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ABSTRACT PURPOSE To quantitatively examine changes in macular oedema after phacoemulsification surgery in eyes with diabetic retinopathy (DR) and in eyes without DR. METHODS Thirty-four eyes

with DR and 34 eyes with no DR scheduled for phacoemulsification surgery were recruited. Foveal thickness and macular volume were measured using optical coherence tomography preoperatively

and at 3, 6, and 12 months postoperatively. Grade of diabetic macular oedema was also examined. RESULTS Preoperatively, there were no significant differences between groups in foveal

thickness and macular volume. The foveal thickness increased by 20.3% in the DR group and by 6.0% in the no DR group at 3 months after surgery, but thereafter decreased gradually. When

comparing the groups, the foveal thickness and macular volume were significantly greater in the DR group than in the no DR group at 3 months postoperatively. The grade of macular oedema

worsened in eight eyes (23.5%) in the DR group, and in one (2.9%) in the no DR group: the incidence was significantly greater in the DR group ( _P_=0.0272). However, the oedema that occurred

after surgery resolved spontaneously in three (33.3%) of the nine eyes. CONCLUSIONS The degree of diabetic macular oedema increases up to 3 months after cataract surgery, but thereafter

decreases gradually. Grade of diabetic macular oedema also worsens up to 3 months, but certain percent of macular oedema that occurs after surgery resolves spontaneously. These changes are

more prominent in eyes with DR than in eyes with no DR. SIMILAR CONTENT BEING VIEWED BY OTHERS ALTERATIONS IN OPTICAL COHERENCE TOMOGRAPHY ANGIOGRAPHY PARAMETERS AFTER CATARACT SURGERY IN

PATIENTS WITH DIABETES Article Open access 11 October 2024 EARLY DMO: A PREDICTOR OF POOR OUTCOMES FOLLOWING CATARACT SURGERY IN DIABETIC PATIENTS. THE DICAT-II STUDY Article 03 August 2021

FOVEAL EVERSION PATTERNS IN DIABETIC MACULAR EDEMA Article Open access 30 July 2022 INTRODUCTION A number of studies have shown that visual outcome following cataract surgery in diabetic

patients depends primarily on the status of macular oedema.1, 2, 3, 4, 5, 6, 7 Previous reports have described many diabetic patients who developed severe maculopathy, retinopathy, and/or

neovascular glaucoma following cataract surgery.5, 8, 9, 10, 11, 12 Because it is important to be able to predict long-term visual effects before cataract surgery is performed, surgeons need

to have a better understanding of the natural course of diabetic macular oedema in addition to diabetic retinopathy (DR) after cataract surgery. It has been demonstrated that DR progresses

in approximately 10–30% of patients after cataract surgery,2, 6, 13, 14, 15, 16, 17 although some authors have hypothesized that the progression of DR after cataract surgery is due simply to

the natural course of the condition, and that the progression is independent of the surgery.18, 19, 20, 21 In these studies, the most significant predictor for progression of DR has been

the status of the DR at the time of the cataract surgery.13, 14, 15, 16, 22, 23 Similarly, diabetic macular oedema has been shown to worsen after cataract surgery,24, 25, 26 although

controversy remains as to the incidence of this worsening.7, 27 Some studies have shown that there are two types of worsening of macular oedema after surgery: transient pseudophakic oedema

that spontaneously resolves such as Irvine–Gass syndrome28, 29, 30 and actual progression of diabetic maculopathy. It has also been suggested that macular oedema tends to show actual

worsening in eyes afflicted with DR at the time of cataract surgery.14 Distinguishing transient oedema from substantial progression of maculopathy is important to the timing of treatment for

the macular oedema, including laser photocoagulation,31 vitrectomy,32, 33, 34 and triamcinolone injection.35, 36, 37 However, until recently, there had been no quantitative study to examine

the progression of diabetic macular oedema after cataract surgery. A recent study described by Kim _et al_38 showed a short-term increase of macular thickness after cataract surgery. The

purpose of the study described herein was to investigate changes in macular oedema after phacoemulsification surgery in eyes with DR and in eyes with no DR. To compare the degree of macular

oedema quantitatively, we measured periodically the foveal thickness and macular volume using optical coherence tomography. MATERIALS AND METHODS PATIENTS All patients with diabetes who were

scheduled for phacoemulsification surgery and intraocular lens (IOL) implantation between May 2004 and July 2005 were consecutively screened for inclusion in this study. In those patients

in whom both eyes underwent surgery, only the eye operated on first was included. Exclusion criteria were cataract due to causes other than age or diabetes, planned extracapsular cataract

extraction, a history of ocular inflammation or surgery, any pathology of the macula or optic nerve due to causes other than diabetes, any anticipated difficulties with the analysis, any

expected problems with follow-up because the patient resided in distant place or had been referred from another clinic, and patient' refusal to participate. Screening was continued

until 35 eyes with DR and 35 eyes with no DR were recruited for this study. At the time of cataract surgery, all patients underwent implantation of a hydrophobic acrylic IOL (MA60AC or

MA50BM; Alcon Laboratories, Fort Worth, TX, USA). The study protocol was approved by the Hospital's Institutional Review Board, and informed consent was obtained from each patient.

SURGICAL PROCEDURES All surgeries were performed by one surgeon (KH) using the same surgical procedures as described previously.39 Briefly, a 3.5-mm scleral incision was made; after

incision, a continuous curvilinear capsulorhexis measuring approximately 5.0 mm in diameter was accomplished using a bent needle. The intent was to make a round capsulorhexis of proper size

(slightly smaller than optic diameter) so that the capsulorhexis edge would circumferentially overlie the IOL optic. After hydrodissection, phacoemulsification of the nucleus and cortical

aspiration were performed. Using a keratome, the wound was enlarged to 4.1 mm for IOL implantation. The lens capsule was then inflated with sodium hyaluronate 1% (Healon; Advanced Medical

Optics, Santa Ana, CA, USA), after which the acrylic IOL was placed in the capsular bag. After insertion, the viscoelastic material was thoroughly evacuated. All surgeries included in the

analysis were uneventful and the IOLs were implanted accurately within the capsular bag. MAIN OUTCOME MEASURES The central retinal (foveal) thickness and macular volume of all patients were

measured by Stratus optical coherence tomography (OCT; Carl Zeiss Meditec, Dublin, CA, USA) a day before surgery, and at 3, 6, and 12 months after surgery. Best-corrected visual acuity and

grade of diabetic macular oedema were determined at each examination. Best-corrected visual acuity on decimal charts was converted to the logarithm of minimal angle of resolution (logMAR)

scale for statistical analysis. Systemic status of the diabetes mellitus, including percentage of haemoglobin A1C, duration of diabetes (years), and types of treatment at the time of

cataract surgery were also examined. During the OCT procedure, each eye underwent six radial scans centred on the fovea. Each radial scan line consisted of 100 samples of 5.92 mm in length,

yielding a total of 600 samples from the six radial scans. Macular volume was calculated as follows. A central macular thickness map measuring 3.45 mm in diameter was generated. The circular

map was subdivided into nine quadrants. The diameters of the middle and inner circles were 2.22 and 1.00 mm, respectively. Mean retinal thickness was calculated for each of the nine

quadrants from the previously obtained radial scans. Multiplying the mean retinal thickness by the area of the quadrant generated the volume for each of the nine quadrants, and the total

macular volume was thus determined as the sum of the volume of the nine quadrants. A fundus examination with full pupil dilation was performed before surgery and at each scheduled

examination, and eyes with DR underwent fluorescein angiography to determine the presence of proliferative changes before surgery and at 12 months after surgery. The macular oedema was

assigned one of the four following grades: 0=no macular oedema, 1=focal macular oedema, 2=diffuse macular oedema, and 3=cystoid macular oedema. Details of the macular oedema grade have been

described previously.26 In brief, focal macular oedema was defined as retinal thickening that occupied less than 1 disc area, while diffuse macular oedema was defined as retinal thickening

of 1 disc area or greater. The grade of macular oedema was determined by a single physician (KH), who was also the surgeon; other examinations were performed by ophthalmic technicians.

STATISTICAL ANALYSIS To compare data between the DR and no DR groups, the Mann–Whitney U test was used for foveal thickness, macular volume, logMAR visual acuity, and other continuous

variables. Discrete variables were compared using the Fisher exact probability test or the _χ_2 test for independence. Simple correlations between the foveal thickness and macular volume and

logMAR visual acuity, and between these and haemoglobin A1C, the duration of diabetes, or the types of treatment were evaluated using the Pearson correlation coefficient. Any differences

showing a _P_-value of <0.05 were considered statistically significant. RESULTS Of the 35 eyes originally enrolled, one in each group was lost to follow-up. One patient in the DR group

refused the examination, and one in the no DR group did not appear for examination because of a scheduling conflict. Therefore, 34 patients (97%) in each group completed the 1-year follow-up

and were included for analysis. Patient characteristics are shown in Table 1. The average age of the patients (±standard deviation [SD]) was 67.9±7.0 years, with a range of 51–81 years;

there were 39 men and 29 women. No statistically significant differences were found between the DR and no DR groups in age, the ratio of left to right eyes, or the presence of hypertension

and nephropathy; the duration of diabetes in the DR group, however, was significantly longer than that in the no DR group (_P_=0.0318), and the percentage of haemoglobin A1C in the DR group

was significantly greater than that in the no DR group (_P_<0.0001). Operative factors are shown in Table 2. No significant differences were found between the two groups in grade of the

nucleus, ultrasound time, ultrasound power emitted, or infusion volume. Twelve eyes in the DR group underwent photocoagulation for the peripheral retina, but no patients underwent retinal

photocoagulation for macular oedema. The mean (±SD) foveal thickness and macular volume in the DR and no DR groups are shown in Figure 1 and 2, respectively. The percentage increases in the

foveal thickness and increases in macular volume from baseline are provided in Table 3. There were no significant differences between the two groups in foveal thickness or in macular volume

before surgery. Foveal thickness increased by 20.3% in the DR group and by 6.0% in the no DR group at 3 months after surgery, and macular volume increased by 7.8% in the DR group and 3.0% in

the no DR group, but thereafter these changes decreased. When comparing groups at 3 months after surgery, the foveal thickness, macular volume, and the percent increases in the DR group

were significantly greater than those in the no DR group. The foveal thickness, macular volume, and percentage increases also tended to be greater in the DR group than in the no DR group at

6 and 12 months after surgery, but the difference did not reach statistical significance. Figure 3 shows the comparison of mean (±SD) logMAR visual acuity between the two groups. Mean visual

acuity in both groups improved significantly by 3 months after surgery (_P_<0.0001), and did not deteriorate postoperatively (_P_=0.9104 in the DR group and _P_=0.9687 in the no DR

group). Only two eyes (5.9%) in the DR group lost more than two decimal lines of visual acuity because of progression of maculopathy. When comparing the two groups, mean visual acuity in the

DR group was significantly worse than that in the no DR group at 3, 6, and 12 months after surgery, despite the fact that there had been no difference before surgery. In addition, logMAR

visual acuity was significantly correlated with both foveal thickness and macular volume at 3, 6, and 12 months after surgery. The grade of macular oedema is shown in Figure 4. The grade of

macular oedema worsened in eight eyes (23.5%) in the DR group but in only one (2.9%) in the no DR group; the incidence of progression in the DR group was significantly greater than that in

the no DR group (_P_=0.0272). However, in three of the nine eyes (33.3%) that had developed macular oedema postoperatively, the oedema resolved virtually by 12 months after surgery. Table 4

shows the simple correlation coefficients between haemoglobin A1C and the foveal thickness and macular volume. Significant association was found between the haemoglobin A1C at the time of

surgery and foveal thickness throughout the follow-up, whereas the associations between the haemoglobin A1C and macular volume did not reach statistical significance. Furthermore, no

significant correlation was found between duration of diabetes and foveal thickness or macular volume. In addition, there were no significant differences in the foveal thickness or macular

volume between the types of treatment, the presence of hypertension, or the presence of nephropathy. Figure 5 and 6 show the horizontal images and maps of the OCT as well as a fundus

photograph of a representative eye that shows transient macular oedema or progression of maculopathy after surgery, respectively. In the eye shown in Figure 5, in which no apparent macular

oedema was seen before surgery, marked cystoid macular oedema occurred at 3 months after surgery. However, this decreased gradually and only a slight oedema was observed at 12 months after

surgery. In the eye shown in Figure 6, diffuse macular oedema with dot and blot haemorrhages and hard exudates was present before surgery. Although the macular thickening gradually

decreased, there was accumulation of hard exudates in the macula, which resulted in severe macular deposition of the exudates at 12 months after surgery. DISCUSSION Our study have shown that

the foveal thickness and macular volume in diabetic patients increases after small incision cataract surgery in eyes both with and without DR: the percent increase from baseline was

greatest at 3 months after surgery, and then decreased gradually. Furthermore, the increase in foveal thickness and in macular volume was greater in eyes with DR than in eyes without DR.

These results indicate that, on average, diabetic macular oedema worsens after cataract surgery, and the worsening is more pronounced in eyes with DR. The grade of diabetic macular oedema

also progressed in 24% of the eyes with DR, but in only 3% of the eyes with no DR. However, three cases of nine (33.3%) of macular oedema that occurred after surgery in eyes with DR had

resolved spontaneously by 12 months. These results suggest that the change in macular oedema in some diabetic patients is transient, while in other diabetics, the macular oedema is

substantial, with marked progression of maculopathy. Mean visual acuity improved significantly after cataract surgery in eyes both with and without DR, and did not worsen in the

postoperative period. Only two eyes ultimately lost more than 2 decimal lines of vision because of marked progression of maculopathy. This indicates that worsening of the macular oedema

after small incision cataract surgery decreases visual acuity only in some cases. Among the parameters studied that reflected the systemic status of diabetes, the haemoglobin A1C level at

the time of surgery in eyes with DR was significantly greater than that in eyes without DR, and was correlated significantly with the foveal thickness. In contrast, duration of diabetes,

types of treatment, and the presence of hypertension or nephropathy were not related to the degree of macular oedema. Although previous studies did not find a significant correlation between

haemoglobin A1C and progression of macular oedema,26, 27 our quantitative study suggests that the percentage of haemoglobin A1C present at the time of surgery may be a significant predictor

for progression of macular oedema. Previous studies showed that diabetic macular oedema progressed in approximately 20–40% of eyes that underwent cataract surgery, but, in a considerable

percentage of these eyes, the macular oedema resolved spontaneously.24, 25, 26, 27 Accordingly, these studies suggested that progression of diabetic macular oedema may be classified as

follows: a transient pseudophakic macular oedema such as Irvine–Gass syndrome, or substantial progression of diabetic maculopathy.24, 25, 27 Our study quantitatively confirmed these two

types of macular oedema. That is, macular thickening generally occurs after cataract surgery, but this resolves with time in most diabetic patients. In some diabetic patients, however,

diabetic maculopathy actually progresses. Both types of macular change are more prominent in eyes with DR than in eyes with no DR. In addition, Funatsu _et al_26 reported the amount of

vascular endothelial growth factor in the aqueous humour to be a significant predictor for progression of macular oedema. Our study showed that haemoglobin A1C is associated with an

increased risk for progression of diabetic macular oedema. Our study showed that macular thickening occurs in most diabetic eyes after cataract surgery, some of which develop clinically

detectable oedema including cystoid macular oedema. Macular thickening after cataract surgery is greater, however, in eyes of diabetics, specifically in eyes with DR, than that in

nondiabetic eyes (unpublished data). This may be explained biologically as follows. It is thought that pseudophakic cystoid macular oedema is caused by cytokines including prostaglandin or

vascular endothelial growth factor, which are released from blood–ocular barrier after cataract extraction. Breakdown of the blood–ocular barrier in diabetic eyes, particularly in eyes with

DR, is known to be greater than that in nondiabetic eyes.40, 41, 42 Indeed, the mean intensity of flare in the DR group was significantly greater than that in the no DR group throughout the

follow-up (unpublished data). Accordingly, macular thickening may be more pronounced in eyes with DR. We acknowledge some limitations to this study. First, the number of eyes with active DR

was small. However, surgeons currently tend to perform retinal photocoagulation when retinopathy is in the early stages. Accordingly, distribution of the stage of DR in this study may

actually reflect more closely the clinical situation. Secondly, the grade of macular oedema and the stage of DR evaluated in this study were relatively simple. However, the goal of the

present study was to quantify the degree of macular oedema, so minute grading of macular oedema was not the primary end point. In conclusion, we have demonstrated that the degree of diabetic

macular oedema generally worsens after cataract surgery, and that the worsening of macular oedema is more prominent in eyes with DR than in eyes without DR at the time of surgery. However,

macular oedema that occurs after cataract surgery resolves spontaneously in some patients for up to a year. Furthermore, percentage of haemoglobin A1C present at the time of surgery may be

predictor for progression of macular oedema. Using a larger sample size, further study is warranted to examine the changes in macular oedema that occur in eyes with active retinopathy.

REFERENCES * Dowler JGF, Hykin PG, Lightman SL, Hamilton AM . Visual acuity following extracapsular cataract extraction in diabetes: a meta-analysis. _Eye_ 1995; 9: 313–317. Article  Google

Scholar  * Zaczek A, Olivestedt G, Zetterstrom C . Visual outcome after phacoemulsification and IOL implantation in diabetic patients. _Br J Ophthalmol_ 1999; 83: 1036–1041. Article  CAS 

Google Scholar  * Cunliffe IA, Flanagan DW, George NDL, Aggarwaal RJ, Moore AT . Extracapsular cataract surgery with lens implantation in diabetics with and without proliferative

retinopathy. _Br J Ophthalmol_ 1991; 75: 9–12. Article  CAS  Google Scholar  * Hykin PG, Gregson RMC, Stevens JD, Hamilton PAM . Extracapsular cataract extraction in proliferative diabetic

retinopathy. _Ophthalmology_ 1993; 100: 394–399. Article  CAS  Google Scholar  * Benson WE, Brown GC, Tasman W, McNamara JA, Vander JF . Extracapsular cataract extraction with placement of a

posterior chamber lens in patients with diabetic retinopathy. _Ophthalmology_ 1993; 100: 730–738. Article  CAS  Google Scholar  * Antcliff RJ, Poulson A, Flanagan DW . Phacoemulsification

in diabetics. _Eye_ 1996; 10: 737–741. Article  Google Scholar  * Early Treatment Diabetic Retinopathy Study Research Group. Results after lens extraction in patients with diabetic

retinopathy: Early Treatment Diabetic Retinopathy Study report number 25. _Arch Ophthalmol_ 1999; 117: 1600–1606. Article  Google Scholar  * Poliner LS, Christianson DJ, Escoffery RF, Kolker

AE, Gordon ME . Neovascular glaucoma after intracapsular and extracapsular cataract extraction in diabetic patients. _Am J Ophthalmol_ 1985; 100: 637–643. Article  CAS  Google Scholar  *

Pavese T, Insler MS . Effects of extracapsular cataract extraction with posterior chamber lens implantation on the development of neovascular glaucoma in diabetics. _J Cataract Refract Surg_

1987; 13: 197–201. Article  CAS  Google Scholar  * Jaffe GJ, Burton TC . Progression of nonproliferative diabetic retinopathy following cataract extraction. _Arch Ophthalmol_ 1988; 106:

745–749. Article  CAS  Google Scholar  * Jaffe GJ, Burton TC, Kuhn E, Prescott A, Hartz A . Progression of nonproliferative diabetic retinopathy and visual outcome after extracapsular

cataract extraction and intraocular lens implantation. _Am J Ophthalmol_ 1992; 114: 448–456. Article  CAS  Google Scholar  * Schatz H, Atienza D, McDonald HR, Johnson RN . Severe diabetic

retinopathy after cataract surgery. _Am J Ophthalmol_ 1994; 117: 314–321. Article  CAS  Google Scholar  * Pollack A, Dotan S, Oliver M . Progression of diabetic retinopathy after cataract

extraction. _Br J Ophthalmol_ 1991; 75: 547–551. Article  CAS  Google Scholar  * Henricsson M, Heijl A, Janzon L . Diabetic retinopathy before and after cataract surgery. _Br J Ophthalmol_

1996; 80: 789–793. Article  CAS  Google Scholar  * Kato S, Fukada Y, Hori S, Tanaka Y, Oshika T . Influence of phacoemulsification and intraocular lens implantation on the course of diabetic

retinopathy. _J Cataract Refract Surg_ 1999; 25: 788–793. Article  CAS  Google Scholar  * Mittra RA, Borrillo JL, Dev S, Mieler WF, Koenig SB . Retinopathy progression and visual outcomes

after phacoemulsification in patients with diabetes mellitus. _Arch Ophthalmol_ 2000; 118: 912–917. CAS  PubMed  Google Scholar  * Chung J, Kim MY, Kim HS, Yoo JS, Lee YC . Effect of

cataract surgery on the progression of diabetic retinopathy. _J Cataract Refract Surg_ 2002; 25: 626–630. Article  Google Scholar  * Tsujikawa A, Otani A, Takanashi T, Ogura Y . Long-term

prognosis of extracapsular cataract extraction and intraocular lens implantation in diabetic patients. _Jpn J Ophthalmol_ 1997; 41: 319–323. Article  CAS  Google Scholar  * Krepler K,

Biowski R, Schrey S, Jandrasits K, Wedrich A . Cataract surgery in patients with diabetic retinopathy: visual outcome, progression of diabetic retinopathy, and incidence of diabetic macular

edema. _Graefes Arch Clin Exp Ophthalmol_ 2002; 240: 735–738. Article  Google Scholar  * Schrey S, Krepler K, Biowski R, Wedrich A . Midterm visual outcome and progression of diabetic

retinopathy following cataract surgery. Midterm outcome of cataract surgery in diabetes. _Ophthalmologica_ 2002; 216: 337–340. Article  CAS  Google Scholar  * Romero-Aroca P,

Fernandez-Ballart J, Almena-Garcia M, Mendez-Marin I, Salvat-Serra M, Buil-Calvo JA . Nonproliferative diabetic retinopathy and macular edema progression after phacoemulsification:

prospective surgery. _J Cataract Refract Surg_ 2006; 321: 1438–1444. Article  Google Scholar  * Pollack A, Leiba H, Bukelman A, Abrahami S, Oliver M . The course of diabetic retinopathy

following cataract surgery in eyes previously treated by laser photocoaguration. _Br J Ophthalmol_ 1992; 76: 228–231. Article  CAS  Google Scholar  * Somaiya MD, Burns JD, Mintz R, Warren

RE, Uchida T, Godley BF . Factors affecting visual outcomes after small-incision phacoemulsification in diabetic patients. _J Cataract Refract Surg_ 2002; 28: 1364–1371. Article  Google

Scholar  * Dowler JGF, Sehmi KS, Hykin PG, Hamilton AMP . The natural history of macular edema cataract surgery in diabetes. _Ophthalmology_ 1999; 106: 663–668. Article  CAS  Google Scholar

  * Dowler JGF, Hykin PG, Hamilton AMP . Phacoemulsification versus extracapsular cataract extraction in patients with diabetes. _Ophthalmology_ 2000; 107: 457–462. Article  CAS  Google

Scholar  * Funatsu H, Yamashita H, Noma H, Shimizu E, Mimura T, Hori S . Prediction of macular edema exacerbation after phacoemulsification in patients with nonproliferative diabetic

retinopathy. _J Cataract Refract Surg_ 2002; 28: 1355–1363. Article  Google Scholar  * Squirrell D, Bhola R, Bush J, Winder S, Talbot JF . A prospective, case controlled study of the natural

history of diabetic retinopathy and maculopathy after uncomplicated phacoemulsification cataract surgery in patients with type 2 diabetes. _Br J Ophthalmol_ 2002; 86: 565–571. Article  CAS

  Google Scholar  * Gass JDM, Norton EWD . Cystoid macular edema and papilledema following cataract extraction. A fluorescein fundoscopic and angiographic study. _Arch Ophthalmol_ 1966; 76:

646–661. Article  CAS  Google Scholar  * Tolentino FI, Schepens CL . Edema of posterior pole after cataract extraction. A biomicroscopic study. _Arch Ophthalmol_ 1965; 74: 781–786. Article 

CAS  Google Scholar  * Schepens CL, Avila MP, Jalkh AE, Trempe CL . Role of the vitreous in cystoid macular edema. _Surv Ophthalmol_ 1984; 28(Suppl): 499–504. Article  Google Scholar  *

Early Treatment Diabetic Retinopathy Study Research Group. Photocoagulation for diabetic macular edema: Early Treatment Diabetic Retinopathy Study report number 1. _Arch Ophthalmol_ 1985;

103: 1796–1806. Article  Google Scholar  * Lewis H, Abrams GW, Blumenkranz MS, Campo RV . Vitrectomy for diabetic macular traction and edema associated with posterior hyaloidal traction.

_Ophthalmology_ 1992; 99: 753–759. Article  CAS  Google Scholar  * Harbour JW, Smiddy WE, Flynn Jr HW, Rubsamen PE . Vitrectomy for diabetic macular edema associated with a thickened and

taut posterior hyaloid membrane. _Am J Ophthalmol_ 1996; 121: 405–413. Article  CAS  Google Scholar  * Tachi N, Ogino N . Vitrectomy for diffuse macular edema in cases of diabetic

retinopathy. _Am J Ophthalmol_ 1996; 122: 258–260. Article  CAS  Google Scholar  * Jonas JB, Sofker A . Intraocular injection of crystalline cortisone as adjunctive treatment of diabetic

macular edema. _Am J Ophthalmol_ 2001; 132: 425–427. Article  CAS  Google Scholar  * Martidis A, Duker JS, Greenberg PB, Rogers AH, Puliafito CA, Reichel E _et al_. Intravitreal

triamcinolone for refractory diabetic macular edema. _Ophthalmology_ 2002; 109: 920–927. Article  Google Scholar  * Jonas JB, Kreissig I, Sofker A, Degenring RF . Intravitreal injection of

triamcinolone for diffuse diabetic macular edema. _Arch Ophthalmol_ 2003; 121: 57–61. Article  CAS  Google Scholar  * Kim SJ, Equi R, Bressler NM . Analysis of macular edema after cataract

surgery in patients with diabetes using optical coherence tomography. _Ophthalmology_ 2007; 114: 881–889. Article  Google Scholar  * Hayashi K, Hayashi H, Nakao F, Hayashi F . Posterior

capsule opacification after cataract surgery in patients with diabetes mellitus. _Am J Ophthalmol_ 2002; 134: 10–16. Article  Google Scholar  * Zaczek A, Zetterstrom C . Aqueous flare

intensity after phacoemulsification in patients with diabetes mellitus. _J Cataract Refract Surg_ 1998; 24: 1099–1104. Article  CAS  Google Scholar  * Oshika T, Kato S, Funatsu H .

Quantitative assessment of aqueous flare intensity in diabetes. _Graefes Arch Clin Exp Ophthalmol_ 1989; 227: 518–520. Article  CAS  Google Scholar  * Moriarty AP, Spalton DJ, Moriarty BJ,

Shilling JS, Ffytche TJ, Bulsara M . Studies of the blood-aqueous barrier in diabetes mellitus. _Am J Ophthalmol_ 1994; 117: 768–771. Article  CAS  Google Scholar  Download references AUTHOR

INFORMATION AUTHORS AND AFFILIATIONS * Hayashi Eye Hospital, Fukuoka, Japan K Hayashi & C Igarashi * Department of Ophthalmology, Saga University Faculty of Medicine, Saga, Japan A

Hirata * Department of Ophthalmology, School of Medicine, Fukuoka University, Fukuoka, Japan H Hayashi Authors * K Hayashi View author publications You can also search for this author

inPubMed Google Scholar * C Igarashi View author publications You can also search for this author inPubMed Google Scholar * A Hirata View author publications You can also search for this

author inPubMed Google Scholar * H Hayashi View author publications You can also search for this author inPubMed Google Scholar CORRESPONDING AUTHOR Correspondence to K Hayashi. ADDITIONAL

INFORMATION The authors have no proprietary interest in any of the materials described in this article and received no financial support. RIGHTS AND PERMISSIONS Reprints and permissions

ABOUT THIS ARTICLE CITE THIS ARTICLE Hayashi, K., Igarashi, C., Hirata, A. _et al._ Changes in diabetic macular oedema after phacoemulsification surgery. _Eye_ 23, 389–396 (2009).

https://doi.org/10.1038/sj.eye.6703022 Download citation * Received: 27 June 2007 * Accepted: 02 October 2007 * Published: 26 October 2007 * Issue Date: February 2009 * DOI:

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currently available for this article. Copy to clipboard Provided by the Springer Nature SharedIt content-sharing initiative KEYWORDS * diabetic macular oedema * phacoemulsification surgery *

optical coherence tomography