|Year : 2018 | Volume
| Issue : 2 | Page : 99-105
NSAIDs eye drops versus steroidal eye drops after phacoemulsification cataract surgery
Safaa A.M Aboud
Department of Ophthalmology, Beni Suef University, Beni Suef, Egypt
|Date of Submission||19-Jan-2017|
|Date of Acceptance||30-Nov-2017|
|Date of Web Publication||7-Jun-2018|
Safaa A.M Aboud
23 Namek Street, Moold El-Naby Square, Beni Suef 62511
Source of Support: None, Conflict of Interest: None
Purpose The aim of this study was to evaluate the efficacy NSAID eye drops in comparison with topical steroids following phacoemulsification cataract surgery.
Patients and methods This prospective study included 120 patients with senile cataract who were subjected to phacoemulsification cataract extraction with foldable posterior chamber intraocular lens implantation. Postoperatively, patients were assigned to two groups: NSAIDs group and steroids group. All patients were subjected to preoperative and postoperative investigations including autorefractometer, slit-lamp examination, indirect ophthalmoscopy, tonometry, and Nassar color plates. Optical coherence tomography was performed for all patients in the last visit.
Results No statistically significant differences were found between both groups in visual acuity (0.20±0.15 in the NSAIDs group and 0.20±0.13 in the steroidal group), corneal edema, or anterior chamber reaction (P>0.05). The mean macular thickness for the steroidal patient group was significantly higher than their counterparts in the NSAIDs group (P<0.05). However, both medications proved their efficacy in preventing complications throughout the study. Intraocular pressure showed spikes in the steroidal group patients from the third week till the end of the study.
Conclusion Both topical NSAIDs and steroids have the same efficacy in preventing inflammation and corneal edema. However, patients subjected to topical steroids were more likely to develop intraocular hypertension and cystoid macular edema.
Keywords: cataract, corneal edema, cystoid macular edema, inflammation, NSAIDs
|How to cite this article:|
Aboud SA. NSAIDs eye drops versus steroidal eye drops after phacoemulsification cataract surgery. Delta J Ophthalmol 2018;19:99-105
|How to cite this URL:|
Aboud SA. NSAIDs eye drops versus steroidal eye drops after phacoemulsification cataract surgery. Delta J Ophthalmol [serial online] 2018 [cited 2018 Jun 22];19:99-105. Available from: http://www.djo.eg.net/text.asp?2018/19/2/99/233928
| Introduction|| |
Cataract surgery is one of the most frequently performed elective surgical procedures in developed countries. The surgical methods have improved significantly over the years, thus decreasing the risk of complications and increasing patients’ and surgeons’ expectations of a successful visual outcome ,,.
Like other types of surgery, cataract surgery induces a surgical inflammatory response. Postoperative ocular inflammation after cataract surgery can be associated with complications, including corneal edema, spikes in intraocular pressure (IOP), cystoid macular edema (CME), and posterior capsule opacification. Uncontrolled inflammation may lead to serious side effects, such as posterior synechiae, uveitis, and secondary glaucoma. Management of inflammation is thus a mainstay in modern cataract surgery ,.
Currently, two drug groups are available to control ocular inflammation: steroids and NSAIDs. Steroids are potent anti-inflammatory agents that work by acting on a number of intercellular inflammatory mediators, whereas NSAIDs work by inhibiting the cyclooxygenase enzymes. The cyclooxygenase enzymes catalyze the release of prostaglandins and thromboxanes. Prostaglandins mediate inflammatory reactions. Preventing the formation of prostaglandins reduces the inflammatory process ,,,,,.
CME occurs because of fluid accumulation occurring a few weeks to months after cataract surgery. It is the most common cause of visual decline after cataract surgery. The prevalence of CME varies from study to study depending on how CME is defined. By using fluorescein angiography, a prevalence of CME of up to 20% has been reported ,, whereas only 2% were diagnosed with CME when loss of visual acuity was required to establish the diagnosis ,.
Usually, CME is subclinical and self-limiting, but in a few patients, it may become chronic, resulting in a permanent visual loss. The cause of CME is believed to be an increased vascular permeability induced by inflammatory mediators such as prostaglandins. There is a tendency toward a higher prevalence of CME in patients with increased postoperative inflammation .
The relationship between inflammation and CME is further supported by the three-fold increase in the risk of CME in patients with a history of uveitis . In addition, macular thickness is greater in patients with complicated cataract surgery compared with uncomplicated cataract surgery . Increased surgical trauma such as iatrogenic iris lesion increases the risk of CME .
Although topical ocular corticosteroids are a vital component of the treatment of postoperative inflammation, their prolonged use can produce side effects, such as elevated IOP, cataract formation (in phakic individuals), and lowered resistance to infection ,. Research has shown that elevated IOP, if left untreated, may lead to progressive optic nerve damage and glaucomatous visual field defects, ultimately culminating in corticosteroid-induced glaucoma .
Deciding which anti-inflammatory agent to use as the standard in patients undergoing cataract surgery is important to ensure a favorable outcome.
This study compares the efficacy of topical steroids with that of topical NSAIDs in reducing postoperative inflammation and preventing CME keeping in mind the possible drawbacks on IOP.
| Patients and methods|| |
In this prospective study, 120 patients with senile cataract (nuclear sclerosis grade 2–3 and immature senile cataract) attending the outpatient clinic of Beni Suef University Hospital were recruited. All patients were subjected to phacoemulsification cataract extraction with posterior chamber intraocular lens (IOL) implantation.
Patients were assigned to the following groups:
This group included 60 patients who received postoperative NSAIDs eye drops, Nevanac (nepafenac ophthalmic suspension 0.1%; Alcon Laboratories Inc., Fort Worth, Texas, USA).
This group included 60 patients who received postoperative steroid eye drops, Econopred plus (prednisolone acetate ophthalmic suspension 1%; Alcon Laboratories).
Patients who had undergone uncomplicated phacoemulsification cataract extraction surgery with foldable posterior chamber IOL implantation were included in the study. Patients with intraoperative complications, local complications associated with cataract, for example, anterior uveitis, and angle closure glaucoma as well as patients with uncontrolled systemic disease such as diabetes were excluded from the study.
All patients were subjected to the following: a preoperative examination including assessment of history, a full ophthalmic examination including uncorrected visual acuity (UCVA) and best-corrected visual acuity (BCVA) using Landolt’s broken ring chart and expressed as logMAR, slit-lamp examination, IOP measurement, and fundus examination using the indirect ophthalmoscope. Ultrasonography was performed in eyes with dense cataract, which impair visualization of the fundus. Biometry was performed to calculate IOL power. Nassar color plates  were used to test for color blindness and for early detection of macular edema.
Postoperative examination included UCVA, BCVA, and IOP measurement by applanation tonometry, fundus examination by indirect ophthalmoscopy, and slit-lamp examination to detect postoperative inflammation in the form of corneal edema and anterior chamber reaction in the form of flare and cells.
Follow-up of patients was performed on the first day, first, second, third, fourth, and sixth weeks postoperatively, with a full ophthalmic examination at each visit. Nassar color plates for color blindness and early detection of macular edema were performed. Optical coherence tomography (OCT) macula using Optvue OCT (OptoVue Inc., Fremont, California, USA) was performed at the last visit at the sixth week.
- Cells in the anterior chamber (slit-lamp examination, using a 1 mm slit beam):
- Grade 0: None.
- Grade 0.50: 1–5 cells.
- Grade 1: 5–15 cells.
- Grade 2: 15–25 cells.
- Grade 3: 25–50 cells.
- Grade 4: >50 cells.
- Flare in the anterior chamber (slit-lamp examination, using a 1 mm slit beam):
- Grade 0: None.
- Grade 1: Faint.
- Grade 2: Moderate (iris/lens details clear).
- Grade 3: Marked (iris/lens details hazy).
- Grade 4: Intense (fibrin/plastic aqueous).
- -Corneal edema (slit-lamp examination):
- Grade 0: No stromal or epithelial edema.
- Grade 1: Slight stromal edema.
- Grade 2: Diffuse stromal edema.
- Grade 3: Diffuse stromal edema with microcystic edema of the epithelium.
- Grade 4: Bullous keratopathy.
Postoperatively, all patients received antibiotic eye drops: one drop five times/day for 1 month and hypertonic eye solution four times/day for 1 month.
The NSAIDs group received NSAID eye drops (Nepafenac 0.1%).
- Week 1: Five times/day.
- Week 2: Three times/day.
- Week 3: Two times/day.
- Week 4: Once daily.
The steroids group received steroid eye drops (Prednisolone acetate 1%).
- Week 1: Five times/day.
- Week 2: Three times/day.
- Week 3: Two times/day.
- Week 4: Once daily.
The study was approved by the Ethical Committee of the Faculty of Medicine, Beni Suef University. The questionnaire included explanations about the purpose of the study and its consequences, and confidentiality of data was assured. Informed consent was obtained from each patient.
Data were analyzed using the software statistical package for social science (version 20; SPSS Inc., Chicago, Illinois, USA). Frequency distribution with its percentage and descriptive statistics with mean and SD were calculated. χ2-Test, t-test, and correlations were performed whenever needed. P values less than 0.05 were considered significant.
| Results|| |
Of the 60 participants in the NSAIDs group, 34 (56.7%) were men and 26 (43.3%) were women, with a mean age of 60.93±4.03 years, compared with 30 (50%) men and 30 (50%) women in the steroids group, and a mean age of 62.83±4.10 years (P>0.05). In the NSAIDs group, 16 (26.7%) patients reported having a medical history of controlled hypertension and eight (13.3%) patients were found to have controlled diabetes compared with only 10 (16.7%) patients with hypertension and four (6.7%) patients with diabetes in the steroidal group. However, no statistically significant differences were found between both groups (P>0.05, [Table 1]).
Although both BCVA and UCVA improved significantly throughout the 6 weeks following the surgery, these increases were almost the same in both the NSAIDs group and the steroidal group. At week 1, BCVA of NSAIDs was 0.91±0.18 compared with 0.89±0.17 in the steroids group (P>0.05) and UCVA was 1.07±0.13 compared with 1.06±0.13 in the steroids group (P>0.05). BCVA figures increased significantly in the third week to reach 0.62±0.18 and 0.66±0.14 in the NSAIDs and the steroid groups, respectively, and UCVA showed a similar increase to 0.83±0.14 and 0.83±0.11 in the NSAIDs and the steroid groups, respectively, with no significant differences noted between both groups whether in BCVA or in UCVA (P>0.05). Three weeks later, BCVA continued to increase, to reach 0.20±0.15 in the NSAIDs group and 0.20±0.13 in the steroidal group, with UCVA following the same trend, achieving a rise of 0.51±0.17 in NSAIDs group and 0.51±0.11 in the steroidal group. Again, no statistically significant differences were found between both groups (P>0.05, [Table 2]).
|Table 2 Comparison between both groups regarding BCVA and UCVA within 6 weeks|
Click here to view
IOP did not show any differences between both groups during the first 2 weeks. However, a sudden refractory increase in IOP of the steroidal group was found from the third week. At week 1, IOP of the NSAIDs group was 17.37±2.91 mmHg compared with 17.17±2.74 mmHg in the steroidal group (P>0.05). At week 3, IOP of NSAIDs decreased to 16.20±2.82 mmHg, whereas IOP of the steroidal group increased to 19.27±3.22 mmHg, resulting in a statistically significant difference between both groups (P<0.05). This difference remained during the following 2 weeks (P<0.05, [Table 3]).
|Table 3 Comparison between both groups in intraocular pressure within 6 weeks|
Click here to view
For the corneal edema, 12 (20%) patients of the NSAIDs group had grade 2–3 edema at day 1 compared with 14 (23.3%) patients of the steroidal group, with no statistically significant difference between both groups (P>0.05). However, grade 2 and 3 edema declined significantly in both groups, with only two cases in the steroidal group at week 1, whereas no cases were reported in both groups at week 2 ([Table 4]).
Furthermore, the anterior chamber reaction, flare and or cells (grade 2 or 3), declined significantly in both groups from eight(13.3%) patients and 10 (16.7%) patients at day 1 in the NSAIDs and steroidal groups, respectively, to only two patients in each group by week 2, with no significant differences between both groups (P>0.05, [Table 5]).
|Table 5 Comparison between both groups in anterior chamber flare within 2 weeks|
Click here to view
This study showed that patients who were subjected to steroidal medications had a normal Nassar test in 73.3%, whereas 15 and 11.7% showed mild and moderate changes, respectively. In the NSAIDs group, 93.4% of the patients were normal and 3.3% had mild and moderate changes, with significant differences between both groups (P=0.013). In addition, these patients had significantly higher rates of macular edema as assessed by OCT (P=0.006). Besides, the mean value of macular thickness for the steroidal patients group was significantly higher than their counterparts in the NSAID group (P=0.001, [Table 6]).
|Table 6 Comparison between both groups in the Nassar color test and optical coherence tomography at sixth week postoperatively|
Click here to view
| Discussion|| |
Surgical trauma to the eye initiates an inflammatory reaction. This reaction includes the release of prostaglandins and the recruitment of neutrophils and macrophages to the site of trauma . Many postoperative complications following the ocular inflammation have been reported, including corneal edema, increases in IOP, and CME ,.
In this study, which included 120 participants assigned to NSAIDs and steroidal groups, UCVA and BCVA improved significantly throughout the duration of follow-up; however, there was no statistically significant difference between both groups in UCVA or BCVA. In consistence with these findings, Asano et al.  did not find any difference between both groups in visual acuity. In contrast, Endo et al.  preferred NSAIDs for visual acuity. Later, Kessel et al.  carried out a meta-analysis on four studies that reported the visual acuity at the longest follow-up (6–8 weeks) after cataract surgery, and concluded that NSAIDs groups achieved better BCVA.
This study also showed spikes in IOP in the steroidal group from week 3 till the end of the follow-up, with statistically significant differences from the NSAIDs group. The mechanism by which topical corticosteroids increase IOP is not fully understood. The glucocorticoid receptor is involved in multiple, diverse signaling pathways, and it is believed that steroid-induced IOP elevation, particularly that observed with long-term use or high doses of corticosteroids, is the result of upregulation or repression of one or more genes unrelated to the indication being treated . Most studies implicate trabecular meshwork (TM) cells and myocilin gene expression in the mechanism of corticosteroid-induced IOP elevation. Corticosteroids appear to decrease the outflow of aqueous humor by inhibiting the degradation and/or enhancing the deposition of extracellular matrix material within the TM and/or cross-linking of actin fibers between TM cells . The TM accounts for the majority of drainage from the eye; it appears that this resistance to aqueous outflow (caused by changes to the TM and its extracellular matrix) eventually leads to an increase in IOP. Indeed, early ultrastructural studies showed an increase in the extracellular ground substance of the corneoscleral trabeculum in steroid-induced glaucoma . Clark and Wordinger  suggested that structural changes in the TM, in turn, result in corticosteroid-induced ocular hypertension, which can progress to secondary iatrogenic open-angle glaucoma.
This study also found that corneal edema decreased significantly throughout the period of follow-up in both groups, but no statistically significant differences between the groups were observed. Similarly, Hozler et al.  reported the efficacy of both types of topical medications in the prevention of edema; however, they concluded that the efficacy was similar in both groups. Besides, Maca et al.  reached the same conclusion; however, they found that topical NSAIDs were more tolerable. In contrast, Asano et al.  found less inflammation and edema with the use of NSAIDs. Kessel et al.  identified six randomized clinical trials that compared the prevalence of CME after the use of topical steroid or NSAIDs. All the studies included in this meta-analysis had a study design in which patients with a history of uveitis, diabetes, or diabetic retinopathy were excluded from participation. In the steroids group, 25.3% of patients had CME at 1 month compared with 3.8% in the NSAIDs group.
This study also showed that both drugs were effective in preventing anterior chamber flare, with no preference of any of them. In agreement with this, Hozler et al. , Asano et al. , and Maca et al.  reached the same conclusion. However, in the meta-analysis of Kessel et al. , the authors concluded that topical NSAIDs were more effective than steroid eye drops in reducing postoperative inflammation measured as the amount of flare by laser flare photometry at 1 week postoperatively. However, steroids with medium to high potency (betamethasone, dexamethasone, loteprednol, and prednisolone) were not significantly different from NSAIDs in controlling inflammation, whereas steroids with low potency (fluorometholone) were significantly less effective in controlling inflammation .
| Conclusion|| |
Both topical NSAIDs and steroids have the same efficacy in preventing inflammation and corneal edema. However, patients who received topical steroids were more likely to develop intraocular hypertension and CME.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Gulkilik G, Kocabora S, Taskapili M, Engin G. Cystoid macular edema after phacoemulsification: risk factors and effect on visual acuity. Can J Ophthalmol 2006; 41:699–703.
Saif MYS, Abdel Khalek MO, Saif ATS, Saif PS, Safina SK. Predictability and accuracy of IOL formulas in high myopia. J Emmetropia 2016; 1:17–21.
Saif MYS, Saif ATS, Saif PS, Abdel Khalek MO, Mahran W. Dry eye changes after phacoemulsification and manual small incision cataract surgery (MSICS). Int J Ophthalmol Eye Res 2016; 4:184–191.
Ursell PG, Spalton DJ, Whitcup SM, Nussenblatt RB. Cystoid macular edema after phacoemulsification: relationship to blood-aqueous barrier damage and visual acuity. J Cataract Refract Surg 1999; 25:1492–1497.
Henderson BA, Kim JY, Ament CS, Ferrufino-Ponce ZK, Grabowska A, Cremers SL. Clinical pseudophakic cystoid macular edema. Risk factors for development and duration after treatment. J Cataract Refract Surg 2007; 33:1550–1558.
Yeh PC, Ramanathan S. Latanoprost and clinically significant cystoid macular edema after uneventful phacoemulsification with intraocular lens implantation. J Cataract Refract Surg 2002; 28:1814–1818.
Arcieri ES, Santana A, Rocha FN, Guapo GL, Costa VP. Blood-aqueous barrier changes after the use of prostaglandin analogues in patients with pseudophakia and aphakia: a 6-month randomized trial. Arch Ophthalmol 2005; 123:186–192.
Bélair ML, Kim SJ, Thorne JE, Dunn JP, Kedhar SR, Brown DM, Jabs DA. Incidence of cystoid macular edema after cataract surgery in patients with and without uveitis using optical coherence tomography. Am J Ophthalmol 2009; 148:128–135.
Akçay BİS, Bozkurt TK, Güney E, Ünlü C, Erdogan G, Akcali G, Bayramlar H. Quantitative analysis of macular thickness following uneventful and complicated cataract surgery. Clin Ophthalmol 2012; 6:1507–1511.
Clark AF, Wilson K, de Kater AW, Allingham RR, McCartney MD. Dexamethasone-induced ocular hypertension in perfusion-cultured human eyes. Invest Ophthalmol Vis Sci 1995; 36:478–489.
El-Harazi SM, Feldman RM. Control of intra-ocular inflammation associated with cataract surgery. Curr Opin Ophthalmol 2001; 12:4–8.
Spaeth GL, Monteiro de Barros DS, Fudemberg SJ. Visual loss caused by corticosteroid-induced glaucoma: how to avoid it. Retina 2009; 29:1057–1061.
Nassar MK, Saif MY, Saif AT, Saif PS. Sensitivity and specificity of Nassar color test in early detection of diabetic macular edema. Al-Basar Int J Ophthalmol 2015; 3:39–43.
Asano S, Miyake K, Ota I, Sugita G, Kimura W, Sakka Y, Yabe N. Reducing angiographic cystoid macular edema and blood-aqueous barrier disruption after small-incision phacoemulsification and foldable intraocular lens implantation: multicenter prospective randomized comparison of topical diclofenac 0.1% and betamethasone 0.1%. J Cataract Refract Surg 2008; 34:57–63.
Endo N, Kato S, Haruyama K, Shoji M, Kitano S. Efficacy of bromfenac sodium ophthalmic solution in preventing cystoid macular oedema after cataract surgery in patients with diabetes. Acta Ophthalmol 2010; 88:896–900.
Kessel L, Tendal B, Jorgensen KJ, Erngaard D, Flesner P, Andresen JL, Hjortdal J. Post-cataract prevention of inflammation and macular edema by steroid and nonsteroidal anti-inflammatory eye drops. Am J Ophthalmol 2014; 121:1915–1924.
Tripathi RC, Parapuram SK, Tripathi BJ, Zhong Y, Chalam KV. Corticosteroids and glaucoma risk. Drugs Aging 1999; 15:439–450.
Kersey JP, Broadway DC. Corticosteroid-induced glaucoma: a review of the literature. Eye 2005; 20:407–416.
Francois J, Benozzi G, Victoria-Troncoso V, Bohyn W. Ultrastructural and morphometric study of corticosteroid glaucoma in rabbits. Ophthalmic Res 1984; 16:168–178.
Clark AF, Wordinger RJ. The role of steroids in outflow resistance. Exp Eye Res 2009; 88:752–759.
Hozler MP, Solomon KD, Sandoval HP, Vroman DT. Comparison of ketorolac tromethamine 0.5% and loteprednol etabonate 0.5% for inflammation after phacoemulsification: prospective randomized double-masked study. J Cataract Refract Surg 2002; 28:93–99.
Maca SM, Amon M, Findl O, Kahraman G, Barisani-Asenbauer T. Efficacy and tolerability of preservative-free and preserved diclofenac and preserved ketorolac eyedrops after cataract surgery. Am J Ophthalmol 2010; 149:777–784.
Duan P, Liu Y, Li J. The comparative efficacy and safety of topical non-steroidal anti-inflammatory drugs for the treatment of anterior chamber inflammation after cataract surgery: a systematic review and network meta-analysis. Graefes Arch Clin Exp Ophthalmol 2017; 255:639–649.
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6]