Many studies of the influence of cataract surgery on diabetic retinopathy have been published. Kato et al.1 report that the progression of retinopathy is not affected by factors such as age, diabetes duration, diabetic treatment method, and hemoglobin A1c level and that the preoperative status of retinopathy may influence the susceptibility of retinopathy to surgical invasion.
Few studies have examined the postoperative course of diabetic retinopathy using the nonoperated fellow eye as a control. Two that have1,2 found that worsening of diabetic retinopathy reflects the natural course of the disease, systemic factors, or both rather than the influence of cataract surgery. In a Japanese study,1 diabetic patients not showing preoperative retinopathy were more susceptible to postoperative retinopathy progression after surgical intervention.
In this study, using the nonoperated contralateral eye as a control, we evaluated whether diabetic retinopathy progresses after cataract surgery and whether the progression is a natural course or caused by the surgery. We also sought to determine the major factors affecting the progression of diabetic retinopathy.
Patients and Methods
This prospective study comprised all cataract surgeries performed by 1 surgeon (J.C.) from August 1, 1997, through January 31, 1999. One eye of 85 diabetic patients who had a similar stage of retinopathy or no retinopathy in both eyes preoperatively had cataract surgery. Exclusion criteria were previous photocoagulation, intraoperative complications (eg, posterior capsule rupture, severe iris damage), secondary surgical intervention, and intraocular surgery performed in the nonoperated eye within 1 year of observation. Ten of 85 eyes were excluded using these criteria. This left 75 eyes, which were evaluated for 1 year, during which the progression of retinopathy in the operated eye was compared with that in the contralateral nonoperated eye, which served as a control.
The preoperative classification of diabetic retinopathy is shown in Table 1. All patients had a similar stage of retinopathy or no retinopathy in both eyes preoperatively. In cases in which the fundus was not visible because of cataract, the retinopathy level on the first postoperative day was used as the preoperative level.
The surgical techniques included continuous curvilinear capsulorhexis and extracapsular cataract extraction (ECCE) through a 10.0 mm corneoscleral incision or phacoemulsification through a 3.0 mm corneal or 7.0 mm corneoscleral incision with in-the-bag implantation of a single-piece poly(methyl methacrylate) (PMMA) or foldable acrylic intraocular lens (IOL), respectively. Topical antibiotics and prednisolone 0.1% were used 4 times daily for 1 month after surgery.
Postoperative examinations included slitlamp biomicroscopy and fundus evaluation through a dilated pupil using stereoscopic fundoscopy at each visit. Fundus photographs were taken to document the progression of retinopathy, defined as deterioration of 1 or more levels according to the Early Treatment Diabetic Retinopathy Study grading.3,4 The postoperative progression of retinopathy was quantified using the stages shown in Table 1.
The patients were assigned to 1 of 2 groups 1 year after cataract surgery. In Group A (n = 23), the progression of retinopathy in the operated eye was attributed to the influence of surgery. In Group B (n = 52), there was no deterioration or a comparable level of deterioration in both eyes or more progression of retinopathy in the nonoperated eye than in the operated eye. Factors evaluated in each group were preoperative macular edema status, surgical technique, renal function, hypertension, age, and duration of and treatment method for diabetes mellitus and whether these factors affected the progression of retinopathy postoperatively.
Patients were further classified according to whether they had preoperative diabetic retinopathy. The same factors evaluated in Groups A and B were studied in this subgroup.
Data analysis was performed using the SPSS statistical program. Paired t tests, unpaired Student t tests, and chi-square tests were used to compare the 2 groups. The level of significance was P < .05.
Preoperatively, 27 of the 75 eyes (36%) had no diabetic retinopathy and 48 (64%) had diabetic retinopathy. Of these 48 eyes, 32 had mild or moderate nonproliferative diabetic retinopathy (NPDR), 13 had severe or very severe NPDR, and 3 had proliferative diabetic retinopathy (PDR) (Table 1).
Diabetic retinopathy was newly developed or further progressed in 23 eyes (30.6%) 1 year after cataract surgery. None of the 27 eyes without retinopathy preoperatively developed it postoperatively. In 23 (47.9%) of the 48 eyes that had preoperative diabetic retinopathy, the retinopathy progressed after surgery. Of eyes in which the retinopathy progressed or developed after surgery, 96.4% had preoperative retinopathy. Significantly more operated eyes (85%) than nonoperated control eyes (15%) had progression of the retinopathy (P < .001). There was no significant difference in the progression of retinopathy between control and operated eyes in patients without preoperative diabetic retinopathy (P > .05) (Table 2).
In the operated eyes, the mean score for the progression of retinopathy (Table 1) increased from 1.45 to 2.04 and in the nonoperated control eyes, from 1.45 to 1.68 (P < .001) (Table 3).
The prevalence of clinically significant macular edema (CSME) at the time of cataract surgery was higher in Group A (progression of retinopathy in operated eye attributable to surgery) than in Group B (no or comparable postoperative deterioration in both eyes).
There was no significant difference between Groups A and B in surgical technique (ie, ECCE or phacoemulsification).
An analysis of the progression of diabetic retinopathy according to the renal function showed a preoperative creatinine level greater than 1.4 mg/dL in 8 patients (34.8%) in Group A and 3 patients (5.7%) in Group B. Fifty-four percent in Group A and 27% in Group B had proteinuria. The difference between groups was significant (P < .05), indicating that patients with diabetic nephropathy are more likely to have progression of diabetic retinopathy after surgery. Of the 48 patients with diabetic retinopathy preoperatively, 8 of 23 (34.8%) in Group A and 3 of 52 (5.7%) in Group B had a preoperative creatinine level greater than 1.4 mg/dL.
There were no significant differences between Groups A and B in the mean patient age or diabetes treatment methods (eg, diet control, oral medication, insulin injection). Hypertension was present in 15.4% in Group B and 8.7% in Group A; however, the difference between groups was not statistically significant (Table 4).
In our study, retinopathy did not develop postoperatively in 27 consecutive patients without retinopathy preoperatively; however, 23 of 48 patients (47.9%) with preoperative diabetic retinopathy had progression of diabetic retinopathy after surgery. The latter percentage differs from that in many recent series of phacoemulsification and ECCE in diabetic patients, which report progression rates of 36%,1 34%,2 38%,5 43%,6 and 25%.7 This is because we analyzed the progression of retinopathy according to whether the patient had preoperative diabetic retinopathy.
Kato et al.1 report that the preoperative status of retinopathy may influence its susceptibility to surgical invasion. They found that patients without retinopathy were more susceptible than those with advanced retinopathy. In contrast, Mittra et al.7 found a strong association between retinopathy progression and NPDR, PDR, and surgery performed by residents. Among these factors, NPDR has consistently been associated with postcataract retinopathy progression. In our study, diabetic retinopathy was more progressed or developed after cataract surgery more often in patients who had preoperative retinopathy. Diabetic patients with any type of retinopathy should be advised that cataract extraction might increase the level of retinopathy.
In our study, the prevalence of CSME at the time of surgery was higher in the operated eyes, which had more progression of diabetic retinopathy. Clinically significant macular edema present in diabetic eyes at the time of surgery is unlikely to resolve spontaneously,8 and the postoperative visual acuity prognosis is not as good as in eyes without edema.9 Careful selection of cases and frequent follow-up may be needed in patients with preoperative CSME to reduce the progression of diabetic retinopathy and unresolved macular edema after cataract surgery.10,11
In a retrospective study of surgical technique, Antcliff and coauthors12 found no significant difference between phacoemulsification and ECCE in visual acuity or retinopathy progression. We also found no significant differences between patients having ECCE through a 10.0 mm incision with implantation of a PMMA IOL and those having phacoemulsification through a 7.0 or 3.0 mm incision with foldable IOL implantation.
Diabetic nephropathy and retinopathy are microangiopathic processes. Thus, those who have diabetic nephropathy are more prone to breakdown of the blood-retinal barrier (BRB), which may facilitate the progression of diabetic retinopathy. In our study, eyes that had diabetic nephropathy had more progression of diabetic retinopathy. If inflammation and BRB breakdown are major factors, aggressive preoperative and postoperative therapy with antiinflammatory medications and more careful control of renal function may prevent the progression of diabetic retinopathy after cataract extraction in cases of diabetic nephropathy.7,13,14
In patients with preoperative diabetic retinopathy, a creatinine level greater than 1.40 mg/dL was a more significant factor in Group A than in Group B. This means that when a patient has preoperative diabetic retinopathy, the presence of diabetic nephropathy can affect the progression of the retinopathy. Therefore, we recommend more frequent follow-up and treatment after cataract surgery in patients with preoperative diabetic nephropathy.
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