Macular oedema

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

The macula supports detailed central vision. When vascular leakage or impaired fluid handling causes fluid to accumulate within its layers, vision may become blurred, distorted or less sensitive to contrast. Cyst-like spaces on an OCT image describe morphology; they do not establish whether the process is diabetic, inflammatory, postoperative or associated with a vascular occlusion. The same scan thickness can have different implications in two patients.

A useful assessment links the time course with retinal findings and previous care. Ask about diabetes, recent cataract or other intraocular surgery, retinal vein occlusion, inflammatory eye disease and previous injections. Establish whether vision never recovered after surgery or improved and then deteriorated. Compare with preoperative imaging where available, because pre-existing diabetic oedema can coexist with a postoperative inflammatory component.

Treatment aims to preserve useful vision while controlling the process producing fluid. Reducing thickness is informative but is not the only outcome. Macular ischaemia, photoreceptor damage, cataract or traction may limit visual recovery after the oedema improves. Explain uncertainty before escalating treatment, and agree how response and adverse effects will be assessed.

Key points

Macular oedema is a finding with a cause, not a single interchangeable treatment indication.
Assess both central visual function and the distribution of fluid on OCT.
Diabetes, retinal vein occlusion, postoperative inflammation and uveitis are important causes.
Central retinal thickness thresholds used in diabetic guidance should not be imposed on postoperative oedema.
Topical steroid and NSAID treatment can be appropriate for postoperative oedema, whereas other causes may need intravitreal treatment.
Steroid therapy requires attention to pressure, infection, lens status and corneal safety.
Persistent fluid should prompt reassessment of cause, adherence and mechanical traction before repeated escalation.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Retinal vascular leakage

Diabetic microvascular injury and retinal vein occlusion disturb capillary function. Their distribution, perfusion changes and accompanying retinal signs help identify why the macula is accumulating fluid.

Inflammatory and postoperative disease

Inflammatory mediators after intraocular surgery or during uveitis can impair retinal barrier function. Pre-existing vascular disease may coexist and complicate attribution of the oedema.

Mechanical contributors

Vitreomacular traction or an epiretinal membrane can distort retinal architecture and contribute to cystic change. Mechanical disease may persist despite control of vascular leakage.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Barrier dysfunction
Leakage across retinal vascular or pigment epithelial barriers allows fluid to accumulate in retinal tissue. VEGF and inflammatory signalling contribute to different degrees across the underlying disorders.
2
Central architectural disruption
Intraretinal fluid separates and distorts the structures needed for detailed vision. Centre involvement can therefore impair reading even when the surrounding retina remains relatively functional.
3
Persistent tissue injury
Longstanding oedema may coexist with photoreceptor damage and macular ischaemia. Removing fluid cannot reliably reverse all structural injury, explaining discordance between anatomical and visual improvement.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Describe central symptoms

Ask about reading, straight lines appearing bent, a blurred central patch and difficulty recognising faces. Test each eye separately. Bilateral disease may become apparent only when one eye is covered, while the absence of pain does not establish a benign cause.

Identify the retinal context

Diabetic microvascular lesions, a sector of haemorrhages after branch vein occlusion, widespread venous changes or inflammatory signs can identify the likely driver. A clear anterior segment does not exclude posterior disease; dilated assessment and imaging may still be necessary.

Recognise postoperative risk

Complicated surgery, prior postoperative oedema in the fellow eye, retinal vein occlusion and diabetic macular disease increase concern. The 2026 RCOphth guidance recommends targeted examination and OCT at three to eight weeks when recovery is unsatisfactory or recognised risk factors are present.

Assess treatment feasibility

A prolonged drop regimen requires adequate dexterity, comprehension and reliable supply. Injections require repeated attendance and aftercare. Ask specifically about difficulties before labelling an apparently unresponsive patient as having treatment-resistant disease.

Red flags requiring action

Painful visual deterioration after ocular surgery or an injection needs urgent assessment for endophthalmitis or another complication.
New macular haemorrhage or distortion can indicate active neovascular AMD and needs its urgent referral pathway.
New peripheral field loss, a curtain or numerous flashes and floaters suggests retinal pathology beyond isolated macular swelling.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Monocular acuity and macular OCTFirst step
Why
Characterise central visual loss and the location of retinal fluid.
Interpretation and limitations
Document centre involvement, thickness, intraretinal cysts, subretinal fluid and traction. Check scan quality and compare with previous images. In diabetic disease, acuity and centre involvement modify how thickness thresholds guide treatment.
02
Dilated slit-lamp and retinal examination
Why
Find the cause and identify concurrent ocular pathology.
Interpretation and limitations
Assess inflammatory activity, haemorrhage pattern, retinal vessels and lens status. A postoperative patient with pain or significant inflammation requires assessment for infection rather than automatic escalation of steroid drops.
03
Intraocular pressure and treatment safety assessment
Why
Establish risk before corticosteroids and monitor adverse effects.
Interpretation and limitations
A previous steroid response, advanced glaucoma or capsule and lens abnormalities can influence route and product choice. Normal baseline pressure does not remove the need for subsequent pressure checks.
04
Angiography and systemic investigations when indicated
Why
Resolve uncertainty about leakage, perfusion or the underlying disorder.
Interpretation and limitations
Specialist fluorescein angiography can clarify leakage and ischaemia where this changes care. Check diabetic or vascular control when relevant; broad inflammatory or thrombophilia panels are not necessary for every patient with macular fluid.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Macular neovascularisation

New central distortion, subretinal fluid or haemorrhage may represent active neovascular disease rather than isolated diabetic or postoperative oedema. Age, examination and additional imaging guide classification.

Vitreomacular interface disease

An epiretinal membrane or vitreous traction may produce distortion and cyst-like spaces. OCT can demonstrate a mechanical relationship that affects treatment selection.

Additional chapter-specific clues

Look for alternative explanations

An epiretinal membrane, vitreomacular traction, neovascular disease or chronic degenerative cavities may change the interpretation of an apparently oedematous scan. Review scan slices and clinical findings rather than accepting the machine-generated thickness map as the diagnosis.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Diabetic diseaseChoose treatment by centre involvement and visionFirst stepOCT confirms diabetic macular oedema and the retinal team has assessed visual function.

1Offer macular laser for non-centre-involving clinically significant oedema, while addressing systemic risk factors alongside retinal care.
2For centre-involving oedema with good vision, defined by NICE as at least 79 ETDRS letters, consider macular laser or observation.
3For centre-involving oedema with visual impairment and central thickness at least 400 micrometres, offer anti-VEGF treatment.
4When centre-involving oedema impairs vision but thickness is below 400 micrometres, consider either anti-VEGF or macular laser; the lower measurement does not exclude injections.
5Assess response after loading, consider adjuvant laser for a suboptimal response, and review longer-term alternatives including steroid or traction-directed surgery when appropriate.

02Postoperative diseaseTreat confirmed postoperative inflammatory oedemaAssessment identifies postoperative macular oedema without infection or another explanation requiring a different pathway.

1Refer to the original surgical provider where possible, aiming for assessment within two weeks and no later than four weeks for uncomplicated postoperative oedema.
2Use a potent topical steroid, such as prednisolone acetate 1%, three to four times daily together with an NSAID eye drop for eight to twelve weeks from diagnosis under ophthalmic supervision.
3Arrange review of acuity, OCT, adherence, ocular surface and pressure; do not leave prolonged corticosteroid treatment without monitoring.
4EscalationIf improvement remains insufficient after eight to twelve weeks, offer periocular steroid injection; earlier escalation may be justified when there is no improvement.
5If periocular treatment is unsuitable, insufficient or followed by recurrence, consider an intravitreal steroid after assessing glaucoma, lens and capsule risks.

03Other causesMatch treatment to vascular or inflammatory diseaseMacular oedema occurs with vein occlusion, uveitis or a possible mechanical retinal abnormality.

1For vein-occlusion oedema, discuss the appropriate anti-VEGF or steroid option and continue surveillance for ischaemic neovascular complications independently of macular dryness.
2For inflammatory oedema, assess whether infection or systemic inflammatory disease changes treatment before using immunosuppressive therapy.
3Review OCT for vitreomacular traction or an epiretinal membrane where medical treatment has not produced the expected response.
4Explain what improvement is achievable when ischaemia or structural damage contributes to poor vision, and offer visual support alongside treatment.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

Suppresses the postoperative inflammatory component when combined with an appropriate topical NSAID.

Prednisolone acetate 1% eye drops, postoperative oedema example

An ophthalmologist may prescribe one drop into the affected eye four times daily as the potent steroid component of the RCOphth eight-to-twelve-week postoperative oedema regimen, then adjust or taper according to response.

Shake the suspension and supervise this prolonged course with regular pressure checks; the SmPC requires strict ophthalmic supervision beyond ten days. Exclude untreated ocular infection, especially epithelial herpes, and consider corneal thinning, delayed healing and steroid-induced glaucoma.

An NSAID drop option alongside a potent steroid for postoperative inflammatory macular oedema.

Ketorolac 0.5% eye drops, Acular

For established postoperative macular oedema, the RCOphth pathway supports ketorolac 0.5%, one drop into the affected eye three or four times daily, alongside a potent steroid for eight to twelve weeks from diagnosis under specialist supervision. This prolonged treatment is off label. The Acular licensed postoperative-inflammation course is one drop three times daily from 24 hours before surgery for up to three weeks afterwards.

Avoid with aspirin or NSAID hypersensitivity; assess asthma, ocular surface disease and corneal healing. Prolonged use with steroid can increase corneal complications. Separate other eye drops by at least five minutes. It is not recommended in pregnancy and should not be used while breastfeeding.

A sustained ocular corticosteroid option for selected diabetic, vein-occlusion or non-infectious posterior inflammatory disease and specialist refractory postoperative care.

Dexamethasone intravitreal implant, Ozurdex

A trained ophthalmologist administers one 700-microgram implant into the affected eye. Re-treatment depends on the licensed indication, response and recurrence; it is not an automatic monthly course. Use for refractory postoperative oedema is off label.

Avoid ocular infection and advanced glaucoma uncontrolled by medicines. Contraindications include aphakia with a ruptured posterior capsule, and specified anterior-chamber or iris/transscleral-fixated lenses with capsule rupture. Other capsule defects can still increase migration risk. Monitor pressure, cataract, infection and retinal complications.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Persistent central visual impairment

Chronic fluid and underlying vascular or inflammatory damage can leave lasting difficulty with reading and detailed tasks, even after the retina becomes anatomically drier.

Treatment-related pressure elevation

Topical, periocular and intravitreal corticosteroids may raise intraocular pressure. A pressure response can threaten the optic nerve and influence future treatment choices.

Procedure and ocular-surface harm

Intravitreal treatment carries infection and retinal injury risks, while prolonged topical therapy can impair corneal healing. The relevant complications depend on the selected route and medicine.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Measure change in acuity, distortion and reading function alongside OCT fluid rather than treating an isolated number as the complete outcome.
During prolonged steroid drops or after steroid injection, arrange pressure and ocular-surface assessment; escalating pain or declining sight requires earlier examination.
After diabetic oedema resolves, NICE recommends hospital monitoring for twelve months, followed by a decision about return to eligible screening or continuing hospital surveillance.
For postoperative disease, reassess at the planned treatment endpoint and earlier if there is no improvement or treatment intolerance; avoid simply renewing drops indefinitely.
Check whether recurrent fluid reflects the expected waning of treatment, missed doses, a new cause or an additional structural problem before selecting the next intervention.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

One threshold does not classify every oedema

The 400-micrometre threshold belongs to a particular NICE diabetic treatment decision. RCOphth does not require that thickness to diagnose clinically relevant postoperative oedema. Symptoms, central involvement and the cause remain essential.

Periocular is a distinct route

For persistent postoperative oedema, the RCOphth pathway offers sub-Tenon's or orbital-floor triamcinolone 40 mg or methylprednisolone suspension 40 mg. These are specialist periocular treatments; preserved triamcinolone is unsuitable for injection into the vitreous.

Anti-VEGF is not a universal fallback

Evidence for anti-VEGF in refractory postoperative oedema is weaker than in diabetic or vein-occlusion disease. RCOphth identifies it as an option when intravitreal steroids are contraindicated, for example in an advanced glaucoma steroid responder.

Licensing and guidance answer different questions

A specialist guideline can support an off-label indication or duration without changing a product's marketing authorisation. Explain the proposed regimen and monitor its particular risks rather than describing a prolonged postoperative oedema course as the routine Acular licence.

A quiet eye may still need review

Macular fluid and pressure elevation can be painless. Conversely, new postoperative pain should not be attributed to oedema without examination. Give safety-net advice based on the direction of symptoms as well as the presumed diagnosis.

11Common pitfallsFrequent interpretation and management errors.

01
Applying diabetic thickness criteria to postoperative oedema or using thickness alone to decide whether vision is affected.
02
Prescribing prolonged steroid drops without checking for infection or arranging intraocular pressure monitoring.
03
Assuming every postoperative visual complaint is macular oedema and missing retinal detachment, endophthalmitis or a refractive problem.
04
Repeating intravitreal treatment without considering ischaemia, traction or irreversible photoreceptor damage.
05
Using a periocular preserved steroid preparation by the intravitreal route or overlooking implant migration risks.