Diabetic retinopathy and screening

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

Diabetic retinopathy is a complication of prolonged metabolic injury to the retinal microcirculation. Its clinical importance lies in two partly independent processes: inadequate perfusion drives abnormal new vessels, while leakage damages the macula. An eye can have substantial peripheral ischaemia with preserved reading vision, or disabling macular oedema without proliferative disease. A useful assessment therefore records retinopathy grade, macular involvement, acuity and the condition of the vitreoretinal interface separately.

Screening detects risk in people who may feel entirely well; hospital eye services investigate and treat disease that has crossed referral thresholds. These are connected services, with different recall rules and responsibilities. A screening photograph is not a comprehensive optometric examination and a satisfactory screening result does not exclude cataract, glaucoma or a new retinal tear. Explain which service is responsible for the next appointment and make that responsibility explicit after treatment or discharge.

Key points

Retinopathy may be advanced while central acuity remains good; screening therefore depends on retinal assessment rather than symptoms.
England invites people with type 1 or type 2 diabetes from age twelve; two consecutive negative routine screens permit a two-year interval.
Microaneurysms and haemorrhages reflect vascular injury; new vessels on the disc or elsewhere identify proliferative disease.
Assess each eye for both retinopathy severity and macular oedema because these can require different treatments concurrently.
NICE usually starts proliferative disease treatment with panretinal photocoagulation, with same-day initiation offered for high-risk features or attendance difficulties.
Coordinate planned rapid substantial HbA1c improvement with ophthalmology so baseline and subsequent retinal assessment accompany metabolic treatment.

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

Metabolic exposure

Longer diabetes duration and sustained hyperglycaemia increase microvascular injury. Blood pressure and renal disease influence risk, while an individual's retinal appearance cannot be predicted from a single recent HbA1c result.

Changing physiological demands

Pregnancy and rapid substantial improvement in glycaemia can alter the short-term course of established disease. They create a need for coordinated retinal monitoring rather than an assumption that previously stable photographs remain representative.

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

1
Barrier breakdown
Injured capillary endothelium and supporting cells permit leakage into the retina. Fluid and lipid accumulation near the fovea disrupt the precise architecture needed for central visual resolution.
2
Capillary closure
Loss of perfused retinal capillaries creates tissue hypoxia. Ischaemic retina releases signals including VEGF that encourage fragile new vessels on the retinal surface or optic disc.
3
Vitreoretinal contraction
Neovascular tissue grows with a fibrous component. Subsequent contraction can distort or detach the retina, while fragile vessels bleed and obscure the clinician's view of the underlying traction.

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

Early vascular lesions

Microaneurysms are small focal capillary outpouchings; dot and blot haemorrhages and hard exudates suggest vascular damage and leakage. These findings can be asymptomatic. Their number, distribution and change over time matter more than a single isolated lesion.

Increasing non-proliferative severity

Widespread haemorrhages, venous abnormalities and intraretinal microvascular abnormalities suggest increasing retinal non-perfusion. Intraretinal vascular remodelling is not the same as new vessels growing into the vitreous. Severe disease warrants closer hospital surveillance even without a symptomatic macular problem.

Proliferative retinopathy

New vessels on the disc or elsewhere are fragile and can bleed into the vitreous. Associated fibrous tissue may contract, pulling the retina away from its normal position. The absence of pain does not indicate a low risk of permanent visual loss.

Macular involvement

Central blur, reading difficulty or distorted straight lines raises concern for diabetic macular oedema, although cataract and refractive change can contribute. Examine the macula and obtain OCT rather than inferring the cause of reduced acuity from peripheral haemorrhages alone.

Red flags requiring action

New vitreous haemorrhage, a progressive field curtain or rapidly falling acuity requires urgent retinal assessment because tractional detachment may threaten the macula.
Painful redness after an intravitreal injection needs immediate contact with the emergency eye service to exclude endophthalmitis.

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
History and monocular visual functionFirst step
Why
Establish the time course and the functional effect in each eye before interpreting photographs.
Interpretation and limitations
Record corrected acuity, new floaters, distortion, field symptoms, previous laser or injections, pregnancy plans and current diabetes treatment. Sudden loss overrides routine recall arrangements. Good acuity can coexist with a peripheral proliferative lesion.
02
Dilated retinal examination and retinal imaging
Why
Determine non-proliferative or proliferative disease and identify haemorrhage, traction and other pathology.
Interpretation and limitations
NICE advises considering ultrawide-field imaging alongside clinical examination when assessing proliferative disease. Images complement an examination; poor image quality or obscured retina requires an alternative assessment rather than a normal screening label.
03
Optical coherence tomography of the macula
Why
Identify retinal thickening, fluid and traction that explain central symptoms and influence treatment.
Interpretation and limitations
OCT is recommended when assessing for diabetic macular oedema. Centre involvement, visual impairment and thickness guide treatment selection together. A thickness value alone does not establish visual prognosis or the cause of every cystic space.
04
Systemic and treatment information
Why
Coordinate retinal decisions with glucose, blood pressure, renal function and medication safety.
Interpretation and limitations
Obtain recent HbA1c and blood pressure results and identify kidney disease. Alert ophthalmology before a treatment expected to cause a rapid substantial HbA1c fall. This supports closer eye assessment and does not justify withholding necessary diabetes care indefinitely.

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

Retinal vein occlusion

A venous occlusion may produce haemorrhage and oedema in a characteristic sector or across one retina. The venous distribution and asymmetry should prevent automatic attribution to diabetes.

Hypertensive injury

Marked blood pressure elevation can cause haemorrhages, cotton-wool lesions and optic-disc swelling. Measure blood pressure and recognise the need for same-day medical assessment when severe hypertension accompanies acute retinal injury.

Non-retinal blur

Cataract, ocular surface disease and changing refraction can reduce acuity without explaining retinal lesions. More than one cause may coexist, so treating the fundus does not guarantee resolution of every visual complaint.

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

01ScreeningMaintain the correct surveillance routeFirst stepThe person has diabetes and no new symptom requiring acute assessment.

1Confirm screening registration from age twelve and establish whether recall is annual, two-yearly or a shorter surveillance appointment.
2In England, explain that a two-year interval follows two consecutive routine screens without retinopathy; other results follow their designated pathway.
3Continue ordinary eye examinations for other causes of visual impairment and give a clear route for reporting new symptoms between screens.

02TreatmentTreat proliferative disease promptlyNew vessels are confirmed on specialist retinal assessment, with or without reduced acuity.

1Offer panretinal photocoagulation at first diagnosis and discuss expected benefit, peripheral or night-vision effects and the consequences of declining treatment.
2Start within four weeks of offering if possible, within six weeks if four is not possible, and complete within four weeks of starting.
3Offer to start on the same day for high-risk characteristics or likely attendance difficulty; arrange practical support rather than simply labelling the person non-adherent.
4If disease remains active after complete laser, offer anti-VEGF therapy; traction requires close collaboration with a vitreoretinal specialist.

03EscalationAddress haemorrhage, traction and concurrent oedemaEscalationVitreous blood, retinal traction or macular fluid complicates the treatment plan.

1Consider temporary anti-VEGF treatment when vitreous haemorrhage or a dense cataract prevents panretinal laser, with specialist surveillance of traction.
2Offer vitrectomy for macula-involving or macula-threatening detachment; consider it for vitreous haemorrhage that has not cleared within three months.
3Assess and treat clinically significant macular oedema as a separate active pathology while optimising systemic vascular risk and retaining surveillance for neovascularisation.

Key medicines and prescribing safety1 treatment · regimens, roles and cautions

A specialist anti-VEGF option for appropriately selected retinal neovascularisation or diabetic macular leakage.

Ranibizumab, Lucentis 10 mg/mL

For an adult selected for treatment of proliferative retinopathy or diabetic macular oedema, inject 0.5 mg in 0.05 mL intravitreally. Begin monthly treatment until maximum acuity and/or absence of disease activity; three or more consecutive monthly doses may be needed. Never inject the same eye less than four weeks apart; subsequently individualise intervals and stop if continued treatment provides no benefit.

Exclude ocular or periocular infection and severe active intraocular inflammation. Review traction, pressure, recent stroke or TIA and the ability to attend. Monitor for infection and pressure rise after injection. Avoid pregnancy unless benefit outweighs risk; wait at least three months after the last dose before planned conception. Breastfeeding is not recommended during Lucentis treatment.

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

Macular visual impairment

Oedema, ischaemia and structural damage can impair reading and face recognition. Anatomical improvement after treatment does not always restore function when photoreceptors or capillary perfusion have been permanently damaged.

Vitreous haemorrhage and detachment

Bleeding can cause sudden obscuration and may conceal a tractional detachment. Ultrasound and vitreoretinal assessment may be needed when a clear view of the retina is unavailable.

Anterior segment neovascularisation

Severe retinal ischaemia can promote new vessels on the iris and drainage angle, leading to painful pressure elevation. This requires urgent specialist treatment alongside control of the retinal ischaemic stimulus.

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

For untreated moderate non-proliferative disease in hospital care, NICE suggests review every six to twelve months; severe or very severe disease generally warrants three-to-six-month review, adjusted to the individual eye.
After treatment for proliferative disease, assess regression two to three months after completion. Continue hospital monitoring for the first twelve months after treatment even when the disease has regressed.
After that first year, return to the screening programme only if eligible and after a clear handover; an eye unsuitable for screening still needs hospital surveillance, often around yearly.
Check practical ability to attend injections and laser, changes in visual function, systemic risk management and psychological impact. A missed high-risk appointment needs active follow-up because the patient may not notice progression.

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

Rapid glucose improvement

A large early fall in HbA1c can coincide with short-term worsening of existing retinopathy. The clinical response is coordinated eye assessment before and after the change, while preserving the long-term benefits of glucose management. Communication is especially important when several teams prescribe independently.

Fenofibrate consideration

NICE advises ophthalmologists to consider fenofibrate for non-proliferative retinopathy in type 2 diabetes. Discuss its off-label retinal indication, renal function, liver monitoring and muscle toxicity with concurrent statins. The exact formulation and renal-adjusted regimen should be agreed with the prescribing team; it does not replace retinal surveillance.

Pregnancy changes surveillance

Pre-existing diabetes requires pregnancy-specific retinal assessment, with additional review when retinopathy is present. Tell both maternity and eye teams promptly about pregnancy. Gestational diabetes alone does not imply the same established-retinopathy screening programme, and treatment choices must account for fetal exposure.

Treatment and visual independence

Panretinal laser may protect sight while reducing peripheral or night function. Discuss driving, mobility and occupational implications before treatment, without presenting these possible effects as a reason to leave dangerous neovascularisation untreated. Low-vision support can help even while active retinal treatment continues.

11Common pitfallsFrequent interpretation and management errors.

01
Do not substitute a normal reading chart result for a retinal examination: the proliferative process can initially spare central vision.
02
Do not describe all diabetic haemorrhages as proliferative disease; the defining finding is pathological neovascularisation, with specialist interpretation when appearances are uncertain.
03
Avoid postponing a new field curtain or vitreous haemorrhage until the next routine screen; acute symptoms need a separate urgent assessment.
04
Do not stop follow-up immediately after successful laser or a dry OCT, because recurrence and other diabetic retinal complications remain possible.