Comm Eye Health Vol. 09 No. 20 1996 pp 58 - 62. Published online 01 December 1996.

Diabetic retinopathy: clinical features and management

P G Hykin BSc FRCS FRCOphth

Consultant Ophthalmic Surgeon, Moorfields Eye Hospital, City Road, London EC1V 2PD

Related content

In the West approximately 1% of the population is diabetic, and at least another 1% are undiagnosed diabetics. Juvenile onset or insulin-dependent diabetes (IDDM) accounts for approximately 10-15% of cases, the remainder being maturity onset or non insulin-dependent diabetics (NIDDM). Diabetic retinopathy remains the major cause of blindness in developed countries in patients under 55 years of age and since it is avoidable in the majority of cases with current treatment techniques, early diagnosis and appropriate management are critically important. In recent years large, prospective Multicentre trials of therapy in the USA, including the Diabetic Retinopathy Study (DRS), the Early Treatment of Diabetic Retinopathy Study (ETDRS), the Diabetes Control Complications Trial (DCCT) and the Diabetic Retinopathy Vitrectomy Study (DRVS), have provided clear management guidelines.


The term, ‘background diabetic retinopathy’ is gradually being replaced by the terms ‘mild’ and ‘moderate non-proliferative diabetic retinopathy’. The term ‘pre-proliferative retinopathy’ is being replaced by the term ‘severe non-proliferative retinopathy’, whilst the term ‘proliferative diabetic retinopathy’ remains unchanged.


Mild non-proliferative diabetic retinopathy

This is the mildest form of non-proliferative diabetic retinopathy and is characterised by the presence of at least one microaneurysm, and also by dot, blot or flame-shaped haemorrhages in all four fundus quadrants of less severity than those shown in Figure 1. Hard exudates and cotton wool spots are not a feature of mild non-proliferative diabetic retinopathy.

Table 1: Diabetic Retinopathy: Clinical Features, Natural History and Management

Level of Retinopathy

Clinical Features

Natural History Rate of progression to PDR at 1 year

Natural History Rate of progression to high-risk disease at 5 years


Mild non-proliferative diabetic retinopathy

More than 1 microaneurysm Haemorrhage and microaneurysms less than in Figure 1



Review 12 months

Moderate non-proliferative diabetic retinopathy

Haemorrhage and microaneurysms more than in Fig. 1 in 1 – 3 quadrants, cotton wool spots, venous beading less than in Fig. 2 and IRMAs less than in Fig. 3



Review 6 – 8 months

Severe non-proliferative diabetic retinopathy

Haemorrhage, microaneurysms more than in Fig. 1 in all quadrants or venous beading more than Fig. 2 in more than 2 quadrants, or IRMA more than Fig. 3 in 1 quadrant



Review 3 – 4 months

Non high-risk characteristic proliferative diabetic retinopathy

One or two high-risk characteristics


Review 2 – 3 months

High-risk characteristic proliferative diabetic retinopathy

Three to four high-risk characteristics

Review 2 months

Note: If clinically significant macular oedema supervenes, these patients should be managed accordingly (see Maculopathy)

Adapted from L Aeillo in Principles and Practice of Ophthalmology, Albert and Jakobiec, WB Saunders: with permission.

Moderate non-proliferative diabetic retinopathy

This is characterised by intraretinal microaneurysms and dot and blot haemorrhages of greater severity than those seen in Figure 1, in one to three quadrants. Cotton wool spots, venous calibre changes, including venous beading, and intraretinal microvascular abnormalities (IRMA), are present but mild.

Severe non-proliferative diabetic retinopathy

At least one of the following should be present: a) haemorrhages and microaneurysms in all four quadrants of the fundus, greater than Figure 1; b) venous beading, more marked than Figure 2 in at least two quadrants, and c) intraretinal microvascular abnormalities, more severe than in Figure 3 in at least one quadrant.

Very severe non-proliferative diabetic retinopathy

This is defined as two or more of the criteria for severe non-proliferative diabetic retinopathy, but without any proliferative diabetic retinopathy.

Proliferative diabetic retinopathy

High-risk characteristics

There are four features of proliferative diabetic retinopathy which are used to determine the level of risk to vision (see below). A patient with one or two characteristics is considered to have non high-risk proliferative retinopathy. A patient with three or four characteristics has high-risk proliferative retinopathy. The characteristics are:

  • any new vessels on the optic disc, or new vessels elsewhere in the fundus

  • new vessels on the disc

  • new vessels on the optic disc greater than those in Figure 4, or an area of new vessels elsewhere in the fundus greater than half a disc area

  • vitreous haemorrhage

Table 2: Treatment of diabetic retinopathy

Proliferative Retinopathy

Clinically Significant Macular Oedema
Retinal microaneurysms

Clinically Significant Macular Oedema
Retinal thickening & areas of non-perfusion

Type of laser

Argon green

Green or yellow (577) argon laser

Green or yellow (577) argon laser

Spot size

500m at the retina, i.e., 250m on setting of laser

50 – 200m

50 – 100m


0.2 – 0.8 watts

0.1 – 0.3 watts

0.1 – 0.3 watts


0.2 seconds

0.1 seconds

0.05 – 0.1 seconds

End point

Faint white burn at level of retinal pigment epithelium (RPE)

Faint whitening of RPE or darkening of microaneurysm

Very faint white burn at level of retinal pigment epithelium (RPE)

How to treat

Do not overlap burns
Do not treat within temporal arcades
Do not treat within one disc diameter of optic disc
Do not treat within two disc diameters temporal to fovea
Avoid retinal arterioles and veins

Apply burns directly to microaneurysms

Place burns at least one burn width apart, to make a grid which includes the area of retinal thickening
Do not treat within 500m of fovea at first session

Number of burns

Approximately 2,000



Number of sessions

Two sessions. Treat the lower half of the retina first (1,000 burns)




Topical steroids and mydriatic after treatment

Signs of resolution

New vessels regressing
Reduced blood flow in new vessels
More fibrous tissue
Less beading of retinal veins

Less retinal thickening/exudate

Less retinal thickening

Indications for retreatment

Fresh new vessels on the optic disc or elsewhere in the fundus
Failure of new vessels to regress

Significant macular oedema after 3 months

Significant macular oedema after 3 months


Between previous burns, avoiding retinal vessels

Do not retreat areas lying in the macular-papular bundle

Treat to within 100m of the edge of the foveal avascular zone

For example, a patient with a one-third disc area of flat, peripheral new vessels, no new vessels on the disc and no vitreous haemorrhage would score one high-risk characteristic and therefore have non-high risk proliferative retinopathy. A patient with new vessels on the disc involving the entire disc surface (Fig. 5) and with vitreous haemorrhage would be graded as high risk.

Tractional retinal detachment

These patients either have peripheral tractional retinal detachment without macular involvement or tractional retinal detachment with macular detachment or traction.

Vitreous haemorrhage

In patients with vitreous haemorrhage in whom no view of the retina is possible, B-scan ultrasonography should be performed to determine whether a tractional or rhegmatogenous retinal detachment (retinal detachment associated with a retinal break/tear/hole) is present.

Neovascularisation of the iris/neovascular glaucoma

At their initial visit, all patients should be examined prior to dilating the pupil, and gonioscopy performed to exclude iris neo-vascularisation.

Maculopathy (Fig.6a;6b)

The terms, ‘diffuse’, ‘exudative’ and ‘ischaemic diabetic maculopathy’ were not employed in the Early Treatment of Diabetic Retinopathy Study (ETDRS). Instead, patients were given macular focal laser therapy based on whether ‘clinically significant macular oedema’ was present or not (Fig. 7). This is defined as:

  1. Retinal thickening at or within 500m (one third of the diameter of the optic disc) at the centre of the macula

  2. Hard exudates at or within 500m at the centre of the macula, if there is thickening of the adjacent retina

  3. An area of retinal thickening greater than one optic disc area in size at least a part of which is within one disc diameter of the centre of the macula.

The ETDRS showed a clear benefit from treating these cases. Fluorescein angiography is performed prior to focal laser therapy to determine where to treat such cases.


Diabetic control and other factors

Clinical trials have conclusively shown that good glycaemic control (less than 155 mg/dL or less than 8.6 mmol/L) substantially reduced the risk of diabetic retinopathy developing and subsequently progressing. Whilst it is probably unwise to give patients specific targets to achieve for their blood glucose, the importance of good control should be stressed. Other factors which should be identified and treated appropriately in diabetic patients include hypertension, renal disease and hyperlipidaemia.

Panretinal photocoagulation for proliferative retinopathy

Clinical trials have unquestionably demonstrated the beneficial effect of pan-retinal photocoagulation (Fig. 8) in high-risk proliferative retinopathy, reducing the risk of severe visual loss (VA < 5/200) from 44% in untreated eyes to 20% in treated eyes at four years’ follow-up.

Indications for Panretinal Photocoagulation

  • High-risk proliferative retinopathy

  • Neovascularisation of the iris

  • Tractional retinal detachment, with or without macular involvement, if active new vessels on the optic disc or elsewhere in the fundus are present

  • Non high-risk proliferative retinopathy if extenuating circumstances exist, such as imminent cataract surgery, pregnancy, when the first eye had a poor outcome after treatment for high risk disease, and poor compliance for follow-up.

Method – See Table 2.

Focal photocoagulation for maculopathy

Clinical trials have shown that the incidence of moderate visual loss at three years’ follow-up in eyes with clinically significant macular oedema was reduced from 30% in untreated eyes to 15% in treated eyes.

Clinically Significant Macular Oedema: the following lesions should be treated

  • Focal leaks greater than 500m from the centre of the macula causing retinal thickening or hard exudates

  • Focal leaks 300m – 500m from the centre of the fovea if treatment will not cause significant damage to the peri-foveal capillary network

  • Areas of diffuse leakage on fluorescein angiography within the macular area

  • A vascular areas within the macular area

Pars plana vitrectomy


  • Vitrectomy is indicated for vitreous haemorrhage, which should be performed early for insulin-dependent diabetics. In non insulin-dependent diabetics vitrectomy should be undertaken if the haemorrhage fails to clear after six months.

  • Complex vitreoretinal surgery is indicated if the macula is detached or threatens to detach, and should be performed early. If there is extensive active neovascularisation panretinal endo-photocoagulation should be undertaken at the end of surgery. If the macula is attached and unthreatened, vitrectomy is not indicated, and pan-retinal photocoagulation should be performed if there is active neovascularisation.

Screening for diabetic retinopathy

Insulin-dependent/juvenile-onset diabetes

  • Dilated fundoscopy examination every year beginning 5 years after diagnosis

  • Examinations more frequently once diabetic retinopathy is diagnosed (Table 1)

Non insulin-dependent/maturity-onset diabetes

  • Dilated fundoscopy examination every year once diabetes diagnosed

  • Examination more frequently once diabetic retinopathy diagnosed (Table 1)

Source references

1 Diabetic Retinopathy Study Report No. 3: Four risk factors for severe visual loss in diabetic retinopathy. Arch Ophthalmol 1979; 97: 658.

2 Diabetic Retinopathy Study Report No. 7: Modification of the Airlie House Classification of Diabetic Retinopathy. Invest Ophthalmol Vis Sci 1981; 21: 210-26.

3 Diabetic Retinopathy Study Report No. 8: Photocoagulation treatment of proliferative diabetic retinopathy. Application of Diabetic Retinopathy Study (DRS findings). Ophthalmology 1981; 88: 583-600.

4 Early Treatment of Diabetic Retinopathy Study Report No. 1: Photocoagulation for diabetic macular edema. Arch Ophthalmol 1985; 103: 1796-1806.

5 Early Treatment of Diabetic Retinopathy Study Report No. 2: Treatment techniques and clinical guidelines for photo-coagulation for diabetic macular edema. Ophthalmology 1987; 94: 761-74.

6 Early Treatment of Diabetic Retinopathy Study Report No. 3: Techniques for scatter and low core photocoagulation treatment of diabetic retinopathy. Int Ophthalmol Clin 1987; 27: 254-64.

7 Early Treatment of Diabetic Retinopathy Study Report No. 4: Photocoagulation for diabetic macular edema. Int Ophthalmol Clin 1987; 27: 265-72.

8 Early Treatment of Diabetic Retinopathy Study Report No. 9: Early photocoagulation for diabetic retinopathy. Ophthalmology 1991; 98: 766-85.

9 Early Treatment of Diabetic Retinopathy Study Report No. 10: Grading diabetic retinopathy from stereoscopic colors, fundus photographs. An extension of the modified Airlie House classification. Ophthalmology 1991; 98: 786-806.

10 Diabetic Retinopathy Vitrectomy Study Report No. 4: Early vitrectomy for severe proliferative diabetic retinopathy in eyes with useful vision. Clinical application of results of a randomised trial. Ophthalmology 1988; 95: 1331-4.

11 Diabetic Retinopathy Vitrectomy Study Report No. 5: Early vitrectomy for severe vitreous hemorrhage in diabetic retinopathy. Four year results for randomised trial. Arch Ophthalmol 1990: 108: 958-64.

Glossary for diabetic retinopathy

Avascular areas: Areas without blood vessels, due to closure of retinal capillaries caused by diabetic changes.

B-scan ultrasonography: Ultrasound technique used to investigate abnormalities in the posterior segment of the eye usually because the retina is not visible as a result of cataract or vitreous haemorrhage.

Capillary leakage: Healthy retinal capillaries do not leak, but in diabetes the capillaries can be damaged and leak blood, serum or lipids which accumulate within the retina.

Compliance: Positive response by a patient to advice given on treatment, with careful following of instructions.

Cotton wool spots: Small, white-grey areas in the retinal nerve fibre layer caused by capillary closure and damage due to ischaemia.

Fovea: A small depression at the centre of the macula

Foveal avascular zone: Physiological area, approximately 500m in diameter, centred on the fovea which does not contain retinal capillaries.

Fluorescein angiography: Technique to investigate details of the retinal vessels and integrity of the retinal pigment epithelium and choroid, obtained by taking serial fundus photographs using a series of filters after intravenous injection of fluorescein dye.

Hard exudates: Yellow-waxy deposits situated in the inner layers of the retina. They are formed by protein and lipid material.

Hyperlipidaemia: High fat content in the blood.

Hypertension: High blood pressure.

Insulin-dependent diabetes (IDDM): Type I diabetes requiring insulin for control, typically presenting in young people (juvenile-onset).

Intraretinal microvascular abnormalities (IRMA): Distinct blood vessel abnormalities affecting very small blood vessels within the retina.

Macula: Central retina

Maculopathy: Abnormal changes affecting the macula (central retina).

Microaneurysms: Visible out-pouching of weakened blood vessel walls, situated in the inner nuclear layer of the retina.

Neovascularisation of the iris: New blood vessels on and in the iris.

Neovascular fronds: Abnormal, new blood vessels, which branch and ‘interlace’.

Neovascular glaucoma: Secondary glaucoma following new vessel formation in the angle of the anterior chamber.

Non insulin-dependent diabetes (NIDDM): Type II diabetes not requiring insulin for control, typically presenting in middle or older age (maturity-onset). Diet and hypoglycaemic agents may be used.

Panretinal photocoagulation: Treatment (of proliferative diabetic retinopathy) by the application of multiple laser burns to the retinal pigment epithelium. Initial treatment may involve the placement of 2,000-3,000 burns.

Pars plana vitrectomy: Removal of the vitreous gel through openings made in the pars plana (a few millimetres posterior to the corneo-scleral limbus).

Retinal pigment epithelium: Layer of pigmented cells lying between the neural retina and the choroid.

Temporal arcades: The main retinal blood vessels which arch above and below the macula on the temporal side of the optic nerve head.

Tractional retinal detachments: Detachment of the retina due to traction of abnormal attachments of the vitreous to the retina, usually in areas of new blood vessels

Vitreous haemorrhage: Blood within the vitreous cavity.

Venous calibre changes/Venous beading: Variation of the retinal veins – size and shape, ‘thick’ and ‘thin’ appearances, lumen differences, sometimes like beads.