Diabetic and hypertensive retinopathy

• Diabetes and chronic hypertension both damage the retinal microcirculation. Diabetic retinopathy (DR) is a leading cause of preventable vision loss in working-age adults; hypertensive retinopathy marks systemic target-organ damage and can be the first sign of accelerated or malignant hypertension.
• Diabetic retinopathy is screened by retinal examination, because it is silent until late. Guidelines differ on the exact interval, but type 1 diabetes needs a first screen from 5 years after onset, type 2 diabetes needs a screen at diagnosis, and pregnancy needs close retinal follow-up.
• Hypertensive retinopathy is graded at the bedside from fundoscopy: arteriolar narrowing and arteriovenous nicking in mild disease, haemorrhages, exudates and cotton-wool spots in moderate disease, and optic disc swelling in severe disease.
• Retinal detachment is an emergency: flashes, new floaters and a curtain across vision need same-day ophthalmology assessment, and macula-on detachments need surgery within about 24 hours.
• Retinitis pigmentosa is an inherited rod-cone dystrophy: night blindness and peripheral field loss come first, diagnosed by fundus signs, electroretinography and genetic testing.
• Laser (panretinal photocoagulation, focal or grid laser) and intravitreal anti-VEGF drugs are the two main sight-preserving treatments for diabetic retinopathy and diabetic macular oedema; the choice and regimen are set by current retinal guidelines.

By the end of this page you should be able to:

1. Define diabetic retinopathy, hypertensive retinopathy, retinal detachment and retinitis pigmentosa, and tell which is inflammatory, degenerative or neovascular in origin.
2. Grade diabetic retinopathy for screening and referral, using the NHS Diabetic Eye Screening Programme definitions and ETDRS levels, and state when retinopathy becomes referable.
3. Grade hypertensive retinopathy with the Keith-Wagener-Barker and Wong-Mitchell systems and link the grade to systemic blood pressure and end-organ damage.
4. Recognise the presentation, mechanism and urgent management of retinal detachment, including macula-on timing.
5. Explain the inheritance, clinical course, diagnosis and current management of retinitis pigmentosa.
6. Describe the place of laser photocoagulation, intravitreal anti-VEGF therapy and surgery in these diseases, and outline screening programmes (NHS DESP, ICO, AAO).

Diabetic retinopathy (DR) is microvascular damage to the retina caused by chronic hyperglycaemia. It is traditionally split into two broad stages: non-proliferative diabetic retinopathy (NPDR), in which damaged capillaries leak and ischaemia builds, and proliferative diabetic retinopathy (PDR), in which ischaemia drives pathological new vessels that can bleed or pull the retina off. Diabetic macular oedema (DME), thickening of the central retina from leakage, is a separate but overlapping threat to central vision and is classed with the retinopathy in most staging systems. The NHS Diabetic Eye Screening Programme (DESP) uses the categories R0 (no retinopathy), R1 (background), R2 (pre-proliferative, split into lower-risk R2L and higher-risk R2H) and R3 (proliferative, either R3A active or R3S stable treated), plus M0/M1 maculopathy and a photocoagulation category. The AAO Preferred Practice Pattern uses an ETDRS (Early Treatment Diabetic Retinopathy Study) level running from level 10-15 (no apparent retinopathy) through levels 20, 35, 43, 47 and beyond, which maps onto mild, moderate and severe non-proliferative disease and proliferative disease. ^[2]

Hypertensive retinopathy is the retinal manifestation of systemic hypertension: chronic elevation of blood pressure injures the arteriolar wall, produces focal and generalised narrowing, arteriovenous (AV) nicking, haemorrhage, exudation and, in severe disease, optic disc swelling. Hypertensive choroidopathy (with Elschnig spots and Siegrist streaks) and hypertensive optic neuropathy overlap with it, and the whole group is often called hypertensive eye disease. A distinction worth making is between chronic hypertensive retinopathy (grades 1-2), which is largely vascular wall change, and acute moderate or severe disease, which reflects leakage and oedema and carries a much worse systemic prognosis.

Retinal detachment is separation of the neurosensory retina from the retinal pigment epithelium. The three types differ by mechanism. Rhegmatogenous retinal detachment (RRD) follows a full-thickness retinal break and is the commonest type; tractional retinal detachment is pulled by fibrovascular membranes, classically in proliferative diabetic retinopathy; and exudative (serous) retinal detachment occurs when fluid accumulates without a break, as in hypertensive choroidopathy, inflammation or tumour. A posterior vitreous detachment with new retinal breaks can precede an RRD and is the common trigger to look for.

Retinitis pigmentosa (RP) is a group of inherited retinal dystrophies in which rod photoreceptors degenerate first, then cones, producing night blindness, progressive peripheral visual field loss and, later, central vision loss. It is non-syndromic when the eye alone is affected and syndromic when extra-ocular features are present (most commonly hearing loss in Usher syndrome). It is also called rod-cone dystrophy, which describes the order of photoreceptor loss.

Diabetic retinopathy occurs in a large minority of people with diabetes. The AAO notes that only 60% of people with diabetes have the recommended yearly screening for DR, which gives a measure of how commonly screening lapses in real practice. ^[1] DR itself becomes more likely with longer diabetes duration and with poor glycaemic and blood pressure control, and its prevalence rises steeply the longer a person has had diabetes.

Chronic hypertensive retinopathy is common in older adults with high blood pressure. One review cites signs of hypertensive retinopathy in 6 to 15% of non-diabetic adults aged 40 years and older, and says this is likely to be an underestimate because milder changes are often missed. ^[8] Hypertensive eye disease is therefore a common finding in general and specialist clinics rather than a rare disease.

Retinal detachment is uncommon but sight-threatening. The annual incidence of rhegmatogenous retinal detachment is approximately 10 to 18 per 100,000 persons. A Dutch study reported an incidence of 18 per 100,000 people (95% CI 11-19) with a peak incidence of 53 per 100,000 people (95% CI 29-57) between 55 and 59 years of age. Prior cataract surgery was present in 34% of detached eyes, ocular trauma in about 10%, and the rate of bilateral non-traumatic detachment was 1.7%. Fellow-eye risk after a non-traumatic detachment in one eye is increased by about 10%, and a phakic fellow eye after pseudophakic retinal detachment carries a 7% risk. ^[6]

Retinitis pigmentosa has a highly variable prevalence. It is estimated at 1 in 750 to 9,000 individuals depending on the study population, and around 1 in 3,000 to 5,000 in Western populations. ^[7] Higher rates are seen in regions with high consanguinity. It is a major cause of inherited blindness outside infancy.

For diabetic retinopathy the risk factors are diabetes itself, duration of disease, hyperglycaemia (glycosylated haemoglobin, HbA1c), systemic hypertension, dyslipidaemia, pregnancy, puberty and renal disease. The AAO stresses that maintaining control of glucose and blood pressure lowers the risk of retinopathy developing and progressing. Paradoxically, rapid, tight glucose control can be followed by accelerated or early onset of DR, an effect reported with semaglutide and other newer agents; this is a warning against abrupt normalisation without retinal monitoring.

For hypertensive retinopathy the driver is elevated blood pressure, both acute and chronic. WHO defines hypertension as a systolic blood pressure greater than 140 mmHg and/or a diastolic blood pressure greater than 90 mmHg. ^[8] Severity of retinopathy tracks both the height and the duration of pressure, and untreated moderate or severe disease is a marker of systemic target-organ damage elsewhere, including kidney disease and higher cardiovascular mortality.

Retinal detachment risk factors include posterior vitreous detachment, high myopia, previous cataract surgery, ocular trauma, family history, lattice degeneration and retinal breaks. tractional detachment is driven by ischaemic retinopathy (especially diabetes), and exudative detachment by inflammation, infection, tumour or severe hypertension.

Retinitis pigmentosa is genetic. It can be inherited as autosomal dominant (15 to 25% of cases), autosomal recessive (5 to 20%) or X-linked recessive (5 to 15%), with rare X-linked dominant, mitochondrial and digenic forms. ^[7] About 20 to 30% of cases have extra-ocular features, most often hearing loss. More than 90 genes are now linked to RP, and next-generation sequencing can solve 60 to 80% of sequenced RP patients. ^[7]

Chronic hyperglycaemia damages retinal capillary pericytes and endothelial cells. The earliest visible change is the microaneurysm: a focal ballooning of a capillary wall. Capillary closure follows, producing retinal ischaemia, and the ischaemic retina releases vascular endothelial growth factor (VEGF). VEGF drives both increased vascular permeability (DME) and new vessel growth (PDR). Non-proliferative disease therefore moves from microaneurysms and dot-blot haemorrhages, through venous calibre change (beading), to intraretinal microvascular abnormalities (IRMA) as ischaemia worsens. Proliferative disease begins when new vessels breach the internal limiting membrane; these vessels are fragile and can haemorrhage into the vitreous or form fibrovascular membranes that contract and tractionally detach the retina.

The eye is the only organ in which the vascular effects of systemic hypertension can be seen directly. Early hypertension causes reversible vasospasm and generalised arteriolar narrowing. Chronic elevation produces structural change: intimal thickening and medial hyperplasia, which narrow the arteriole and compress the crossing venule (AV nicking), and hyaline degeneration (copper or silver wiring). Severe hypertension breaks the blood-retina barrier, producing retinal haemorrhages, cotton-wool spots from focal ischaemia of the nerve fibre layer, hard exudates and, if intracranial pressure rises, optic disc swelling. A choroidopathy with Elschnig spots and Siegrist streaks can be added in young patients with acute severe elevations. The vascular changes of mild (grades 1-2) retinopathy are only modestly associated with blood pressure, which is why many guidelines do not count mild retinopathy alone as target-organ damage.

In rhegmatogenous detachment, liquefied vitreous passes through a full-thickness break into the subretinal space, separating retina from pigment epithelium and cutting off the photoreceptors from their blood supply. Symptoms follow the mechanics: flashes from vitreoretinal traction, floaters from debris or haemorrhage, then a peripheral shadow or curtain as the detachment extends. Central vision falls only when the macula detaches. Photoreceptor apoptosis begins within hours of macular detachment, which is why speed matters. In tractional detachment, fibrovascular membranes contract; in exudative detachment, fluid accumulates under an intact retina because of choroidal or retinal pigment epithelial dysfunction. ^[9]

RP starts with loss of rod function. Because rods sit outside the fovea and serve dim light and peripheral vision, the first symptoms are night blindness and difficulty with暗 light, followed by constricted fields. Cone loss comes secondarily, so central acuity and colour vision are affected later; tunnel vision results. On fundoscopy the classic triad is a pale disc, attenuated retinal vessels and mid-peripheral bone-spicule-like pigmentation, although a non-pigmented form exists. Secondary cataract and cystoid macular oedema are common and add to visual disability.

DR is asymptomatic for a long time. When symptoms appear they are usually from DME or advanced disease: blurred or distorted central vision, difficulty reading, floaters from vitreous haemorrhage, or sudden vision loss from tractional detachment. Background (R1) disease has microaneurysms and small haemorrhages but normal vision. Pre-proliferative (R2) disease shows increasing haemorrhage counts, venous beading and IRMA. Proliferative (R3) disease may declare itself through vitreous haemorrhage, neovascularisation of the iris or rubeotic glaucoma. The key clinical point is that vision can be normal with vision-threatening retinopathy, so waiting for symptoms is not a safe strategy; this is why screening programmes exist.

Most chronic hypertensive retinopathy is found incidentally and does not affect vision. Symptoms of severe disease are reduced visual acuity, visual field defects, metamorphopsia from macular oedema or serous detachment, and headache or other features of hypertensive crisis. On fundoscopy the examiner looks for arteriolar narrowing, AV nicking, copper or silver wiring, haemorrhages, cotton-wool spots, hard exudates and disc swelling. Optic disc swelling distinguishes malignant from accelerated hypertension and is an emergency.

Patients describe a sudden increase in floaters, brief peripheral flashes (photopsia), and a dark curtain or shadow moving across the visual field, often from the periphery toward the centre. When the macula detaches, central vision drops sharply. Some inferior detachments are silent and progress slowly. Pain is usually absent but mild discomfort and redness can occur and be mistaken for uveitis. A careful dilated examination is needed because small shallow detachments can be subtle, and indirect ophthalmoscopy with scleral indentation is the best method. A relative afferent pupillary defect can occur with extensive detachment.

Night blindness (nyctalopia) is usually the first symptom, often in childhood or adolescence, followed by bumping into objects and difficulty with peripheral vision. Photopsia and photophobia are common. Central vision holds until mid to late disease; some patients reach counting-fingers vision by the fourth or fifth decade, but fewer than 1% progress to no light perception. ^[7] Associated signs include cataract, cystoid macular oedema and Coats-like exudative vasculopathy. Visual function and mobility are usually the main patient-reported problems.

The table separates the commoner masqueraders. For diabetes-related findings, retinal vein occlusion, hypertensive retinopathy, radiation retinopathy and anaemia can look similar; for a pigmented retinopathy, inherited and acquired causes must be distinguished.

For the four diseases here, the useful tests are largely ocular and metabolic.

• Fundoscopy and retinal imaging. Dilated fundus examination is the gold standard screen for DR; validated digital imaging is an effective alternative for screening. For hypertensive disease, fundoscopy documents the grade, and colour fundus photography plus optical coherence tomography (OCT) is used for Elschnig spots, serous detachments and vessel measurements.
• OCT and OCT angiography. Macular OCT measures retinal thickness and fluid in DME and retinal detachment, and OCT angiography can show capillary non-perfusion and neovascularisation without dye.
• Fluorescein angiography. This maps areas of capillary non-perfusion and leakage in diabetic disease and guides laser. In hypertensive choroidopathy it shows delayed choroidal filling and Elschnig-spot hyperfluorescence.
• Visual function testing in RP. Best-corrected visual acuity, perimetry (Goldmann kinetic perimetry or computerised and microperimetry), full-field electroretinography following ISCEV (International Society for Clinical Electrophysiology of Vision) standards, and multimodal imaging (wide-field fundus, SD-OCT, fundus autofluorescence) are the core tests. Full-field ERG shows diminished rod-driven responses early and eventually extinguished photopic and scotopic responses in end-stage disease.
• Genetic testing. In RP this is indispensable: targeted gene panels first, then whole-exome or whole-genome sequencing if the panel is negative. In syndromic cases it also guides family counselling.
• Systemic tests. HbA1c, blood pressure measurement, renal function and lipid profile are part of the work-up of any DR or hypertensive retinopathy; women of childbearing age need pregnancy testing and obstetric liaison when retinopathy is found in pregnancy.

Two grading frameworks are used worldwide and are worth knowing both, because they answer slightly different questions.

NHS DESP retinopathy grades. R0 is no retinopathy. R1 is background retinopathy. R2 is pre-proliferative retinopathy, split into:

• R2L (lower risk): more than 20 intraretinal haemorrhages or microaneurysms in 1 to 3 of the four quadrants, 8 or more blot haemorrhages, venous beading in one quadrant, or IRMA less than ETDRS standard photograph 8a. ^[2]
• R2H (higher risk): more than 20 intraretinal haemorrhages or microaneurysms in each of the four quadrants, venous beading in two or more quadrants, or moderate IRMA equal to or worse than Airlie House ETDRS standard photograph 8a in one or more quadrants. ^[2]

R3A is active proliferative retinopathy and R3S is stable treated proliferative retinopathy. Maculopathy is M0 (none) or M1 (referable maculopathy): exudate groups greater than or equal to half a disc area, retinal thickening within one disc diameter of the fovea, or visual acuity worse than 6/12 with microaneurysms or haemorrhages within one disc diameter of the fovea. ^[2] Treatment decisions and recall intervals follow from these grades.

ETDRS levels used by AAO and others. No apparent retinopathy (levels 10, 14, 15) is recalled annually. Mild NPDR (level 20) equals level R1. Level 35 mild NPDR (levels 35a-35e) carries approximately a 6.2% one-year risk of progression to PDR (level 30 risk 6.2%, level 41 11.3%, level 45 20.7% in NHS DESP summaries), with recall at 4 to 6 months. Level 43 (moderate NPDR) has an 11.3% one-year risk and 3 to 6 month recall. Level 47 (moderately severe NPDR) has a 20.7% risk and 4 month recall. Level 53 (severe NPDR) and beyond tip toward proliferative disease and need prompt treatment. ^[2]

Screening rules by type. People with type 1 diabetes should have annual screening from 5 years after onset, whereas people with type 2 diabetes should have a prompt screen at diagnosis and at least yearly thereafter. Women with diabetes who become pregnant need early and close retinal follow-up throughout pregnancy, but no eye examination is required for gestational diabetes. Young patients need closer follow-up during puberty because of accelerated progression. ^[1]

Keith-Wagener-Barker (1939), four grades. Grade 1: mild generalised retinal arteriolar narrowing. Grade 2: definite focal narrowing and AV nicking. Grade 3: grade 2 signs plus retinal haemorrhages, exudates and cotton-wool spots. Grade 4: severe grade 3 retinopathy plus papilloedema (malignant hypertension). This is the system most widely cited and it carries the classic prognostic thresholds from the original cohort. ^[8]

Wong and Mitchell (2004), three grades. Mild: one or more of generalised or focal arteriolar narrowing, AV nicking or arteriolar wall opacity (copper or silver wiring). Moderate: one or more of retinal haemorrhage (blot, dot or flame-shaped), microaneurysm, cotton-wool spot or hard exudate. Severe: moderate retinopathy plus optic disc swelling. This simplified system is easier at the bedside and is the one most often used for risk stratification today. ^[8]

Escalation by grade: mild disease is referred to a general practitioner within about a week, moderate disease within one to two days, and severe disease or choroidopathy with malignant hypertension demands immediate blood pressure measurement and emergency department referral.

RP is classified by mode of inheritance (autosomal dominant, autosomal recessive, X-linked recessive and rare forms) and by whether it is non-syndromic or syndromic, with Usher syndrome as the commonest syndromic form. Severity is tracked by visual field loss, visual acuity and structural imaging rather than by a single score, although clinical trial outcome measures such as microperimetry retinal sensitivity and full-field stimulus threshold are used in research.

Systemic control first. Controlling glucose and blood pressure lowers the risk of retinopathy developing and progressing. Each retinal decision is made against this background: there is no retinal treatment that substitutes for metabolic control.

Panretinal photocoagulation (PRP, scatter laser). PRP ablates ischaemic peripheral retina to reduce VEGF drive and to prevent neovascularisation and vitreous haemorrhage. It remains an important treatment for proliferative DR, and one anti-VEGF pivotal trial showed that with ranibizumab 0.3 mg monthly, only 1% of patients needed PRP over the study period versus 12% of sham-treated patients, and that focal or grid laser was needed in 38% versus 72%, confirming that anti-VEGF controls disease but does not replace PRP for everyone. ^[4] PRP is also used for severe non-proliferative disease when follow-up is unreliable. Side effects include peripheral visual field constriction, night-vision difficulties, macular oedema worsening and reduced acuity.

Focal and grid laser for diabetic macular oedema. Macular (focal or grid) laser targets leaking microaneurysms in clinically significant macular oedema and remains useful, especially for non-centre-involving oedema and where injections cannot be delivered or maintained.

Intravitreal anti-VEGF. Anti-VEGF drugs (ranibizumab, aflibercept, and off-label bevacizumab) are effective for centre-involving DME with vision loss and reduce DR severity and treat proliferative DR. Dosing from the labels:

• Ranibizumab: 0.3 mg (0.05 mL of a 6 mg/mL solution) by intravitreal injection once a month (approximately 28 days).^[4]
• Aflibercept: 2 mg (0.05 mL of a 40 mg/mL solution) by intravitreal injection every 4 weeks (approximately 28 days) for the first 5 injections, then every 8 weeks (2 months). It may be given as frequently as every 4 weeks.^[5]

Anti-VEGF injections are usually preceded by topical povidone-iodine preparation because non-use has been linked to an unacceptably high risk of endophthalmitis. All intravitreal injections carry small risks of endophthalmitis, retinal detachment and, rarely, retinal vasculitis.

Centre-involving DME with good vision. In eyes with good visual acuity and centre-involving DME, treatment may reasonably be deferred until visual acuity is affected (20/30 or worse); in practice this threshold is often used to delay anti-VEGF rather than to treat immediately.^[1]

Vitrectomy. Pars plana vitrectomy is used for non-clearing vitreous haemorrhage, tractional macular detachment and for removing membranes in advanced disease. Prompt vitrectomy is considered in people with at least severe non-proliferative disease and poor follow-up; in real-world care it is also used for rubeosis and neovascular glaucoma.

Corticosteroid implants. Intravitreal dexamethasone or fluocinolone acetonide implants are an option for DME, particularly pseudophakic eyes or where anti-VEGF response is inadequate, accepting the risks of cataract and raised intraocular pressure. Regional availability and licensed indications vary, so follow local guidance.

There is no specific ocular treatment for chronic mild to moderate hypertensive retinopathy; management is control of blood pressure and the underlying cause. The presence of grade 3 or 4 retinopathy (or choroidopathy) should be reported to the treating physician as target-organ damage, and in malignant hypertension the eye findings guide how urgently blood pressure is lowered. Optometrists and ophthalmologists who discover these signs in undiagnosed patients should arrange blood pressure measurement and primary-care follow-up: within about a week for mild, within one to two days for moderate, and emergency referral for severe or choroidopathy.^[8] Choroidopathy can resolve on imaging after blood pressure is controlled. Care is coordinated with the primary care physician or emergency department, and the eye changes are monitored to demonstrate resolution.

This is a surgical emergency. Small breaks and asymptomatic detachments can sometimes be treated with laser or cryotherapy to seal the break, but once the retina is detached, surgery is needed.

Timing. Macula-on (fovea-on) RRD should be repaired within about 24 hours because repair within that window gives better final best-corrected visual acuity than later surgery. If the macula is already detached, repair should be within two days, because longer delays substantially worsen visual outcome; retinal repair within three days of symptom onset gives better acuity than four to seven days. Photoreceptor apoptosis begins within about 12 hours of detachment. Preoperative posturing (face turned so the detachment sits uppermost) can slow progression to the fovea.^[9]

Surgical options. Scleral buckling (an external silicone band indenting the sclera) suits uncomplicated detachments and is widely available in low-resource settings; vitrectomy (pars plana vitrectomy with internal tamponade by gas or silicone oil) is needed for complex detachments, vitreous traction, giant tears and proliferative vitreoretinopathy; pneumatic retinopexy (an intravitreal gas bubble with posturing) is suitable for a selected minority. More than 95% of uncomplicated RRDs can be repaired successfully, although more than one procedure is sometimes needed; visual recovery depends on macula status and delay, so early macula-sparing repair matters. ^[6] After surgery, intraocular gas means poor early vision, posturing as directed until the gas is absorbed (about 5 days for short-acting SF6, 6 to 8 weeks for C3F8), no air travel and no volatile gas anaesthesia until the gas is absorbed; worsening vision or severe pain needs urgent review for raised pressure or redetachment.

Patient advice. A recent onset of retinal detachment is referred immediately, usually directly to the surgeon who will operate. Macula-on patients should be warned to avoid exertion, to posture as advised and to return urgently if a curtain develops. Prophylactic laser or cryotherapy treats symptomatic breaks caused by posterior vitreous detachment, but prophylactic treatment of asymptomatic breaks or degenerative lesions has not been shown to reduce detachment risk.

There is no cure for the underlying degeneration, but several measures slow complications or preserve useful vision.

• Monitoring and treat associated problems. Cataract extraction and treatment of cystoid macular oedema (for example oral or topical carbonic anhydrase inhibitors in selected cases) can improve vision; Coats-like exudation needs retinal control.
• Vitamin A and lutein have been studied for slowing progression, with inconsistent evidence; any supplementation should be clinician-directed (excess vitamin A is hepatotoxic and teratogenic).
• Genetic therapy. Voretigene neparvovec is an FDA-approved gene therapy for RPE65-associated inherited retinal dystrophy, delivered by subretinal injection; it requires a confirmed mutation and viable photoreceptors, and many RP patients are not eligible because the causative gene is not identified or the retina is too advanced.^[7]
• Visual rehabilitation. Low-vision aids, mobility training, LED illumination, contrast enhancement and orientation training are mainstays.
• Psychological and family support. Studies report that anxiety or depression occurs 5 to 6 times as often in RP as in the general population, and genetic counselling before and after testing helps with inheritance, recurrence risks and family planning.^[7]
• Emerging research. Gene-specific and gene-independent therapies (antisense oligonucleotides, RNA editing, optogenetics, retinal implants) are in trials; patients should be referred to specialist centres and registries rather than promised specific outcomes.
• Counselling. Patients should be advised to report sudden changes that might signal retinal detachment or macular oedema.

• Diabetic retinopathy. DME, proliferative vitreous haemorrhage, tractional retinal detachment, rubeotic glaucoma and clinically significant macular ischaemia. An RRD can occur in PDR. Anti-VEGF and PRP reduce these risks but do not abolish them.
• Hypertensive retinopathy. Macular oedema, serous retinal detachment, retinal arteriolar occlusion, and in severe disease retinal pigment epithelium and choroidal ischaemia (Elschnig spots). Systemically it flags accelerated or malignant hypertension and higher stroke, coronary and renal risk.
• Retinal detachment. Proliferative vitreoretinopathy (scarring that prevents reattachment), macular damage, secondary ocular hypertension, uveitis and cataract; after surgery, redetachment, cataract progression and silicone-oil complications in some. Delayed macula-off repair worsens visual outcome: repair within about 3 days gives better acuity than repair after 4 to 7 days. ^[9]
• Retinitis pigmentosa. Cataract, cystoid macular oedema, Coats-like exudation, epiretinal membrane and, in late disease, a small group developing choroidal neovascularisation or retinal detachment. Quality of life, educational and occupational impact can be large.

Prognosis depends on the condition and its stage.

• Diabetic retinopathy is treatable at most stages: early disease is controlled by systemic factors; vision-threatening disease needs laser or anti-VEGF; adherence to screening and treatment determines how much sight is preserved. The AAO-highlighted deficiencies in screening uptake show why late presentation is still common.
• Hypertensive retinopathy of mild to moderate grade often improves once blood pressure is controlled, and the retinal findings recede. Severe or malignant disease left untreated has a poor prognosis.
• Retinal detachment has an excellent anatomical prognosis (over 95% of uncomplicated cases repaired) but functional recovery depends on macula status and delay. Macula-on repair within a day gives the best visual outcomes.
• Retinitis pigmentosa is slowly progressive and highly variable. People with autosomal dominant disease may retain useful vision to old age; X-linked and recessive disease moves faster. Most patients retain some light perception even in late disease, and early diagnosis helps planning, low-vision support and family counselling.^[7]

Screening matters most for diabetic retinopathy because it is silent early and treatable. Three guideline sources shape practice:

• AAO Diabetic Retinopathy Preferred Practice Pattern (edition 2024, published February 2025). People with type 1 diabetes need annual screening from 5 years after onset; people with type 2 need a prompt screen at diagnosis and at least yearly thereafter. The AAO recommends glycaemic and blood pressure control, warns that rapid tight glucose control can accelerate DR, advises early and frequent retinal follow-up in pregnancy, closer follow-up during puberty, defines when treatment of centre-involving DME may be deferred (20/30 or worse), affirms that anti-VEGF agents treat DME and reduce DR severity, that PRP remains important for PDR, and that povidone-iodine should be used for intravitreal injections. Only about 60% of people with diabetes receive the recommended yearly screen.^[1]
• NHS Diabetic Eye Screening Programme (England, grading definitions updated 4 December 2025). This defines the R0 to R3 and M0/M1 grades and recall intervals used to decide referral: digital two-field retinal photography, with grading into no retinopathy, background, pre-proliferative (higher or lower risk), active or stable proliferative, and referable or non-referable maculopathy. ETDRS final grades from 10/14/15 through to 47 map onto these categories and give a stated one-year risk of progression to PDR for each level (6.2%, 11.3%, 20.7%).^[2]
• ICO Guidelines for Diabetic Eye Care (2017 edition). These offer tiered recommendations for low, intermediate and high-resource settings, covering screening and evaluation for potentially blinding eye problems and treatment of DR and other ocular complications of diabetes, and are maintained as a working document.^[3]

Prevention beyond diabetes control includes hypertension control (which reduces both hypertensive retinopathy and progression of DR), smoking cessation, weight and lipid management, and trauma protection. Screening for RP is familial and genetic rather than population-based, and genetic counselling is central.

Pregnancy. Diabetic retinopathy can progress rapidly in pregnancy and needs early examination and close follow-up; gestational diabetes does not require an eye examination. Hypertensive choroidopathy in pre-eclampsia and eclampsia is a medical emergency because these conditions carry serious maternal and fetal risk. Urgent blood pressure control and obstetric management are required; the eye findings are a sign, not the disease to treat.

Children. RP often presents in childhood with night blindness and needs paediatric ophthalmology and genetic services; severe non-proliferative or proliferative diabetic disease is uncommon in children but accelerated progression around puberty means tighter DR follow-up in young people with diabetes. Retinal detachment in children may follow trauma or syndromic connective-tissue disease and can be silent at first; check the fellow eye.

Older adults. Hypertensive retinopathy and age-related macular disease are common. Post-cataract-surgery patients have higher RRD risk and must be taught the symptoms; co-existing cognitive or mobility problems can delay diagnosis.

Immunocompromised patients. Cytomegalovirus retinitis, which presents with haemorrhagic necrotising retinitis, is a different entity and needs ophthalmology and infectious-disease input; it should not be confused with DR or hypertensive retinopathy.

• Diabetic and hypertensive screening. A trained observer using a direct ophthalmoscope through a dilated pupil can detect vision-threatening retinopathy without imaging, and non-mydriatic cameras with telemedicine grading are effective where broadband allows. Follow the resource-tier guidance in the ICO guidelines for deciding what is essential versus optimal.^[3]
• Hypertension. Measure blood pressure routinely; grade retinopathy by bedside fundoscopy. Mild disease means arrange follow-up within a week, moderate within days, severe same-day emergency referral.
• Retinal detachment. Scleral buckling needs little equipment and can save sight where vitrectomy is unavailable; the keys are recognition (flashes, floaters, curtain) and prompt referral, with posturing in the transfer. Avoid air travel with intraocular gas.
• RP. Genetic testing may be unavailable; the diagnosis rests on history and fundus findings, and rehabilitation and genetic counselling information should still be given.
• General points. dilated retinal examination should be a routine skill for clinicians; network with the nearest retinal surgeon and reduce avoidable delays.

• Diabetic retinopathy is staged from none (R0) through background (R1), pre-proliferative (R2 lower or higher risk), active or stable proliferative (R3A or R3S), with maculopathy M0 or M1; screening starts at 5 years after onset for type 1 and at diagnosis for type 2, and is yearly thereafter. ^[1]
• Only about 60% of people with diabetes receive the recommended yearly DR screen, so missed screening is a more common cause of vision loss than failed treatment. ^[1]
• Maintaining glucose and blood pressure control lowers DR risk; rapid, tight glucose control can transiently worsen DR, so retinal monitoring is needed when control is intensified.
• Systemic anti-VEGF plus PRP remains central: anti-VEGF treats centre-involving DME and reduces DR severity, PRP remains important for PDR, and centre-involving DME with good acuity can often be observed until acuity falls to 20/30. ^[1]
• Ranibizumab 0.3 mg intravitreally monthly and aflibercept 2 mg intravitreally monthly for five doses then every two months are representative anti-VEGF regimens for DR and DME. ^[4][5]
• Hypertensive retinopathy is graded Keith-Wagener-Barker 1 to 4 or Wong-Mitchell mild, moderate and severe; grade 4 (disc swelling) is malignant hypertension and an emergency, with immediate blood pressure measurement and referral. ^[8]
• Hypertensive retinopathy is a marker of systemic target-organ damage; encourage blood pressure control and report new findings.
• RRD incidence is about 10 to 18 per 100,000 per year, with a peak around 55 to 59 years; 34% of detached eyes have had cataract surgery and 10% ocular trauma. ^[6] Macula-on repair should occur within 24 hours and macula-off repair within two days. ^[9]
• Preoperative posturing can slow a macula-on detachment; patients should be warned about flashes, floaters and curtains and to attend immediately.
• Retinitis pigmentosa is a rod-then-cone dystrophy: night blindness first, then peripheral loss, then tunnel vision. It is diagnosed by fundus signs, full-field ERG and genetic testing, and inherited as autosomal dominant 15 to 25%, autosomal recessive 5 to 20% and X-linked 5 to 15%. ^[7]
• Over 90 RP genes are known and sequencing solves 60 to 80% of patients; voretigene neparvovec is licensed only for RPE65-associated disease. Less than 1% reach no light perception. ^[7]
• About 20 to 30% of RP has extra-ocular features (Usher syndrome most common); arrange genetic counselling. ^[7]
• In low-resource settings, dilated fundoscopy, blood pressure control, scleral buckling and visual rehabilitation produce most of the benefit.

This topic connects with retinal vascular occlusion, where blockage of central vessels is a separate but related threat to sight. It also connects with stroke and hypertensive emergencies (because retinal findings often mirror cerebral and renal target-organ damage), diabetes mellitus and its complications, hypertension management, inherited retinal dystrophies and low-vision rehabilitation. Planned future MedGrasp topics include AMD and macular disease; reference them only once they are published. Plain text is used for all links; no other MedGrasp topics are linked within this page.