulotomy. J Cataract Refract Surg 1995; 21:132-135
12. Bradford JD, Wilkinson CP, Fransen SR. Pseudophakic retinal detachments; the relationships between retinal tears and the time following cataract surgery at which they occur. Retina 1989; 9:181-186
13. Javitt JC, Tielsch JM, Canner JK, et al. National outcomes of cataract extraction; increased risk of retinal complications associated with Nd: YAG laser capsulotomy; the Cataract Patient Outcomes Research Team. Ophthalmology 1992; 99:1487-1497; discussion by CP Wilkinson, 1497–1498
14. Greven CM, Sanders RJ, Brown GC, et al. Pseudophakic retinal detachments; anatomic and visual results. Ophthalmology 1992; 99:257-262