Medically reviewed by Shaun Larsen, OD – Doctor of Optometry, Southern College of Optometry.

Last clinically reviewed: July 2026 | Next scheduled review: July 2027

How this guide differs from our condition atlas. Our main eye disease atlas describes what each condition is. This page answers the next question: how is it graded, what did the scan show, and what does the number on my report mean? If you have been handed an OCT printout, told you have "moderate NPDR" or "intermediate AMD", or given a central subfield thickness in microns, this is the page that explains it.

A note before the images

Retinal photographs illustrate typical presentations. Real disease varies with fundus pigmentation, media clarity, camera field and stage, and a normal-looking photograph does not exclude early glaucoma or diabetic change that only OCT will detect. These images are here to help you understand what your clinician is describing – not to grade your own eyes. Staging determines treatment, and it is done on a dilated examination with imaging, by a clinician.

There are numerous eye diseases that could compromise your vision, with the most prevalent ones including:

Macular Degeneration

Macular degeneration refers to deterioration or breakdown of the macula located within your retina (light-sensitive tissue at the back of your eye). The macula provides central vision that allows for fine details like threading a needle, driving or reading – but when its function stops functioning normally your central vision becomes dim or even blurry, with distortion such as straight lines appearing bent or crooked; it is one of the primary causes of severe vision loss in people over 50.

How AMD is staged

Staging is based on drusen size and pigmentary change, because these predict progression risk. Drusen are measured against the width of a retinal vein at the disc margin, which is approximately 125 µm.

No AMD – no drusen, or only drupelets under 63 µm.

Early AMD – medium drusen, 63–125 µm, without pigmentary abnormality.

Intermediate AMD – large drusen over 125 µm, or medium drusen with pigmentary abnormality. This is the stage at which AREDS2 supplementation has proven benefit.

Late AMD – either geographic atrophy involving the centre, or neovascular (wet) AMD.

Reticular pseudodrusen (subretinal drusenoid deposits) sit above the retinal pigment epithelium rather than beneath it, are best seen on near-infrared reflectance and OCT, and independently raise progression risk. They are easily missed on colour photography alone.

The AREDS Simplified Severity Scale is the tool used to counsel patients on risk. One point is assigned per eye for the presence of large drusen and one for pigmentary abnormality, giving a score of 0–4 across both eyes; five-year risk of progressing to advanced AMD rises steeply with each point, from a few percent at 0 to around 50% at 4. If you have intermediate AMD, this is the number worth asking your clinician for – it is far more informative than being told you have "some macular changes".

Macular degeneration typically presents itself in either its dry or wet forms; typically the former involves yellow protein deposits called drusen slowly building up under the retina, eventually leading to its thinning and weakening over time. Ten to fifteen percent of cases progress into more serious wet form macular degeneration involving abnormal blood vessels growing under retina leaking fluid or blood, accounting for approximately 90% of the severe vision loss attributable to AMD.

Drusen are not blood vessels and they do not leak. They are accumulations of lipid, protein and cellular debris between the retinal pigment epithelium and Bruch’s membrane. Leakage of fluid or blood is the defining feature of the neovascular form, in which new vessels grow from the choroid into or beneath the retina. This distinction is frequently blurred in patient-facing material and it matters, because it separates a condition monitored over years from one that requires treatment within days.

What the OCT scan shows in AMD

Drusen appear as dome-shaped elevations of the RPE band with variable internal reflectivity.

Intraretinal fluid – dark cystoid spaces within the retinal layers. Generally the strongest indicator of active neovascular disease.

Subretinal fluid – a dark space between the neurosensory retina and the RPE.

Pigment epithelial detachment (PED) – elevation of the RPE from Bruch’s membrane, which may be drusenoid, serous or fibrovascular.

Subretinal hyperreflective material – often fibrosis or haemorrhage; a poor prognostic sign when it involves the fovea.

Outer retinal atrophy with choroidal hypertransmission – the signature of geographic atrophy on OCT. Fundus autofluorescence remains the reference standard for measuring GA lesion area.

Central subfield thickness is the number most often quoted from an OCT report – the average retinal thickness in the central 1 mm circle. It is used to track response to treatment, but note that a thickness in the normal range does not by itself mean the disease is inactive: small amounts of subretinal fluid can persist with a normal-looking thickness value, which is why the clinician reads the actual B-scan rather than the number alone.

Treatment, stated precisely, because the previous version conflated two different things. AREDS2 supplementation (500 mg vitamin C, 400 IU vitamin E, 10 mg lutein, 2 mg zeaxanthin, 80 mg zinc, 2 mg copper) is for intermediate dry AMD, or advanced AMD in one eye, where it reduces the risk of progression to advanced disease by roughly 25%. It is not a treatment for established wet AMD, it does not prevent AMD in people who do not have it, and it does not recover lost vision. Products still containing beta-carotene use the superseded formula – beta-carotene was removed because it raised lung cancer risk in smokers and former smokers.

Furthermore, injectable medications like Avastin or Lucentis may help counteract the growth and leakage of abnormal blood vessels; the current anti-VEGF options also include aflibercept 2 mg and 8 mg, brolucizumab, and faricimab, a bispecific antibody targeting both VEGF-A and angiopoietin-2. The newer agents were developed mainly to lengthen the interval between injections rather than to improve peak acuity, because treatment burden is the principal reason real-world outcomes fall short of trial results.

Regimens are individualised – fixed interval, treat-and-observe, or treat-and-extend, in which the interval lengthens while the macula stays dry and shortens when fluid returns. Photodynamic therapy and thermal laser are now reserved for narrow indications such as polypoidal choroidal vasculopathy.

For geographic atrophy, two complement inhibitors – pegcetacoplan (C3) and avacincaptad pegol (C5) – were FDA-approved in 2023 and slow lesion growth. Their limits should be stated plainly: the pivotal trials did not show improvement in visual function, treatment is by ongoing intravitreal injection, and reported risks include intraocular inflammation, increased conversion to neovascular AMD, and rare ischaemic optic neuropathy and retinal vasculitis. Whether the anatomical benefit justifies the burden remains genuinely debated among retina specialists.

Warning signs that require examination within days, not at the next routine visit: new distortion of straight lines, a new central grey or dark patch, or sudden central blurring. Untreated neovascular AMD can destroy central vision within weeks, and vision lost to subretinal scarring does not return.

Keratoconus

Keratoconus is a progressive [corneal dystrophy] that results in blurry vision due to an irregular shape of the cornea, often first noticed during teen or early 20 years but can develop at any age. Strictly it is a corneal ectasia rather than a dystrophy – a progressive biomechanical weakening and thinning of the stroma that allows normal intraocular pressure to bow the cornea into a cone. Initial symptoms may be mild-moderate and correctable with eyeglasses or traditional contact lenses; as the condition worsens, rigid gas permeable (RGP) contacts or hybrid or scleral lenses may become necessary as more surface area of cornea is covered by rigid lenses.

Risk factors: vigorous or habitual eye rubbing (the principal modifiable factor, and strongly linked to atopic disease and obstructive sleep apnoea), atopy – hay fever, asthma, eczema – family history, Down syndrome, and connective tissue disorders including Ehlers–Danlos syndrome. Treating the underlying allergy so the eyes stop itching is a legitimate part of management.

The cornea is a thin transparent layer on the front of your eye that helps focus light onto the retina. When someone has keratoconus, their normally round cornea thins out and bulges into a cone-like shape, preventing light entering their eye from being focused onto their retina correctly, leading to distortion of vision.

How keratoconus is staged and what the numbers mean

The Amsler–Krumeich classification grades severity in four stages using mean keratometry, refractive error, corneal thickness and the presence of scarring – from stage 1 (eccentric steepening, K under 48 D, myopia/astigmatism under 5 D) to stage 4 (K over 55 D, thinnest pachymetry under 200 µm, central corneal scarring). Newer tomography-based indices such as the Belin/Ambrósio deviation value have largely superseded it for detecting early and subclinical disease.

Parameters that appear on your topography report:

Kmax – maximum keratometry, the steepest point on the cornea, in dioptres. The primary parameter used to define progression.

Thinnest pachymetry – the minimum corneal thickness in microns and its location.

Posterior elevation at the thinnest point – frequently the earliest measurable abnormality, which is why anterior-surface-only topography can miss early disease.

Index of surface variance / index of vertical asymmetry – quantify irregularity and inferior steepening.

Progression is defined by change over serial scans, conventionally a documented increase in Kmax with corroborating change in pachymetry or refraction. A single scan cannot establish progression, which is why repeat imaging at defined intervals is standard in younger patients.

Keratoconus can be diagnosed by performing a slit lamp examination and topographical map of the cornea. Scheimpflug tomography adds posterior surface and full pachymetric mapping and is now preferred where available. Your physician will also consider your medical history, family history and symptoms you are experiencing. Teenagers or young adults should notify their ophthalmologist of any changes to their vision such as blurriness and need for frequent eyeglass or contact lens adjustments; failure to treat may lead to more severe visual distortion that requires corneal transplant.

Corneal cross-linking (CXL) is the omission that most needs correcting here, because it is the only treatment shown to halt progression. Riboflavin is applied to the stroma and activated with UV-A light, generating reactive oxygen species that create additional covalent bonds between collagen fibrils and stiffen the tissue. The standard epithelium-off Dresden protocol debrides the central epithelium (riboflavin cannot cross intact epithelium), instils riboflavin, then irradiates at 3 mW/cm² for 30 minutes for a total dose of 5.4 J/cm². Accelerated protocols deliver the same total energy at higher irradiance over less time. A minimum stromal thickness of 400 µm is required to keep the endothelium below its UV damage threshold.

Two things patients consistently misunderstand about CXL: it stabilises rather than restores – modest flattening and acuity gain are common but are not the objective – and timing is the whole point, because it prevents future loss and cannot recover past loss. Documented progression is the trigger; waiting until vision is poor forfeits the benefit. Since CXL became widely available the proportion of keratoconus patients progressing to corneal transplant has fallen substantially.

Visual rehabilitation is a separate track from stabilisation, and runs alongside it: spectacles and soft torics in mild disease, then custom soft keratoconus lenses, corneal RGPs, piggyback and hybrid designs, and scleral lenses, which vault the cornea entirely and land on the conjunctiva – now the mainstay for moderate-to-advanced disease. Intrastromal ring segments regularise selected cones. Deep anterior lamellar or penetrating keratoplasty is reserved for central scarring or contact lens intolerance.

Retinal Detachment

The retina is a layer of light-sensitive tissue located inside your eyeball’s inner backwall and contains millions of photoreceptors that convert light entering your eye into electrical impulses that travel back to your brain and become visual images. When this process happens, vision forms; should the retina detach, this could result in severe loss.

Retinal detachments are medical emergencies that, if left untreated promptly, could lead to permanent blindness. They typically manifest as sudden flashes of light such as cobwebs or curtains moving across your vision; or as an expanding dark shadow encroaching upon central vision (similar to curtains moving).

The symptom triad, stated precisely – because the sentence above merges three distinct symptoms into one: (1) photopsia, brief arcing flashes in the peripheral vision, most noticeable in dim light, caused by vitreous traction on the retina; (2) new floaters, often a sudden shower of small dark specks representing pigment or blood; (3) a progressive peripheral shadow or curtain. Because the retinal image is inverted, a shadow in the upper field corresponds to a detachment in the lower retina.

Macular status is the single strongest predictor of final vision. A macula-on detachment repaired promptly frequently retains excellent acuity; once the macula detaches, outcomes fall substantially and continue to decline with each day of delay. This is why the symptom triad warrants same-day examination rather than a routine appointment.

Detachments often begin with retinal tears that go unrepaired, which allow fluid from vitreous gel to pass through and collect underneath, pulling away from its blood supply and pulling the retina away from its connection with its blood source. Detachment may then take various forms. For instance:

Rhegmatogenous Retinal Detachment – This type is the most prevalent, occurring when a hole or tear allows fluid to pass through and collect underneath the retina, detaching it from its underlying blood supply . It may occur naturally with age or trauma, or due to certain medical conditions like diabetic retinopathy or cataracts. Most breaks arise during posterior vitreous detachment, when the vitreous gel separates from the retina and pulls at points of firm adhesion. Risk factors: age, high myopia, prior cataract surgery, blunt trauma, lattice degeneration, and personal or family history of detachment.

Tractional Retinal Detachment – Caused by scar tissue on the retina’s surface, this form is similar to rhegmatogenous detachment but with one important difference: there is no retinal break. Contracting fibrovascular membranes mechanically pull the retina forward. The dominant cause is proliferative diabetic retinopathy; it is also seen in sickle-cell retinopathy, retinopathy of prematurity, and penetrating trauma.

Exudative (serous) Retinal Detachment – named in the list above but never previously defined. Fluid accumulates beneath the retina from a leaking source, with no break and no traction. Causes include Coats’ disease, choroidal tumours, posterior scleritis, Vogt–Koyanagi–Harada disease, central serous chorioretinopathy, and severe hypertensive or pre-eclamptic choroidopathy. The subretinal fluid characteristically shifts with head position. Treatment is directed at the underlying cause, not at the retina – which is exactly why identifying the mechanism correctly determines management. (Note that Coats’ disease belongs here, not under tractional detachment.)

Repair. Breaks without detachment can often be sealed in clinic with laser retinopexy or cryotherapy. Established rhegmatogenous detachment requires surgery: pneumatic retinopexy for selected superior breaks, scleral buckling, or pars plana vitrectomy with gas or silicone oil tamponade. Primary reattachment succeeds in the large majority of cases; proliferative vitreoretinopathy is the principal cause of failure.

Diabetic Retinopathy

Diabetes can damage the light-sensitive retina at the back of the eye. Damaged vessels bleed or leak fluid, blurring and distorting vision. With advanced diabetic retinopathy, abnormal new blood vessels begin growing on the retina to compensate for those that have closed or bled; eventually these new blood vessels bleed or swell, blocking vision altogether resulting in blindness – leading to detachment from its original position and blindness; diabetic retinopathy being the number one cause of blindness among working-age adults (roughly 20–74 years) in the United States and other high-income countries – therefore regular eye exams with dilation as well as controlling blood sugar is key when living with diabetes.

The severity scale – what "mild", "moderate" and "severe" actually mean

Grading follows the International Clinical Diabetic Retinopathy Severity Scale, derived from the Early Treatment Diabetic Retinopathy Study. These are the terms that appear on your report:

No apparent retinopathy – no abnormalities.

Mild NPDR – microaneurysms only.

Moderate NPDR – more than microaneurysms, less than severe.

Severe NPDR – defined by the 4-2-1 rule: extensive intraretinal haemorrhages in all 4 quadrants, or definite venous beading in 2 or more quadrants, or prominent intraretinal microvascular abnormalities (IRMA) in 1 or more quadrant – with no neovascularisation. A high proportion of these eyes progress to proliferative disease within a year, which is why this grade sharply shortens the follow-up interval.

Proliferative DR – neovascularisation of the disc, retina or iris, and/or vitreous or preretinal haemorrhage.

Diabetic macular oedema is graded separately and can occur at any of the stages above. The decisive distinction is whether it is centre-involving – within the central 1 mm subfield on OCT – because that determines whether treatment is indicated. Note that macular oedema does not cause floaters; floaters in diabetes usually signal vitreous haemorrhage.

Non-proliferative diabetic retinopathy (NPDR) is the initial stage of this disease. Damaged blood vessels swell and leak clear fluid and fats onto the retina, creating deposits which cause reduced or blurred vision. Those yellow deposits are hard exudates – lipid and protein residue left behind after fluid resorbs – and their arrangement in a ring (circinate) pattern indicates a leaking source at the centre. Treatment in this phase typically is not necessary unless vision has already become significantly impaired. The important qualifier: "no treatment needed" does not mean "no monitoring needed". Early and even moderately advanced diabetic retinopathy is entirely asymptomatic, so waiting for symptoms means presenting at the stage where damage is irreversible. When this is the case, laser scatter laser photocoagulation treatment can be conducted. Laser surgery uses laser light to destroy damaged blood vessels, which helps prevent bleeding and scarring of the retina. If bleeding becomes severe, vitrectomy surgery may need to be performed; otherwise keeping glucose levels under control, quitting smoking, and having regular dilated eye exams are the best ways to lessen risk of vision loss.

Current treatment hierarchy: intravitreal anti-VEGF is first-line for centre-involving macular oedema with reduced acuity, and also regresses neovascularisation; corticosteroid implants are an alternative, particularly in pseudophakic eyes; focal/grid laser retains a role for non-centre-involving oedema; panretinal photocoagulation remains the definitive treatment for proliferative disease, ablating ischaemic peripheral retina to lower VEGF drive. PRP costs peripheral field and night vision – a trade patients should be told about – but it durably prevents severe loss and does not depend on indefinite return for repeat injections. Vitrectomy is used for non-clearing vitreous haemorrhage or tractional detachment threatening the macula.

Screening intervals: type 1 diabetes – first dilated examination five years after diagnosis; type 2 – at diagnosis, because retinopathy is often already present; pre-existing diabetes in pregnancy – before conception or in the first trimester, as pregnancy accelerates progression. At least annually thereafter, and more often with established disease.

Macular Edema

Macular edema, the abnormal accumulation of fluid in the central retina that results in blurry vision, is a result of blood-retinal barrier breakdown, allowing proteins and solutes into retinal tissue and leading to fluid accumulation. Recent treatments include using vascular endothelial growth factor blockers or corticosteroids which reduce inflammatory mediators that disrupt it as ways to manage this complication.

Left untreated, macular edema can result in significant [visual impairment] or even blindness. The common mechanism is breakdown of the inner or outer blood–retinal barrier, allowing fluid to accumulate in the extracellular space. Raised intraocular pressure is not a cause of macular oedema. The principal causes are diabetic retinopathy, retinal vein occlusion, uveitis, post-surgical inflammation (Irvine–Gass syndrome after cataract surgery), neovascular AMD, vitreomacular traction and epiretinal membrane, and certain drugs – notably topical prostaglandin analogues in predisposed eyes, latanoprost among them, and taxane chemotherapy.

What it looks like on OCT: intraretinal cystoid spaces (dark, round, mainly in the inner nuclear and outer plexiform layers), subretinal fluid, retinal thickening, and in chronic cases disruption of the ellipsoid zone – the last of which predicts poorer visual recovery even after fluid resolves. In cystoid macular oedema, fluorescein angiography shows the characteristic petalloid leakage pattern radiating from the fovea.

Preventing macular edema requires annual comprehensive dilated eye exams; pregnant women with diabetes should undergo additional exams as directed by their healthcare providers.

Treatment is directed at the cause:

Diabetic macular oedema – intravitreal anti-VEGF first-line for centre-involving disease; corticosteroid implants as an alternative; focal/grid laser for non-centre-involving oedema with discrete leaking microaneurysms.

Vein-occlusion oedema – anti-VEGF or corticosteroid implant.

Uveitic oedema – control the inflammation: topical, periocular, intravitreal or systemic corticosteroid, and steroid-sparing immunomodulation.

Post-cataract (Irvine–Gass) – topical NSAID with corticosteroid; usually self-limiting.

Vitreomacular traction or epiretinal membrane – pars plana vitrectomy with membrane peel, since the cause is mechanical and no drug will relieve traction.

Drug-induced – withdraw the causative agent where possible.

Fluorescein angiography and OCT are diagnostic, not therapeutic. OCT is the tool used to detect, quantify and monitor macular oedema, and central subfield thickness is the metric tracked between visits.

Glaucoma

Glaucoma is an eye disease that affects the optic nerve that transmits visual messages to the brain, and is the leading cause of irreversible blindness worldwide – cataract causes more blindness overall, but cataract-related loss is reversible with surgery, whereas glaucomatous damage is not. It develops due to increased pressure within the eye caused by fluid buildup; often without symptoms and only becoming noticeable once significant vision loss has taken place; that is why having regular eye exams is so essential.

An important correction to that framing: raised intraocular pressure is the principal modifiable risk factor, not the definition of the disease. A substantial proportion of open-angle glaucoma occurs at pressures that never exceed the statistically normal ceiling of 21 mmHg – this is normal-tension glaucoma. Patients reassured that their pressure is fine are sometimes falsely reassured. Conversely, many people with pressures above 21 mmHg never develop glaucoma at all; that is ocular hypertension, a risk state rather than a disease.

Your eyes continuously produce fluid to keep them moist and healthy, which drains out through drainage angles in your eye. However, if the drainage angle becomes blocked or clogged up it can increase intraocular pressure (IOP) leading to an increase in eye internal pressure which leads to glaucoma; damage to optic nerve can then result in permanent vision loss. The fluid in question is aqueous humour, secreted by the ciliary body into the posterior chamber; it is not tear film, and it has no role in keeping the eye surface moist – a distinction worth making because patients frequently conflate the two.

Open-angle glaucoma is the most prevalent form of glaucoma, typically developing slowly without pain or symptoms. Over time, peripheral vision will progressively decline into tunnel vision; if this is your situation it is essential that we meet regularly so we can identify it early and provide preventative treatments.

Closed-angle glaucoma is less common but often progresses much more rapidly than its open counterpart. Here, eye drainage suddenly becomes blocked leading to an exponentially high increase in eye pressure resulting in symptoms like blurry vision, rainbow halos around lights, intense eye pain and nausea and vomiting. Acute angle closure is an ocular emergency requiring same-day treatment – permanent damage can occur within hours. Anyone with this combination of symptoms should attend an emergency department or ophthalmologist immediately. Because the nausea and vomiting can dominate the picture, acute angle closure is sometimes mistaken for a gastrointestinal or neurological problem, delaying diagnosis.

How glaucoma is staged and monitored

Severity is graded on visual field loss, commonly using the Hodapp–Parrish–Anderson criteria (early, moderate, advanced) based on mean deviation and the depth and location of defects. The parameters that appear on your reports:

Mean deviation (MD) – average sensitivity loss across the field in decibels; more negative is worse.

Pattern standard deviation (PSD) – how uneven the loss is. Localised glaucomatous damage raises PSD; diffuse loss from cataract does not.

Visual field index (VFI) – expressed as a percentage of a normal field, used to plot rate of progression over time.

Peripapillary RNFL thickness on OCT – in microns, with sector analysis. Detects structural loss before it becomes measurable on fields.

Vertical cup-to-disc ratio – which must be interpreted relative to disc size, since a large healthy disc has a large physiologic cup. See our separate guide on large optic nerves without glaucoma.

Rate of progression is the number that actually drives management. A person losing 0.2 dB per year and a person losing 2 dB per year need entirely different levels of intervention, and the difference is invisible on any single test. This is why serial testing matters more than any one result, and why keeping monitoring appointments is itself part of treatment.

How to read your imaging report

A short glossary of the terms that appear most often on printouts handed to patients:

OCT (optical coherence tomography) – a cross-sectional scan of the retinal layers at micron resolution. No dye, no radiation, takes seconds.

Central subfield thickness (CST) – average retinal thickness in the central 1 mm circle, in microns. Typically around 250–300 µm in normal eyes, device-dependent. Used to track macular oedema.

Ellipsoid zone (EZ) – a bright band representing photoreceptor inner segment mitochondria. Its integrity is one of the better structural predictors of visual potential.

RNFL – retinal nerve fibre layer. Reported as average and by sector, colour-coded green/yellow/red against a normative database.

GCC or GCL-IPL – ganglion cell complex / ganglion cell–inner plexiform layer. Assesses cell bodies in the macula; often detects damage earlier than RNFL.

FAF (fundus autofluorescence) – images RPE lipofuscin. The reference standard for measuring geographic atrophy.

OCTA – OCT angiography; maps blood flow without dye injection.

FA / ICG – fluorescein and indocyanine green angiography; dye-based, still the standard for characterising leakage and choroidal disease.

On the colour coding: green, yellow and red on OCT reports indicate where your measurement falls against a normative database – they are statistical flags, not diagnoses. Red simply means the value sits outside the range of most people in the reference population. False positives are common in high myopia, large or tilted discs, and eyes with coexisting macular disease, because such eyes are under-represented in normative databases. Always read the flag alongside the actual scan image and your clinical findings.

When to seek care urgently

Same day: sudden painless loss of vision; a curtain or shadow crossing the field; a sudden shower of floaters with flashes; severe eye pain with redness, haloes and nausea; sudden double vision; eye injury or chemical splash; new vision loss with headache, scalp tenderness or jaw pain in anyone over 50 (possible giant cell arteritis – sight- and life-threatening).

Within days: new distortion of straight lines; a new central grey or dark patch; new floaters without flashes; progressive blurring over days.

Routine: gradual blurring over months, night glare, difficulty with small print, changes in colour perception.

References

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