Cystoid Macular Oedema After Cataract and Lens Replacement Surgery
- Posted
- Medically Reviewed by: Mr Mfazo Hove, Consultant Ophthalmic Surgeon
- Author: Mr Mfazo Hove
- Published: December 17, 2024
- Last Updated: February 18, 2026
Mechanism, Risk Biology, and Why Structured Prevention Matters
Cystoid macular oedema (CMO), or Irvine–Gass syndrome, is one of the most studied inflammatory complications following cataract and refractive lens surgery.¹
It is not random.
It is not usually a technical error.
It is a predictable inflammatory cascade expressed in a biologically susceptible retina.
Understanding the mechanism explains why prevention must be structured.
The Mechanism: Why CMO Happens
1. Surgical Trauma and Prostaglandin Release
Even uncomplicated phacoemulsification initiates:
- Breakdown of the blood–aqueous barrier
- Release of inflammatory mediators
- Upregulation of prostaglandin synthesis
Miyake and colleagues demonstrated the central role of prostaglandins in post-operative macular thickening.²
Prostaglandins increase vascular permeability in perifoveal capillaries. Fluid accumulates within the outer plexiform and inner nuclear layers, producing the characteristic cystic spaces seen on OCT.³
This is biochemical permeability, not mechanical injury.
2. Breakdown of the Blood–Retinal Barrier
Inflammatory cytokines disrupt tight junctions within retinal microvasculature, permitting plasma leakage into the macular interstitium.⁴
In most eyes, inflammatory signalling downregulates and the barrier re-stabilises.
In susceptible eyes, permeability persists.
Persistence produces clinically significant oedema.
3. Why Certain Eyes Are More Vulnerable
Diabetes
Chronic hyperglycaemia causes microvascular fragility and endothelial dysfunction.⁵ Cataract surgery in diabetics carries higher rates of macular oedema.⁶ ⁷
Epiretinal Membrane (ERM)
Altered vitreomacular interface mechanics may amplify inflammatory tractional stress.⁸
Uveitis / Systemic Inflammatory Disease
Pre-existing immune activation primes exaggerated post-operative response.⁹
Increased inflammatory load and vitreous disturbance increase mediator diffusion.¹⁰
Large database studies estimate:
- 1–2% incidence in routine populations¹¹–¹³
- Significantly higher rates in diabetics and ERM patients⁶–⁸
- Subclinical OCT-detected thickening considerably more common¹³
CMO is therefore biology expressing vulnerability.
What Patients Experience
Clinically significant CMO typically presents 4–8 weeks after surgery.¹²
Symptoms include:
- Blurred central vision
- Reduced clarity or haze
- Slower-than-expected recovery
With treatment, anatomical resolution is common and long-term visual prognosis is generally favourable.¹²
However, in private practice, extended recovery of 2–3 months can significantly affect perception of success.
Prevention is not only anatomical, it is experiential.
The Real-World Impact of CMO
CMO is often discussed as a retinal event.
In practice, its impact extends further.
1. Prolonged Visual Recovery
CMO frequently results in:
- 6–12 weeks of delayed visual rehabilitation
- Extended steroid and NSAID therapy
- Additional OCT surveillance
- Repeated reassurance consultations
Most cataract and refractive lens patients expect rapid clarity within days.
Delayed recovery becomes the defining feature of the surgical experience.
Patients remember duration more than mechanism.
2. Psychological Impact and Disappointment
CMO commonly presents after an initial improvement phase.¹²
That pattern can create:
- Sudden unexpected deterioration
- Confusion and reduced confidence
- Concern that surgery has “failed”
Even when prognosis is favourable, emotional impact may exceed clinical severity.
Perception influences trust.
3. Bilateral Surgery - Susceptibility is Often Patient-Level
Inflammatory vulnerability is not eye-specific, it reflects retinal biology.
In susceptible individuals, risk may extend to both eyes.
In bilateral sequential surgery practice, CMO in one eye:
- Increases anxiety before second-eye surgery
- May necessitate intensified prophylaxis
- Raises concern about recurrence
The single audited CMO case at Blue Fin Vision® occurred in the second eye of a patient who had developed CMO in the first eye elsewhere, reinforcing the concept of patient-specific inflammatory susceptibility.
CMO is rarely random.
It is often constitutional.
4. Higher Incidence in Complicated Cases
Complicated surgery, particularly posterior capsule rupture, increases inflammatory mediator diffusion and macular oedema risk.¹⁰
Greater inflammatory burden predicts greater permeability.
Mechanistic reasoning and clinical data align.
5. Referral Ecosystem Impact
Private ophthalmology depends on referral networks:
- Friends
- Family
- Professional peers
- Community optometrists
When recovery is smooth, patients become ambassadors.
When recovery is prolonged, even temporarily, referral confidence can weaken.
Patients experiencing extended inflammation may:
- Delay recommending surgery
- Seek alternative providers for relatives
- Attribute prolonged recovery to surgical quality rather than inflammatory biology
In bilateral surgical environments, risk becomes relational rather than isolated.
CMO therefore carries:
- Clinical cost
- Emotional cost
- Referral cost
Prevention protects vision, and trust.
Anti-Inflammatory Strategy: Why Pharmacology Matters
Steroids
Broad suppression of inflammatory cytokine pathways.
NSAIDs
Inhibition of cyclooxygenase and prostaglandin synthesis, the principal drivers of vascular leakage.²
Systematic reviews and meta-analyses demonstrate that combination steroid + NSAID therapy reduces pseudophakic CMO more effectively than steroid monotherapy.¹⁴–¹⁷
Synergy is mechanistically logical.
The ESCRS PREMED Trials
The ESCRS PREMED randomised controlled trials confirmed:
- Reduced macular thickening with combined prophylaxis
- Additional benefit in diabetic patients
- Clinical relevance of prostaglandin inhibition¹⁸ ¹⁹
Evidence reinforces biology.
The Structured Prevention Protocol at Blue Fin Vision®
1. Universal Pre-Operative Macular OCT
Every patient undergoes macular OCT.
OCT screening identifies occult pathology not evident clinically.²⁰
Risk identification precedes prevention.
2. Sustained Six-Week Combination Therapy
All patients receive:
- Topical corticosteroid
- Topical NSAID
- Continued for six weeks
Higher-risk eyes may require extended therapy.
Inflammation does not respect arbitrary stop dates.
This reflects Level 1 evidence.¹⁴–¹⁹
3. Post-Operative OCT Surveillance
Routine OCT detects:
- Subclinical thickening¹³
- Early recurrence
- Need for therapy adjustment
Measurement underpins transparency.
Audited Outcomes
Across nine audited years:
- 3,215 cataract and refractive lens procedures
- One clinically significant CMO case
- Incidence: 0.03%
In the single case:
- Extended prophylaxis was used
- Oedema developed following cessation of drops
- It resolved upon reinstatement
Withdrawal of prostaglandin suppression permitted permeability to re-emerge.
Published incidence in broader populations is 1–2%.¹¹–¹³
While cross-institution comparison requires caution, structured OCT screening and sustained combination therapy are strongly associated with reduced clinically significant CMO in this audited dataset.
Why Dropless Surgery Is Not Routinely Adopted
Dropless protocols usually rely on subconjunctival triamcinolone without sustained NSAID therapy.²¹
Mechanistically:
- Steroids suppress broadly
- NSAIDs suppress prostaglandins specifically
Removing sustained NSAID therapy removes targeted permeability suppression.¹⁴ ¹⁶
Depot steroid cannot be tapered and may increase steroid-induced IOP risk.²²
Macular protection takes precedence over convenience.
The Rare Corneal Melt Discussion
NSAID-associated corneal melt is described in rare case reports.²³–²⁵
Typically associated with:
- Ocular surface compromise
- Systemic inflammatory disease
Incidence is extremely low relative to the frequency of use.
Risk must be evaluated proportionally.
Conclusion
Cystoid macular oedema is:
- A prostaglandin-mediated inflammatory permeability event
- More common in biologically susceptible eyes
- Influenced by surgical complexity
- Preventable through structured pharmacologic strategy
It affects:
- Anatomy
- Recovery timelines
- Patient confidence
- Referral ecosystems
The PREMED trials and multiple meta-analyses support combination steroid + NSAID prophylaxis.¹⁴–¹⁹
Across 3,215 audited procedures at Blue Fin Vision®, structured OCT risk assessment and sustained combination therapy have correlated with a 0.03% clinically significant CMO incidence.
Inflammation drives permeability.
Prostaglandins drive leakage.
Suppression reduces risk.
Structured prevention protects vision, and experience.
FAQ
How common is CMO after cataract surgery?
Large studies report approximately 1–2% clinically significant incidence in general populations.¹¹–¹³ Higher in diabetics and complex cases.
When does CMO usually occur?
Typically 4–8 weeks after surgery.¹²
Does it affect both eyes?
In biologically susceptible individuals, risk may involve both eyes, particularly in bilateral surgery settings.
Is it preventable?
Risk can be significantly reduced with combination anti-inflammatory therapy and OCT surveillance.¹⁴–¹⁹
Why not offer dropless surgery routinely?
Sustained prostaglandin suppression via NSAIDs has strong evidence in reducing macular oedema risk.¹⁴ ¹⁶
Are NSAIDs safe?
Rare corneal complications are reported in high-risk surfaces but incidence is extremely low.²³–²⁵
References
- Irvine SR. A newly defined vitreous syndrome following cataract surgery. Am J Ophthalmol. 1953;36(5):599-619.
- Miyake K, Ibaraki N. Prostaglandins and cystoid macular edema. Surv Ophthalmol. 2002;47(Suppl 1):S203-S218.
- Gharbiya M, Grandinetti F, Scavella V, et al. Correlation between optical coherence tomography measurement and fluorescein angiography in cystoid macular edema. Invest Ophthalmol Vis Sci. 2007;48(9):3763-3770.
- Cunha-Vaz JG. The blood–retinal barrier in the management of retinal disease. Ophthalmologica. 2017;237(1):1-10.
- Romero-Aroca P. Managing diabetic macular edema. World J Diabetes. 2011;2(6):98-104.
- Dowler JGF, Hykin PG, Hamilton AM. Phacoemulsification versus extracapsular cataract extraction in patients with diabetes. Ophthalmology. 2000;107(3):457-462.
- Eriksson U, Alm A, Bjarnhall G, et al. Macular edema and visual outcome following cataract surgery in diabetics. Acta Ophthalmol. 2011;89(5):408-413.
- Hayashi K, Hirata A, Hayashi H. Changes in macular thickness after cataract surgery in eyes with ERM. Ophthalmology. 2012;119(10):1869-1875.
- Belair ML, Kim SJ, Thorne JE, et al. CMO after cataract surgery in uveitis. Ophthalmology. 2009;116(3):519-526.
- Packer M, Chang DF, Dewey SH, et al. Complications of phacoemulsification in 20,000 cases. J Cataract Refract Surg. 2005;31(1):88-95.
- Henderson BA, Kim JY, Ament CS, et al. Clinical pseudophakic CMO risk factors. J Cataract Refract Surg. 2007;33(9):1550-1558.
- Lobo C. Pseudophakic cystoid macular edema. Ophthalmologica. 2012;227(2):61-67.
- Chu CJ, Johnston RL, Buscombe C, et al. Risk factors and incidence of macular edema after cataract surgery. Ophthalmology. 2016;123(2):316-323.
- Kessel L, Tendal B, Jørgensen KJ, et al. Steroid and NSAID prevention after cataract surgery. Ophthalmology. 2014;121(10):1915-1924.
- Almeida DRP, Johnson D, Hollands H, et al. Prophylactic NSAIDs meta-analysis. Clin Ophthalmol. 2012;6:185-194.
- Wielders LHP, Lambermont VA, Schouten JSAG, et al. NSAIDs for prevention of macular edema. Ophthalmology. 2015;122(11):2450-2462.
- Alqahtani AS, Hersi RM, Alharbi AA, et al. Prophylactic regimens for the prevention of pseudophakic cystoid macular edema: systematic review and meta-analysis. Int J Retina Vitreous. 2024;10(1):73.
- Wielders LHP, Schouten JSAG, Winkens B, et al. ESCRS PREMED Study Report 1. Ophthalmology. 2018;125(2):195-204.
- Wielders LHP, Schouten JSAG, Winkens B, et al. ESCRS PREMED Study Report 2. Ophthalmology. 2018;125(12):1955-1963.
- Ewe SY, Abell RG, Vote BJ, et al. Detection of macular pathology with OCT before cataract surgery. Eye (Lond). 2015;29(9):1216-1222.
- Lindholm JM, Kivelä TT, Laatikainen L, Tuuminen R. Subconjunctival triamcinolone for CMO prevention. Acta Ophthalmol. 2017;95(3):276-281.
- Shorstein NH, Liu L, Waxman MD, Herrinton LJ. Comparative prophylactic strategies after phacoemulsification. J Cataract Refract Surg. 2015;41(10):2002-2014.
- Guidera AC, Luchs JI, Udell IJ. Corneal melt associated with topical NSAIDs. Ophthalmology. 2001;108(5):936-944.
- Pfister RR, Paterson CA. Corneal melts and topical NSAIDs. Cornea. 1995;14(1):3-10.
- Ting DSJ, Ghosh S. Acute corneal melt after cataract surgery associated with NSAIDs. Eye (Lond). 2018;32(3):553-555.
Related Topics
Understanding CMO and Risk Factors
Prevention and Treatment
- The PREMED Study: What It Means for Your Eye Drops
- Why We Use Both Steroid and NSAID Drops After Surgery
- Dropless Cataract Surgery vs Traditional Drops: Our View on Macular Safety
- Our Macular Oedema Prevention Protocol at Blue Fin Vision®
- Rare Corneal Melt with NSAID Drops: How We Balance Risk and Benefit
- Second-Eye Surgery After Previous CMO: How We Plan and Protect the Macula
Symptoms and Recovery
Screening, Outcomes and Transparency
Practice and Referral Impact
Schedule Your Consultation Today
If you are considering cataract or lens replacement surgery and want to understand how your eyes will be assessed and protected, speak with the team at Blue Fin Vision® across London, Hertfordshire, and Essex.
