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 Table of Contents  
CASE REPORT
Year : 2022  |  Volume : 60  |  Issue : 1  |  Page : 71-73

Anti VEGF for post op CME- Boon or Bane!


1 Department of Retina Vitreous, Aravind Eye Hospital, Puducherry, India
2 Department of Uvea Services, Aravind Eye Hospital, Puducherry, India

Date of Submission12-Aug-2021
Date of Decision10-Nov-2021
Date of Acceptance06-Dec-2021
Date of Web Publication22-Mar-2022

Correspondence Address:
Dr. Roshni Mohan
Department of Retina and Vitreous, Aravind Eye Hospital, Thavalakuppam, Puducherry - 605 007
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/tjosr.tjosr_127_21

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  Abstract 


Cataract surgery has advanced in techniques and instrumentation over the years, but complications such as cystoid macular edema (CME) do occur even after uneventful surgery. The incidence of pseudophakic CME (detected by optical coherence tomography) is 30%–40% after uncomplicated phaco cataract surgeries. Risk factors for the development of CME include prolonged duration of surgery, iris handling and diabetes. Corticosteroids are the mainstay of treatment of postoperative inflammation and CME. In certain situations where steroids are contraindicated anti-vascular endothelial growth factor (VEGF) agents are used as the second line agents for the treatment of CME. Here, we describe a case of postoperative uveitis with CME which showed good response with single dose intravitreal anti-VEGF injection-Bevacizumab.

Keywords: Anti-vascular endothelial growth factor, bevacizumab, corticosteroids, cystoid macular edema, phacoemulsification


How to cite this article:
Mohan R, Arthi M, Balamurugan S. Anti VEGF for post op CME- Boon or Bane!. TNOA J Ophthalmic Sci Res 2022;60:71-3

How to cite this URL:
Mohan R, Arthi M, Balamurugan S. Anti VEGF for post op CME- Boon or Bane!. TNOA J Ophthalmic Sci Res [serial online] 2022 [cited 2022 Jun 29];60:71-3. Available from: https://www.tnoajosr.com/text.asp?2022/60/1/71/340347




  Introduction Top


Cystoid macular edema (CME) remains one of the most common causes of defective vision postcataract surgery.[1] It is caused by the breakdown of blood ocular barrier which continues up to 6 weeks postcataract surgery.[2] The incidence of clinically significant CME, defined as visual acuity worse than 20/40 is 13%–15% postcataract surgery.[3] Although it resolves spontaneously in majority of patients, it can produce visual morbidity in some.


  Case Report Top


A 58-year-old female presented with complaints of pain, redness, and defective vision in the left eye (OS) for 2 weeks. She had undergone OS uncomplicated phacoemulsification with in the bag hydrophobic acrylic intraocular lens for Grade 2 nuclear sclerosis a month before the onset of symptoms. She had no history of systemic or ocular illness. At presentation, her best-corrected visual acuity (BCVA), right eye (OD) was 20/60, OS 20/30. OD was unremarkable with nuclear cataract. OS showed PCIOL with 360° posterior synechiae, variable anterior chamber depth, and normal IOP. Fundus evaluation OS showed pigment dispersion in the anterior vitreous and mild vitreous haze, rest of the fundus was unremarkable. She was treated for postoperative inflammation with 1% prednisolone acetate eye drops eight times a day and 0.1% Nepafenac drops. She followed up elsewhere and was on and off topical steroids when symptomatic. She was diagnosed with 360° peripheral anterior synechiae (PAS) with secondary angle closure elsewhere and had undergone laser peripheral iridotomy (PI) for the same. Four months later, the patient was still symptomatic with painful red eye. Examination of OS revealed BCVA 20/60, IOP 30 mmhg, persisting iritis, and a patent PI. Steroid response was suspected; she was advised to taper topical and oral steroids and started on antiglaucoma medications (AGM) along with topical nonsteroidal anti-inflammatory drug (NSAID). Two weeks later, she presented with persistent inflammation but normal IOP. She was advised to taper topical steroids and continue AGM.

Subsequently 2 weeks later, her BCVA was 20/200 OS, IOP was normal and eye was quiet. Fundus examination showed glaucomatous cupping of optic disc with thin epiretinal membranes.

A month later, she had reactivation of anterior segment inflammation with slight elevation of IOP to 25 mm hg. Optical coherence tomography (OCT) OS showed CME with neurosensory detachment. Uveitic workup was done (including HLA B51 and rheumatology workup for recurrent uveitis) which turned out to be negative. Anterior segment OCT was done which revealed a well centered optic with no tilt or regional elevation of iris. She was started on topical low potent steroid therapy, loteprednol 0.5% eye drops along with AGM.

Two weeks later, intraocular inflammation had reduced, IOP was under control but CME persisted [Figure 1]a. IOL explantation was deferred due to advanced disc damage and risk of increase in inflammation. She underwent intravitreal injection Bevacizumab 1.25 mg/0.05 ml for CME under guarded prognosis after obtaining appropriate consent from the patient regarding the secondary role of anti-VEGF in pseudophakic CME.
Figure 1: (a) showing cystoid macular edema with Neurosensory detachment (*), IRF (arrow head), Epiretinal membrane (Downward arrow). (b) Showing resolving CME. (c) Showing resolved CME with epiretinal membrane

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One month postinjection, BCVA was 20/125 and there was reduction in the CME (CMT 367 μ) with no flare up of inflammation and IOP within normal limits [Figure 1]b and [Figure 1]c. She was explained about the need for filtration surgery in future to maintain her vision and prevent IOP fluctuations. The patient was lost to follow-up thereafter.


  Discussion Top


Postcataract surgery inflammation can lead to suboptimal visual recovery, more so when it is complicated by secondary glaucoma and inflammatory CME. The risk factors for the development of postoperative CME include prolonged duration of diabetes, use of pupil expansion devices and African − American race.[4] Postsurgical uveitis is defined as inflammation persisting 6 months or longer with persistent need for immunotherapy without any alternative etiology. In the study conducted by Patel et al., 27 out of 17757 eyes developed chronic postoperative uveitis with no history of previous uveitis or immunological disorders.[5] In our patient, the duration of surgery, intraoperative manipulation, and use of intracameral drugs could not be elicited because surgery was performed elsewhere. The position of IOL was confirmed by AS OCT and ultrasound biomicroscopy.

Loteprednol etabonate suspension 0.5% is the only C-20 ester corticosteroid approved for use in the treatment of corticosteroid-responsive inflammatory conditions including postoperative ocular inflammation.[6] This alone or in combination with NSAIDs may provide effective and safe inflammation control in steroid responders. The retrometabolic drug design allows the corticosteroid to be active at its site of action and then undergo predictable hydrolysis to inactive metabolites, resulting in reduced incidence of steroid response.

VEGF is known to increase the vascular permeability, cause the breakdown of blood retinal barrier and result in macular edema. Various studies have shown that anti-VEGF agents are efficacious in the treatment of refractory postoperative CME by counteracting these effects and maybe helpful in patients with steroid response.[7],[8] Arevalo et al. used Bevacizumab for treatment of pseudophakic CME in 25 patients and concluded the it is a viable short-term alternative. Seventy-one percent of patients showed significant improvement in BCVA with reduction of CMT and only 12 patients required retreatment [Table 1]. Its use has improved structural outcomes, but the functional outcome is not clear. It has definitely added value to our armamentarium of agents used to treat inflammatory CME.
Table 1: Comparison between our patient and the patients in Arevalo et al study

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Our patient developed a combined mechanism glaucoma-secondary angle closure due to persistent inflammation that induced formation of PAS and steroid response leading to advanced cupping which precluded use of ocular or periocular steroids for treatment of CME. Hence, we had to resort to intravitreal anti-VEGF. Since patient was not affordable for intravitreal Ranibizumab injection, we had to opt for Bevacizumab after obtaining necessary consent from the patient. This helped us in the management of this patient such as visual acuity improvement and significant reduction of central macular thickness.

Postoperative inflammation is not an infrequent complication of cataract surgery. Loteprednol can be used safely to control inflammation and anti-VEGF agents can be used for the treatment of pseudophakic CME in steroid responders. Although short-term efficacy of anti-VEGF agents is proven, long-term studies are required to establish the optimum dosing, interval and response of pseudophakic CME to anti-VEGF injections.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient (s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Tsilimbaris MK, Tsika C, Diakonis V, Karavitaki A, Pallikaris I. Macular Edema and Cataract Surgery. London: InTech. 2013:323-36.  Back to cited text no. 1
    
2.
Irvine SR. A newly defined vitreous syndrome following cataract surgery interpreted according to recent concepts of the structure of the vitreous, the Seventh Francis I. Proctor lecture. Am J Ophthalmol 1953;36:601-19.  Back to cited text no. 2
    
3.
Lardenoye CW, van Kooij B, Rothova A. Impact of macular edema on visual acuity in uveitis. Ophthalmology 2006;113:1446-9.  Back to cited text no. 3
    
4.
Neatrour K, McAlpine A, Owens TB, Trivedi RH, Poole Perry LJ. Evaluation of the etiology of persistent iritis after cataract surgery. J Ophthalmic Inflamm Infect 2019;9:4.  Back to cited text no. 4
    
5.
Patel C, Kim SJ, Chomsky A, Saboori M. Incidence and risk factors for chronic uveitis following cataract surgery. Ocul Immunol Inflamm 2013;21:130-4.  Back to cited text no. 5
    
6.
Dua HS, Attre R. Treatment of post-operative inflammation following cataract surgery – A review. Eur Ophthalmic Rev 2012;6:98-103.  Back to cited text no. 6
    
7.
Arevalo JF, Fromow-Guerra J, Quiroz-Mercado H, Sanchez JG, Wu L, Maia M, et al. Primary intravitreal bevacizumab (Avastin) for diabetic macular edema: Results from the Pan-American collaborative retina study group at 6-month follow-up. Ophthalmology 2007;114:743-50.  Back to cited text no. 7
    
8.
Mason JO 3rd, Albert MA Jr., Vail R. Intravitreal bevacizumab (Avastin) for refractory pseudophakic cystoid macular edema. Retina 2006;26:356-7.  Back to cited text no. 8
    


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