Prednisolone versus dexamethasone for prevention of pseudophakic cystoid macular edema.

OBJECTIVE: Prevention of cystoid macular edema (CME) is important to achieve good surgical outcomes after cataract surgery. Although many options for management exist, control of postoperative inflammation with topical steroids is one of the most commonly employed. We evaluated the difference in incidence of pseudophakic CME in patients treated with prednisolone or dexamethasone topical steroids. METHODS: The study was a retrospective chart review of patients who had undergone phacoemulsification at the Cole Eye Institute of the Cleveland Clinic. Reviewable patient charts had to indicate the topical steroid used and whether or not an additional medication (e.g., nonsteroidal anti-inflammatory drugs [NSAIDs]) was used after surgery. Excluded were patients who underwent combination procedures (e.g., trabeculectomy), perioperative anti-vascular endothelial growth factor or intraocular steroid, eyes with epiretinal membrane or prior retinal vein occlusion, those who developed postoperative endophthalmitis, patients with less than 3 months of follow-up, and patients who received topical NSAIDs. Pseudophakic CME was defined as new or worsening macular edema on optical coherence tomography within the first 3 months after cataract extraction. RESULTS: In total, 1135 patient charts were included in the analysis; 721 patients were treated with prednisolone acetate, and 414 were treated with dexamethasone. Patient characteristics were similar between the 2 treatment groups. No significant difference was found in the rate of postoperative CME for patients receiving prednisolone or dexamethasone (4.0% vs 4.1%, p = 0.94). CONCLUSIONS: There was no significant difference in the rate of pseudophakic CME when either prednisolone acetate or dexamethasone sodium phosphate was used after cataract surgery.

Ocular safety comparison of non-steroidal anti-inflammatory eye drops used in pseudophakic cystoid macular edema prevention.

Non-steroidal anti-inflammatory drug (NSAID) eye drops are widely used to treat ocular inflammatory conditions related to ophthalmic surgical procedures, such as pseudophakic cystoid macular edema, and they have been used for off-label treatments. The most commonly used NSAIDs are diclofenac and ketorolac and the new molecules bromfenac and nepafenac have also been used. We used primary human keratocytes in cell culture in combination with a novel technology that evaluates dynamic real-time cytotoxicity through impedance analysis. This study also included classic cell viability tests (WST-1(®) and AlamarBlue(®)), wound healing assay, Hen's Egg Test and an ex vivo histopathological assay. NSAIDs were shown to have important cytotoxicities and to retard the healing response. Furthermore, the new eye drops containing bromfenac and nepafenac were more cytotoxic than the more classical eye drops. Nevertheless, no immuno-histochemical changes or acute irritation processes were observed after the administration of any eye drops tested. Due to cytotoxicity and the total absence of discomfort and observable injuries after the administration of these drugs, significant corneal alterations, such as corneal melts, can develop without any previous warning signs of toxicity.

Controversies in NSAIDs Use in Cataract Surgery.

Pseudophakic cystoid macular edema (PCME) remains the most common cause of poor visual outcome following cataract surgery. Whereas acute PCME may resolve itself spontaneously, some patients will suffer from vision impairment and will be difficult to treat. Although PCME has already been described approximately 50 years ago, its pathophysiology remains uncertain and a multitude of mechanisms have been suggested. As broad as the mechanisms, as many are the treatment options. Topical nonsteroidal anti-inflammatory agents (NSAIDs) and corticosteroids either as mono- or combined therapy are a commonly used first line approach. When ineffective, systemic treatment with these agents may be an option. Alternatively, intravitreal application of corticosteroids and anti-vascular endothelial growth factor (anti-VEGF) may offer an effective option, if first-line treatment fails. A critical evaluation of the current literature revealed that the optimal treatment of PCME remains unclear and requires further investigation. In addition, prevention should be of foremost importance and remains an open issue. Identification of risk factors, application of NSAIDs and consequent follow-up are potential essential steps in the avoidance of this complication.

[Aphakic and pseudophakic glaucoma following pediatric cataract surgery]. / Aphakie- und Pseudophakieglaukom nach Kataraktoperation im Kindesalter.

Modern surgical techniques allow congenital cataract surgery to be performed much more successfully. The development of a secondary glaucoma is the most dreaded postoperative complication (one third of all pediatric secondary glaucomas). Due to the limited value of the available literature, data on prevalence are unreliable. A 10-year postoperative incidence of 10-25% is given in the literature for developing secondary glaucoma and the frequency increases with the duration of follow-up. A major risk factor seems to be the age at the time of surgery. The younger the patient is at the time of surgery the higher the risk of secondary glaucoma. A microcornea seems to be another risk factor in multivariate analysis. The following postoperative changes might be involved in the pathogenesis: peripheral anterior synechia, high iris insertion and membranous material over the trabecular meshwork. Additionally postoperative inflammation, reaction to lens epithelial cells, perioperative barotrauma and loss of anterior segment architecture might also be responsible. In order to evaluate the optimal age window for congenital cataract surgery and risk factors for the development of secondary glaucoma, a prospective longitudinal study is mandatory.

Prophylaxis of pseudophakic cystoid macular edema with intraoperative pegaptanib.

PURPOSE: The purpose of this study was to determine the efficacy of an intraoperative intravitreal pegaptanib injection during phacoemulsification in preventing the development of pseudophakic cystoid macular edema (CME) following cataract surgery. METHODS: This prospective, controlled pilot study was carried out at the Department of Ophthalmology, Nuevo Hospital Universitario y Politécnico La Fe, Valencia (Spain). Five hundred patients with cataract and healthy retina were included in the study. Patients were assigned in a 1:1 ratio to receive an intraoperative intravitreal pegaptanib injection (n=250) or not (control group, n=250) associated with standardized phacoemulsification surgery and postoperative treatment. Any surgical complication was considered as an exclusion criterion. The main outcome measure was the incidence of CME at 4 weeks postsurgery, defined as a central foveal thickness greater than 350 µm as measured by spectral-domain optical coherence tomography with associated cystoid changes. RESULTS: The incidence of CME by the fourth postoperative week was 0.4% (n=1) in the pegaptanib group and 4.4% (n=11) in the control group (P=0.009). CONCLUSIONS: Prophylactic use of intravitreal pegaptanib immediately after phacoemulsification was effective in preventing CME by the fourth postoperative week. The inclusion of intravitreal pegaptanib injection in the prophylaxis of pseudophakic CME will be considered for complicated cases in forthcoming studies.

[Studies on clinical pathophysiology of pseudophakic/aphakic eyes--a journey of 4 decades].

My prime years as an ophthalmologist began as intraocular lenses (IOLs) were just entering into the developmental stage, and I took on as my mission to contribute to perfecting safe and reproducible cataract/IOL implantation surgery. Identifying surgical and/or IOL-related complications consumed time; however, these complications soon became predictable and even preventable with the use of sensitive biological parameters and preclinical evaluation. This was a simple goal for me to pursue my studies on cataract/IOL implantation surgery. I discuss in this review article, based on my previous research, clinico-pathophysiological problems of these intra- and postoperative eyes. The early phase of cataract/IOL implantation surgery development began with a debate as to which is physiologically superior: intracapsular cataract extraction (ICCE) or extracapsular cataract extraction (ECCE). From the perspective of transporting substances from intraocular fluids to extraocular space, which we studied using a nonphysiological substance, fluorescein, ECCE was confirmed to be physiologically superior to ICCE. The transport mechanism of both physiological and nonphysiological substances from intraocular fluids (such as vitreous and aqueous humor) is believed to be related to the pathogenesis of various ocular disorders. Following the fluorescein study, I next focused my attention on biosynthesis and active transport of prostaglandin (PG), which are inflammatory mediators. My studies revealed that PG were more likely to accumulate in ICCE eyes than in ECCE eyes; higher intraocular concentration of PG was also confirmed in eyes with persistent aphakic or pseudophakic cystoid macular edema (CME). While conducting the above studies and having made some observations, I postulated another hypothesis on the pathogenesis of aphakic or pseudophakic CME as follows: topical application of nonsteroidal antiinflammatory drugs (NSAIDs) to eyes with PG, which are biosynthesized intra- and postoperatively during the healing process of uveal tissues and lens epithelial cells, prevents CME. Based on this hypothesis experimental studies were then started, and in 1977 I became the first in the world to prove that topical application of indomethacin, one of the NSAIDs, controls the incidence of CME in ICCE eyes. Thereafter, some 40 follow-up studies have been conducted worldwide, and recent meta-analysis has established the efficacy of indomethacin. Macular edema and CME are recently of significant interest as complications in various ocular disorders. Compared to other forms of CME, the pathophysiology of CME associated with aphakic/ pseudophakic eyes is relatively simple, its natural history is well understood and its reproducibility is high. It is possible that the other forms of macular edema or CME having more complicated pathogenesis may be interpreted by understanding the formation mechanism of aphakia/pseudophakic CME. Our studies have shown how chemical mediators (PG) are systematically involved in the development of aphakic/pseudophakic CME, and that they concurrently cause blood-aqueous barrier disruption and CME, decrease oscillatory potential of the full field ERG, and decrease choroidal blood flow at an early postoperative period, and this has recently been proven. All these phenomena, however, can be effectively prevented by topical application of NSAIDs. I believe these findings provide significant information when considering the pathogenesis and treatment of CME associated with other ocular disorders. Using the primitive method of an early phase, I discovered that anti-PG eye drops can treat disrupted blood-aqueous barrier, and confirmed that the blood-aqueous barrier function is indeed a very sensitive function. I next applied fluorophotometry and laser flaremetry. Using blood-aqueous barrier function as a parameter, the following were evaluated: consensual reaction of blood-aqueous barrier disruption, method of IOL fixation, racial differences in disruption of the aqueous barrier function, drugs used perioperatively, biocompatibility of IOL materials, and effects of preservative agents. Research on preservative agents disclosed that the preservative agent in anti-glaucoma drops more strong by induced pseudophakic CME than the anti-glaucoma agent itself. Thus, this introduced a new concept called Our desire to closely observe the endosurface of the iris, ciliary processes and anterior vitreous face, all of which are closely related to phacoemulsification techniques, posterior chamber lens fixation, and active transport of PG, led me to the development of "Posterior video technique" (Miyake-Apple View). The technique since then has been used to evaluate cataract surgical techniques, to analyze complications, to review IOL designs and fixation techniques, to pre-clinically evaluate surgical devices, and to study variations of local anatomy related to cataract/IOL surgery. The method is also useful as an educational as well as a presentational tool, and it has now been accepted world-wide. The pathogenesis of aphakic/pseudophakic CME, physiological evaluation centering on blood-aqueous barrier function, and preclinical evaluation using the Posterior video technique have all played a significant role in establishing today's safe cataract/IOL implantation surgery.

[Posterior capsule opacification in pseudophakic eyes--etiopathogenesis, clinical picture, possibilities of prevention and therapy]. / Zmetnienie torebki tylnej soczewki w oczach pseudofakijnych--etiopatogeneza, obraz kliniczny, profilaktyka i leczenie.

Posterior capsule opacification (PCO) is a late complication after the cataract surgery, currently occurring most often. The epithelial cells which migrate to the surface of the posterior capsule participate in the mechanism of PCO formation. Clinical opacification of the posterior capsule appears as the foggy form, creasing, pearl mass and fibrosis. PCO can be cured by laser or surgical capsulotomy. The factors influencing a size and intensity of PCO are as follows: age of patient, other diseases, method of surgery and type of the implanted artificial intraocular lens. Prevention against PCO during surgery should include accurate hydrodissection, removing of cortical mass, polishing of the capsule and intracapsular fixation of the lens. It is necessary to carry out further studies on possibilities of PCO prevention.

Recent developments in pseudophakic dysphotopsia.

PURPOSE OF REVIEW: Photic phenomena associated with intraocular lenses can degrade visual performance following intraocular lens implantation. Postoperative dysphotopsia introduces glare, halos, starbursts and shadows in a small number of patients. Understanding the optical mechanisms behind the introduction of these artifacts can lead to improved lens design and a reduction in the deleterious effects of stray light. This review looks at the improvement efforts of recent years to illustrate the systematic hunt for lens problems. RECENT FINDINGS: Improvements in edge designs have diminished the effects of positive dysphotopsia. However, negative dysphotopsia remains poorly understood and a variety of lens designs and materials can cause negative dysphotopsia. In other efforts, a testing procedure has been developed to improve understanding of the visual percept of a patient suffering dysphotopsia. This test should enlighten practitioners to the deficits their patients face and provide clues to the root causes of the problems. SUMMARY: Intraocular lenses can introduce stray light artifacts into the eye. These artifacts manifest themselves as glare, halos, starbursts and shadows. While positive dysphotopsia (glare, halos and starbursts) has been largely attributed to edge effects of the implant, negative dysphotopsia remains somewhat mysterious and appears to be more related to the patient's anatomical structure than to specific lens designs or materials.