Cystoid macular edema related to cataract surgery and topical prostaglandin analogs: Mechanism, diagnosis, and management

doi:10.1016/j.survophthal.2020.02.004

Survey of Ophthalmology

Volume 65, Issue 5, September–October 2020, Pages 496-512

https://doi.org/10.1016/j.survophthal.2020.02.004 Get rights and content

Abstract

Cystoid macular edema (CME) is a form of macular retina thickening that is characterized by the appearance of cystic fluid-filled intraretinal spaces. It has classically been diagnosed upon investigation after a decrease in visual acuity; however, improvements in imaging technology make it possible to noninvasively detect CME even before a clinically significant decrease in central vision. Risk factors for the development of CME include diabetic retinopathy, retinal vein occlusion, uveitis, and cataract surgery. It has been proposed that eyes with elevated intraocular pressure after cataract surgery, including those treated with prostaglandin analog eye drops, may be at higher risk for the development of CME. We summarize the current knowledge of the molecular mechanisms underlying CME, the potential role of ocular surgery and topical glaucoma medication in increasing the risk of CME, the newly developed imaging methods for diagnosing CME, and the clinical management of CME.

Section snippets

Introduction to cystoid macular edema

Cystoid macular edema (CME) is characterized by retinal thickening at the macula, associated with cystic changes in the outer plexiform and inner nuclear layers.¹⁰² These cystic changes occur from the accumulation of fluid arising from inner and outer blood-retinal breakdown of the perifoveal capillaries, which is mediated by a number of inflammatory molecules.⁴⁰ CME may be classified as acute or chronic, whereby CME is present for less or more than 6 months, respectively. Clinical CME is

Diagnosis of CME

The traditional methods for evaluating macular thickening include slit-lamp biomicroscopy, indirect ophthalmoscopy, and fundus photography.¹⁰⁶^,¹⁰⁸ Although these methods identify exudates, hemorrhages, and microaneurysms, their usefulness is limited in identifying specific anatomic details at the vitreoretinal interface, and they are dependent on the extent of edema and the observer's level of experience and skill.¹⁰⁶ Therefore, postoperative CME is conventionally diagnosed by decreased visual

Pathology and pathophysiology of CME

Although the classic picture of CME is characterized by cysts in the outer plexiform layer, cysts initially form in the inner nuclear layer and, upon disease progression, they appear in the outer plexiform layer and the subretinal space.¹⁰² This is coupled with capillary loss, which is observed in both the superficial capillary plexus and the deep capillary plexus during pseudophakic CME, but normalizes upon CME resolution.²⁰^,¹⁰⁴ This suggests that capillary nonperfusion in pseudophakic CME is

CME in patients with glaucoma

The risk of CME in patients who receive postoperative PGAs after IOP-lowering glaucoma surgery has not yet been characterized. There are limited reports on CME after incisional glaucoma surgeries like trabeculectomy. One small study reported CME after trabeculectomy combined with intraoperative mitomycin C in 1 of the 26 operated eyes (3.8%), all of which had post-keratoplasty glaucoma.⁴⁴ It has been reported, however, that trabeculectomy may lead to increased macular thickness. In one

The role of PGs in the development of pseudophakic CME

Endogenous PGs are lipid mediators that are produced from the cleavage of membrane phospholipids by phospholipase A2 to arachidonic acid. Arachidonic acid is subsequently metabolized by the cyclooxygenase (COX) enzymes (COX1 and COX2) to eventually produce thromboxanes and PGs (PGD₂, PGE₂, PGI₂, and PGF_2α).⁸⁷ A summary of the ocular localization of PG receptors is provided in Table 2. Analogs of PGF_2α are commonly used to lower IOP in patients with open-angle glaucoma by increasing uveoscleral

Clinical experience with CME in topical PGA users

In one recent investigation, PGAs have recently been recommended for the prophylactic treatment of IOP elevation after uncomplicated cataract surgery.⁴² As previously mentioned in this review, the use of PGAs typically does not cause CME in phakic patients with a normally functioning blood-ocular barrier but may increase the incidence of CME after cataract surgery.³^,³⁰^,¹²⁹ In a retrospective study comprising data from 1659 cataract surgeries, preoperative use of PGAs was associated with a

Management of pseudophakic CME

PGA-related CME can be effectively treated with discontinuation of the PGA and appropriate treatment of the CME.⁴^,⁶³ In pseudophakic CME, the most commonly used treatment strategy is to suppress postsurgical inflammation using topical NSAIDs or corticosteroids, either separately or as a combined treatment.³³^,³⁹ A summary of the medical interventions used to treat pseudophakic CME is provided in Table 3. Corticosteroids are commonly used to treat pseudophakic CME because of their well-known

Expert opinion and conclusions

Pseudophakic CME seems to be more common than previously appreciated and may be underreported after cataract surgery. In several published studies and case reports, CME was detected only upon the report of decreased visual acuity; however, advances in OCT and OCT angiography technology allow noninvasive detection, quantification, and monitoring of CME. This makes it possible to assess CME objectively, but independently from central visual function. In addition, this means that CME may be

Method of literature search

•
A thorough literature search was done on Medline from 1950 to 2019 using the main search term “(cystoid macular edema) OR (cystoid macular oedema OR CME OR CMO)” AND the following terms “prostaglandin AND cataract surgery”, “prostaglandin”, “bimatoprost”, “travoprost”, “latanoprost”, “tafluprost”, “unoprostone”, “phakic”, “(phakic) AND (glaucoma)”, “diagnosis”, “(prostaglandin) AND (management)”, “management”, “(treatment) AND pseudophakic”, “glaucoma filtration surgery”, “glaucoma filtration

Disclosures

G Holló is a consultant for Mundipharma, Novartis, and Santen. T Aung is a consultant for Alcon, Allergan, Belkin Laser, Mundipharma, Novartis, ONL Therapeutics, PH Pharma, Santen, and Sun Pharma and has received grant support from Allergan, Novartis, and Santen. L Cantor is a consultant for Carl Zeiss Meditec and Santen and has received grant support from Allergan, Bausch and Lomb, and InnFocus. M Aihara is a consultant for Santen and has received grants and personal fees from Alcon Japan,

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Mechanisms of blood-retinal barrier disruption related to intraocular inflammation and malignancy
2024, Progress in Retinal and Eye Research
Blood-retinal barrier (BRB) disruption is a common accompaniment of intermediate, posterior and panuveitis causing leakage into the retina and macular oedema resulting in vision loss. It is much less common in anterior uveitis or in patients with intraocular lymphoma who may have marked signs of intraocular inflammation. New drugs used for chemotherapy (cytarabine, immune checkpoint inhibitors, BRAF inhibitors, EGFR inhibitors, bispecific anti-EGFR inhibitors, MET receptor inhibitors and Bruton tyrosine kinase inhibitors) can also cause different types of uveitis and BRB disruption. As malignant disease itself can cause uveitis, particularly from breast, lung and gastrointestinal tract cancers, it can be clinically difficult to sort out the cause of BRB disruption. Immunosuppression due to malignant disease and/or chemotherapy can lead to infection which can also cause BRB disruption and intraocular infection.
In this paper we address the pathophysiology of BRB disruption related to intraocular inflammation and malignancy, methods for estimating the extent and effect of the disruption and examine why some types of intraocular inflammation and malignancy cause BRB disruption and others do not. Understanding this may help sort and manage these patients, as well as devise future therapeutic approaches.
The role of retinal glial cells and related factors in macular edema
2024, Biochemical and Biophysical Research Communications
Macular edema (ME) has emerged as a leading cause of visual impairment, representing a critical clinical manifestation and complication associated with many eye diseases. In the occurrence and development of ME, retinal glial cells like Müller cells and microglial cells play vital roles. Moreover, growth factor and cytokines associated with them, such as vascular endothelial growth factor (VEGF), pigment epithelium-derived factor (PEDF), hypoxia-inducible factor-1α (HIF-1α), angiopoietin-like protein 4 (ANGPTL4), interleukin-6(IL-6), interleukin-8 (IL-8), monocyte chemoattractant protein-1 (MCP-1), prostaglandin, etc., also take part in the pathogenesis of ME. Changes in these cytokines can lead to retinal angiogenesis, increased vascular permeability, blood-retinal barrier (BRB) breakdown, and fluid leakage, further causing ME to occur or deteriorate. Research on the role of retinal glial cells and related cytokines in ME will provide new therapeutic directions and effective remedies. This article is a literature review on the role of Müller cells, microglial cells and related factors in ME pathogenesis.
Synergic effects of EP2 and FP receptors co-activation on Blood-Retinal Barrier and Microglia
2023, Experimental Eye Research
Macular edema (ME) is caused with disruption of the blood-retinal barrier (BRB) followed by fluid accumulation in the subretinal space. Main components of the outer and inner BRB are retinal pigment epithelial (RPE) cells and retinal microvascular endothelial cells, respectively. In addition, glial cells also participate in the functional regulation of the BRB as the member of 'neurovascular unit'. Under various stresses, cells in neurovascular units secrete inflammatory cytokines. Neuroinflammation induced by these cytokines can cause BRB dysfunction by degrading barrier-related proteins and contribute to the pathophysiology of ME. Prostaglandins (PGs) are crucial lipid mediators involved in neuroinflammation. Among PGs, a novel EP2 agonist, omidenepag (OMD) acts on not only the uveoscleral pathway but also the conventional pathway, unlike F prostanoid (FP) receptor agonists. Moreover, the combination use of the EP and the FP agonist is not recommended because of the risk of inflammation. In this study, we investigated effects of OMD and latanoprost acid (LTA), a FP agonist, on BRB and microglia in vitro and in vivo.
To investigate the function of outer/inner BRB and microglia, in vitro, ARPE-19 cells, human retinal microvascular endothelial cells (HRMECs), and MG5 cells were used. Cell viability, inflammatory cytokines mRNA and protein levels, barrier morphology/function, and microglial activation were evaluated using proliferation assays, qRT-PCR, ELISA, immunocytochemistry, trans-epithelial electrical resistance, and permeability assay. Moreover, after vitreous injection into the mouse, outer BRB morphology, glial activation, and cytokine expression were assessed. Each OMD and LTA alone did not affect the viability or cytokines expression of the three types of cells. In ARPE-19 cells, the co-stimulation of OMD and LTA increased the mRNA and protein levels of inflammatory cytokines (IL-6, TNF-α, and VEGF-A) and decreased the barrier function and the junction-related protein (ZO-1 and β-catenin). By contrast in HRMECs, the co-stimulation affected significant differences in the mRNA levels of some cytokine (IL-6 and TNF-α) but enhanced the barrier function. In MG5 cells, the cytokines mRNA and size of Iba1-expressed cell were increased. A non-steroidal anti-inflammatory inhibited the barrier dysfunction and the junction-related protein downregulation in ARPE-19 cells and activation of MG5 cells. Also in vivo, the co-stimulation induced outer BRB disruption, cytokine increase, and retinal glial activation. Therefore, the co-stimulation of EP2 and FP induced the inflammatory cytokine-mediated outer BRB disruption, the enhanced inner BRB function, and the microglial activation. The BRB imbalance and the intrinsic prostaglandin production may be involved in OMD-related inflammation.
Efficacy and safety of combined 27-G vitrectomy and Ahmed valve using same sclerotomy site for the tube placement: A case series
2023, Archivos de la Sociedad Espanola de Oftalmologia
Presentamos una serie retrospectiva describiendo la viabilidad y los resultados de la cirugía combinada de vitrectomía mínimamente invasiva con 27-G e implante de válvula de Ahmed® (IVA). Cuatro ojos de 4 pacientes fueron operados de vitrectomía 27-G e IVA en la cavidad vítrea empleando la misma esclerotomía. Se recogieron los datos pre y postoperatorios hasta 12 meses, incluyendo el tipo de glaucoma, la presión intraocular, la medicación hipotensora y las complicaciones. En todos los casos se pudo implantar el tubo en la cavidad vítrea, aunque en 2 ojos fue necesaria una pequeña ampliación. Al año, la presión y las medicaciones se redujeron (41,5 ± 19,1 a 14,5 ± 3,1 mmHg y 3 [3-3] a 1,5 [1,5-3,5], respectivamente). Tres pacientes desarrollaron edema macular. En conclusión, la primera serie publicada de la cirugía combinada 27-G e IVA muestra una reducción de la presión y los fármacos hipotensores; en la mitad de los casos fue necesario ampliar la esclerotomía para el implante del tubo.
We report a retrospective case series describing the feasibility and outcomes of combined 27-G minimally invasive vitrectomy surgery (MIVS) and Ahmed® glaucoma valve (AGV) placement. Four eyes of four patients underwent a combined MIVS using 27-G technology and AGV implantation with the tube placement in the vitreous cavity. Preoperative and postoperative data up to 12 months were collected including the type of glaucoma, intraocular pressure (IOP), glaucoma medications, and complications. All AGVs tubes were placed in the vitreous cavity using the same sclerotomy, although a slight wound enlargement was required. After one year, IOP and glaucoma medications were reduced (41.5 ± 19.1 to 14.5 ± 3.1 mmHg and from 3 [3-3] to 1.5 [1.5-3.5]). Three patients developed cystoid macular edema. The first-reported cases of combined MIVS-27-G and AGV showed a reduction of IOP and antiglaucoma medication. Placing the tube using the same sclerotomy location is feasible but a slight enlargement may be required.
Transient Increase of Flicker Electroretinography Amplitudes after Cataract Surgery: Association with Postoperative Inflammation
2023, Ophthalmology Science
To determine the characteristics and cause of the increase in the amplitude of flicker electroretinography (ERG) after cataract surgery.
Prospective, observational clinical study.
Thirty patients who underwent cataract surgery.
Flicker ERGs were recorded with the RETeval system without mydriasis. The central macular thickness (CMT) was measured by OCT and the aqueous flare value (AFV) by laser flare-cell photometry. These examinations were performed before surgery and 1 day, 1 week, 1 month, 2 months, and 3 months after surgery. Linear regression analysis through the origin was used to compare the correlations between the relative changes in flicker ERG amplitudes and the changes in the CMT and AFV at different times after the surgery.
The amplitude of flicker ERGs, CMT, and AFV.
The mean amplitude of flicker ERGs increased significantly by 31% at 1 week after surgery (P < 0.001); a significant increase in the amplitudes was not present at 3 months after the surgery. The mean AFV was significantly increased at 1 day after surgery (P < 0.001), and the CMT was significantly increased at 1 to 3 months after surgery (P < 0.001). The changes in flicker ERG amplitudes at 1 week after surgery were significantly associated with the changes in the CMT at 1 to 3 months after surgery (P < 0.05), and they were weakly associated with the changes in AFV at 1 day after surgery (P = 0.05).
These results suggest that the increase in the amplitude of flicker ERGs after cataract surgery is a transient phenomenon that has a peak at 1 week after surgery. The increase of flicker ERG amplitude was associated with measures that are frequently used to evaluate postoperative inflammation.
Proprietary or commercial disclosure may be found after the references.
Prophylactic interventions for preventing macular edema after cataract surgery in patients with diabetes: A Bayesian network meta-analysis of randomized controlled trials
2022, eClinicalMedicine
Citation Excerpt :
Accordingly, several perioperative interventions have been proposed to reduce the incidence rate of PME in diabetes underwent cataract surgery. Nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit prostaglandins synthesis during surgical inflammatory response.6 Thus, NSAIDs is used as one of the common perioperative interventions in preventing PME.8
Diabetes significantly increases the risk of postoperative macular edema (PME) after cataract surgery, leading to potential worst post-operative outcomes. This study aims to compare the effect of different prophylactic interventions in improving postoperative anatomic and visual acuity outcomes of diabetes patients who underwent cataract surgery.
We searched MEDLINE, Embase, Web of Science databases from inception until February 2nd, 2022, for studies including studies reporting PME events and/or best-corrected visual acuity (BCVA) outcomes. Random-effects Bayesian network meta-analysis was performed to compare the efficiency of intravitreal anti-vascular endothelial growth factor injections (anti-VEGF), nonsteroidal anti-inflammatory drugs (NSAIDs) and topical steroids eye drop at 1 week, 1 month, 3 months, 6 months after cataract surgery.
The total of 2566 participants from 17 randomized controlled trials were included in the network meta-analysis, with moderate risk of bias and no evidence of publication of bias. Compared to placebo/steroid eye drop alone, patients received additional topical NSAIDs or intravitreal anti-VEGF injections had lower risk of PME at 1 month (NSAIDs: OR=0·221, 95% Confidence interval [CI], 0·044–0·755, I²=0·0%, 5 studies; anti-VEGF: OR=0·151, 95%CI, 0·037–0·413, I²=0·0%, 5 studies) and 3 month (NSAIDs: OR=0·370, 95%CI, 0·140–0·875, I²=0·0%, 8 studies; anti-VEGF: OR=0·203, 95%CI, 0·101–0·353, I²=0·0%, 4 studies) after cataract surgery. Further, additional anti-VEGF exhibited better BCVA outcome at 1 month (mean difference of LogMAR: -0·083, 95%CI, -0·17 to -0·014, I²=62·0%, 5 studies), and 3 months (mean difference of LogMAR: -0·061, 95%CI, -0·11 to -0·011, I²=0·0%, 5 studies) after cataract surgery. Such additional benefits did not reach statistic significant at 6 months after surgery.
Our data suggests that compared to placebo/steroid eye drop alone, additional prophylactic anti-VEGF intervention could be considered for preventing the occurrence of PME after cataract surgery in patients with diabetes.
Research and Development of Special (2020-1-2052); Science & Technology Project of Beijing Municipal Science & Technology Commission (Z201100005520045, Z181100001818003).

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Major reviewCystoid macular edema related to cataract surgery and topical prostaglandin analogs: Mechanism, diagnosis, and management

Abstract

Section snippets

Introduction to cystoid macular edema

Diagnosis of CME

Pathology and pathophysiology of CME

CME in patients with glaucoma

The role of PGs in the development of pseudophakic CME

Clinical experience with CME in topical PGA users

Management of pseudophakic CME

Expert opinion and conclusions

Method of literature search

Disclosures

J Cataract Refract Surg

Am J Ophthalmol

Can J Ophthalmol

Am J Ophthalmol

Am J Ophthalmol

Am J Ophthalmol

Ophthalmology

Ophthalmology

J Cataract Refract Surg

J Cataract Refract Surg

Am J Ophthalmol

Surv Ophthalmol

Ophthalmology

J Cataract Refract Surg

J Cataract Refract Surg

J Cataract Refract Surg

Am J Ophthalmol

Am J Ophthalmol

Ophthalmology

Ophthalmology

Ophthalmology

Am J Ophthalmol

J Cataract Refract Surg

Am J Ophthalmol Case Rep

Surv Ophthalmol

J Cataract Refract Surg

Ophthalmology

J Cataract Refract Surg

Am J Ophthalmol

J Cataract Refract Surg

Ophthalmology

Effects of benzalkonium chloride on the blood-aqueous and blood-retinal barriers of pseudophakic eyes

J Ocul Pharmacol Ther

Five-year, multicenter safety study of fixed-combination latanoprost/timolol (Xalacom) for open-angle glaucoma and ocular hypertension

J Glaucoma

The effects of prostaglandin analogues on the blood aqueous barrier and corneal thickness of phakic patients with primary open-angle glaucoma and ocular hypertension

Eye (Lond)

Blood-aqueous barrier changes after the use of prostaglandin analogues in patients with pseudophakia and aphakia: a 6-month randomized trial

Arch Ophthalmol

Intravitreal bevacizumab for refractory pseudophakic cystoid macular edema: the Pan-American Collaborative Retina Study Group results

Ophthalmology

Reversible cystoid macular edema following uneventful microinvasive Kahook Dual Blade goniotomy in a pseudophakic patient: a case report

J Glaucoma

Short-term safety and efficacy of intravitreal bevacizumab for pseudophakic cystoid macular edema

Retina

Efficacy and safety of benzalkonium chloride-free fixed-dose combination of latanoprost and timolol in patients with open-angle glaucoma or ocular hypertension

Clin Ophthalmol

Accumulation and apparent active transport of prostaglandins by some rabbit tissues in vitro

J Physiol

The effects of experimental uveitis on anterior uveal prostaglandin transport and aqueous humor composition

Invest Ophthalmol

Intravitreal triamcinolone acetonide in refractory pseudophakic cystoid macular edema: functional and anatomic results

Eur J Ophthalmol

Use of ocular hypotensive prostaglandin analogues in patients with uveitis: does their use increase anterior uveitis and cystoid macular oedema?

Br J Ophthalmol

Acute pseudophakic cystoid macular edema imaged by optical coherence tomography angiography

Retina

Etiology and treatment of the inflammatory causes of cystoid macular edema

J Inflamm Res

Diagnosis of macular edema

Ophthalmologica

Successful treatment of chronic pseudophakic macular edema (Irvine-Gass syndrome) with interferon alpha: a report of three cases

Ocul Immunol Inflamm

Omidenepag isopropyl ophthalmic solution 0.002%: first global approval

Drugs

The incidence, pathogenesis and treatment of cystoid macular edema following cataract surgery

Trans Am Ophthalmol Soc

Major review
Cystoid macular edema related to cataract surgery and topical prostaglandin analogs: Mechanism, diagnosis, and management