What is Diabetic Eye Disease: Proliferative Diabetic Retinopathy

Proliferative diabetic retinopathy is an eye disease that affects diabetics. It occasionally also affects individuals with pre-diabetic metabolic abnormalities (e.g. metabolic syndrome). The condition is characterised by the growth of tiny abnormal blood vessels (a process called neovascularisation) in the eye, and fibrous growth in the retina (the light-sensing area of the eye) and surrounding vitreous fluid (a layer of jelly-like substance that protects the retina and separates it from the lens).
Neovascularisation (abnormal blood vessel growth) in diabetic retinopathy occurs in response to retinal ischaemia (lack of blood flow to the retina). New vessels may grow on the optic disc (where the optic nerves enter the eye) or elsewhere in the eye. Because the blood vessels are abnormal, they may bleed into the retina or vitreous fluid, causing spots of blood in the eye that block vision.
Proliferative retinopathy is a sight-threatening condition. The abnormal blood vessel growth that characterises the disease also creates a risk of macular oedema. Macular oedema occurs if fluid from the vessels leaks and disturbs vision in the macula (the section of the eye that regulates clear, sharp vision). It is the leading cause of blindness in working-age people.
Proliferative diabetic retinopathy can be further classified in terms of the likelihood that it will cause vision loss. Classifications are:

  • Non-high risk (also termed early proliferative): Cases where abnormal blood vessel growth is limited and there is no haemorrhage in the vitreous;
  • High risk or sight-threatening: Cases where the abnormal blood vessel growth occurs in the optic disc area and covers more than a quarter of the disc surface, or cases where abnormal blood vessel growth occurs in other areas and causes bleeding in the vitreous fluid.

Other categories of diabetic retinopathy include the following.

Non-proliferative diabetic retinopathy

Non-proliferative diabetic retinopathy, previously called background retinopathy, is the earliest stage of diabetic eye disease. It is characterised by the development of microaneurysms (enlarged areas of blood vessels which occur due to weak vessel walls). The condition often has no symptoms. Individuals with non-proliferative diabetic retinopathy may lose vision as a result of macular oedema or if their condition progresses to proliferative diabetic retinopathy.

Non-proliferative retinopathy For more information, see Non-Proliferative Diabetic Retinopathy.

Diabetic macular oedema

At all stages of non-proliferative diabetic retinopathy, there is also a risk of macular oedema, a sight-threatening condition that occurs as a consequence of the vascular changes of diabetic retinopathy. Macular oedema is the most common cause of diabetes-associated vision loss. It occurs when abnormal new blood vessels burst and bleed into the macula.

Ischaemic maculopathy

Ischaemic maculopathy is an untreatable form of diabetic retinopathy characterised by the loss of capillaries (tiny blood vessels) in the macula and impaired blood flow to the macula.

Statistics on Diabetic Eye Disease: Proliferative Diabetic Retinopathy

Proliferative diabetic retinopathy pictureDiabetic retinopathy is common amongst diabetics, and the likelihood of a diabetic developing the condition increases with the length of time they have had diabetes. The risk of retinopathy also varies depending on the age at diabetes diagnosis, the person’s age, and whether or not they have non-proliferative diabetic retinopathy.
In Australia, new cases of proliferative diabetic retinopathy are diagnosed in 2.9% of diabetics every 5 years. Incidence is higher in the elderly and Indigenous Australians, and those with non-proliferative retinopathy. For example, one study reported 1.5% of all diabetics developed proliferative retinopathy in 5 years, compared to 4.2% of those with existing non-proliferative retinopathy. An estimated 1.2% of the diabetic population develop sight-threatening disease each year, which may be either proliferative retinopathy or, more commonly, macular oedema.
The prevalence of retinopathy amongst diabetics increases with progression of the disease (as metabolic changes become more pronounced) and as duration since diabetes diagnosis increases. After 10 years diabetes duration, 7% of patients have evidence of retinopathy, and after 25 years some 90% will be affected by retinopathy of varying degrees. Evidence of retinopathy is almost universal amongst diabetics 30 years after onset. A US-based study estimated that 72% of diabetics develop proliferative retinopathy at some stage.
However, prevalence and severity of diabetic retinopathy appears to be declining. The decline is assumed to result from better diabetes management and treatment, which means that diabetics are able to control their blood sugar levels, blood pressure and other metabolic imbalances more effectively by modifying their diets or using medications.

Risk Factors for Diabetic Eye Disease: Proliferative Diabetic Retinopathy

Diabetes is the key risk factor for proliferative diabetic retinopathy, and all individuals with type 1 diabetes mellitus or type 2 diabetes mellitus are at risk of developing diabetic retinopathy. Some individuals with impaired glucose metabolism who do not develop diabetes are also at risk of diabetic retinopathy.
In these groups of patients, risk factors for development and progression of the disease include:

  • Duration of diabetes: The risk of retinopathy increases as the length of time since diabetes diagnosis increases;
  • Pre-pubertal diabetes onset: Individuals who develop diabetes before they go through puberty have a high risk of retinopathy;
  • Type 1 diabetes: Individuals with type 1 diabetes are more likely to develop retinopathy that those with type 2 diabetes;
  • Poorly controlled blood sugar levels: Individuals with diabetes who do not effectively control their blood sugar using dietary modifications and/or medications have an increased risk of diabetic retinopathy. The extent of risk increases in line with the extent of blood sugar abnormalities;
  • Poor blood pressure control;
  • High cholesterol;
  • Pregnancy: Associated with an increased risk of developing non-proliferative retinopathy. May also be associated with more rapid progression of existing retinopathy;
  • Kidney impairment: Associated with diabetic retinopathy, although it appears that diabetic retinopathy leads to kidney impairment rather than vice versa;
  • Genetic susceptibility: Diabetic retinopathy appears to be a genetic condition, but the genetics of it are not well understood;
  • Alcohol: Does not increase the risk or progression of diabetic retinopathy, but individuals who consume moderate amounts of alcohol have a 1.8 times higher risk of vision loss if they do develop retinopathy. Because alcoholic drinks contain a lot of calories and diabetics must control their calorie intake, consuming alcohol makes it very difficult to follow a diabetic diet. Non-compliance with a diabetic diet increases the risk of retinopathy;
  • Gender: A US-based study reported that male diabetics were more than twice as likely to develop retinopathy than female diabetics;
  • Ethnicity: A US study reported higher prevalence of retinopathy in non-Hispanic black diabetics (39%) compared to non-Hispanic white diabetics (26%). Sight-threatening retinopathy also occurred in a significantly greater proportion of non-Hispanic black (9%) than white (3%) individuals.

Early diabetes diagnosis

Early diabetes onset (before age 30) is associated with a higher risk of diabetic retinopathy. Amongst individuals who were diagnosed with diabetes before age 30, proliferative retinopathy affects 25% after 15 years duration, and 55% after 20 years (compared to 20% of individuals diagnosed after age 30 with 20 years disease duration).

Diabetes type

In patients with type 2 diabetes, available evidence suggests that 40% have some type of retinopathy. 8.2% have severe, sight-threatening retinopathy. Evidence regarding the prevalence of retinopathy in type 1 diabetes is more limited; one study reported 82% prevalence for any type or severity of retinopathy, and 32% prevalence for sight-threatening retinopathy. This suggests type 1 diabetics have a higher risk of retinopathy than type 2 diabetics. Some recent research has reported higher risk in those with type 2 diabetes, which may indicate fewer new cases of retinopathy in type 1 diabetics due to improvements in blood sugar control.
There are also differences in the nature of retinopathy depending on diabetes type. Those with type 1 diabetes are most likely to experience vision loss due to proliferative retinopathy, whereas those with type 2 diabetes are most likely to experience vision loss as a result of macular oedema.

Poor glucose control

The risk of retinopathy increases with increasing severity of blood sugar abnormalities. Individuals with impaired glucose tolerance who do not develop diabetes (e.g. those with metabolic syndrome) also have a risk of diabetic retinopathy. Of those who do not develop diabetes, 7.9% show signs of diabetic eye disease.
Evidence also shows associations between blood sugar levels and reduced progression of diabetic retinopathy, and that optimal regulation of blood sugar levels with diabetes treatments reduces development and progression of diabetic retinopathy. Optimal blood sugar control can reduce the development and progression of retinopathy by up to 54% in type 1 diabetic patients, and up to 25% in type 2 diabetic patients.


Evidence also suggests that blood pressure-reducing therapies reduced the risk of diabetic retinopathy in diabetic patients with hypertensiion.

Progression of Diabetic Eye Disease: Proliferative Diabetic Retinopathy

Progression of vascular changes

Proliferative diabetic retinopathy pictureProliferative diabetic retinopathy is a condition that can cause severe vision loss and blindness. It develops as a complication of diabetes and becomes more likely with duration and severity of diabetes or blood sugar abnormalities. The growth of abnormal blood vessels in the retina characterising proliferative disease occurs as a result of lack of blood flow to the retina, caused by non-proliferative diabetic retinopathy. Visual loss may occur if the new blood vessels leak or if the retina becomes detached from the layers supporting it. Retinal detachment occurs when fibrous growth causes the retina to pull away from the underlying epithelial cells (also called tractional retinal detachment).


Abnormalities in glucose metabolism (which regulates blood sugar levels) and retinopathy have a number of common pathways. Chronic hyperglycaemia (high blood sugar) is accepted as the most common pathway through which diabetic retinopathy develops. Different stages of the development of retinopathy can also be linked to other pathways affecting glucose metabolism.
Pathways linked to the development of proliferative disease include:

There is considerable crossover between these pathways. The chemicals involved in each pathway influence each other. As a result, it is unlikely that treatments targeting a single pathway will be completely effective.
In addition to these pathways, increased oxidative stress (an excess of free radicals that can damage body tissues and cells) is associated with high blood sugar and diabetes. Each of the above pathways is associated with the production of free radicals. This indicates that treatments also aiming to reduce free radicals may be more successful than those targeting any single pathway.

Sorbitol and aldose reductase pathway

The sorbitol–aldose reductase pathway is the pathway through which aldose reductase catalyses the reduction of glucose to sorbitol. In individuals with high blood sugar levels, excess sorbitol accumulates and causes damage to blood vessel walls. Sorbitol accumulation also causes damage to retinal pericytes, which regulate the growth and function of capillaries in the retina. When pericytes become damaged, they cannot prevent blood vessel proliferation, and neovascularisation (abnormal new blood vessel growth) occurs.
The sorbitol–aldose reductase pathway is linked to the development of non-proliferative diabetic retinopathy, from which proliferative disease develops. It also plays a direct role in the neovascularisation characterising proliferative disease. Changes in the sorbitol–aldose reductase pathway lead to the development of precursors of advanced glycation end-products, which impair the function of proteins and cause damage to cells (discussed below).

Retinal blood flow changes

Retinal blood flow is altered in all stages of diabetic retinopathy. Blood flow increases to counteract the effect of contracted or occluded blood vessels, which impair blood flow in the early, non-proliferative stages of the disease.
In the later stages of disease when larger retinal arteries widen to counter the effect of blocked capillaries, blood flow decreases. Reduced blood supply to the retina leads to a lack of retinal oxygen. In an attempt to correct oxygen levels by improving blood flow, the body releases vascular endothelial growth factors (VEGFs). These stimulate the growth of new blood vessels.

Increased protein kinase C activity

Protein kinase C refers to a group of proteins that regulate the chemicals which stimulate cell growth (growth factors), transmit signals to the brain (neurotransmitters) and regulate hormone production. In particular, protein kinase C regulates the production of endothelial growth factor, the growth factor that regulates vascular cells such as those that form blood vessels. Endothelial growth factor is an important mediator of neovascularisation in the eye.
The protein kinase C pathway also mediates blood flow to the retina. Increased protein kinase C activity causes the vascular changes characteristic of diabetic retinopathy. In addition, activation of the protein kinase C pathway is associated with increased production of reactive oxygen species, which increases oxidative stress. As mentioned above, oxidative stress plays a role in the development of diabetic retinopathy.

Development of advanced glycation end-products

Advanced glycation end-products (AGEs) are the result of glycation (bonding of a carbohydrate to a protein or other chemical). With ageing, blood sugars cause irreversible damage to many proteins by binding to them through glycation and glycosylation. This binding causes degradation of the protein, which leads to the formation of AGEs.
While AGEs develop naturally with ageing, it progresses more quickly in diabetics than in non-diabetics. The AGEs resulting from glycation cause cell damage by impairing the function of regulatory proteins. In particular, AGEs are known to alter the function of collagen, a protein that mediates the function of blood vessels.
AGEs also result in the production of reactive oxygen species, which contribute to retinopathy by increasing oxidative stress.

Angiotensin enzyme expression and coagulation pathway

Components of the angiotensin–renin enzyme system affect cell growth, blood pressure and the permeability of blood vessels. These enzymes are found in many of the eye’s structures and regulate several ocular processes, including the production of blood vessels and retinal pigment cells.
Increased concentrations of the enzymes involved in the angiotensin–renin system are associated with the development of diabetic retinopathy. Treatment with either angiotensin-converting enzyme (ACE) inhibitors or angiotensin II type 1 receptor blockers (medicines that affect the angiotensin system) has been shown to inhibit the abnormal growth of new blood vessels in the retina.
The angiotensin–renin system is linked to the blood coagulation pathway. Diabetic retinopathy is associated with changes to the coagulation pathway, which is regulated by vascular endothelial growth factors (involved in regulating blood vessel structure) and connective tissue growth factors (such as collagen). These are produced in increasing quantities in retinopathy.

Other mechanisms that influence the development of diabetic retinopathy

A number of other mechanisms are thought to influence the development of diabetic retinopathy, including:

  • Inflammation and dysfunction of blood vessel cells;
  • Hypertension: Increases inflammation in the retina;
  • Changes to the retinal barrier, which usually functions to prevent blood flowing into the retina;
  • Vascular changes, specifically the widening of retinal veins and arterioles, which occurs in the early stages of diabetes; and
  • Pregnancy: Can lead to inflammation and damage to the blood vessel system.

Progression of symptoms

In the early stages of diabetic retinopathy (non-proliferative retinopathy) a person typically has no symptoms. The first noticeable symptoms are usually vision changes, which appear when a person develops proliferative retinopathy. Vision changes worsen and cause vision loss over time.
Macular oedema may occur at the same time as proliferative diabetic retinopathy. It initially causes blurred vision, but can progress very rapidly to complete and permanent vision loss. Vision loss related to macular oedema can occur at any stage of non-proliferative or proliferative disease.
Proliferative retinopathy is characterised by neovascularisation (i.e. the growth of new, abnormal blood vessels in the eye’s retina and surrounding vitreous fluid). New blood vessels grow in response to lack of blood flow to the retina, which occurs in the non-proliferative stage of the disease due to blood vessel damage.The new blood vessels are fragile and the risk of bleeding is high. Bleeding typically occurs at night during sleep.

Symptoms of Diabetic Eye Disease: Proliferative Diabetic Retinopathy

Proliferative diabetic retinopathy pictureSymptoms of proliferative retinopathy include:

  • Floating spots in the vision;
  • Areas of shadow in the vision; or
  • Missing spots in the vision.

Diabetic retinopathy often has no obvious symptoms until major bleeding occurs in the proliferative stage of the disease, causing vision loss. All people with diabetes should have their eyes examined regularly, as eye examinations can identify retinopathic changes before symptoms occur, allowing treatment to be started before vision loss occurs. Treatments for diabetic retinopathy cannot restore vision that has already been lost, but can help prevent vision loss. Screening to diagnose diabetic retinopathy in the early stages and early treatment are therefore of vital importance.
Up to one third of diabetics with retinopathy are undiagnosed. It is therefore likely that your doctor will enquire about the last time you had an eye examination during a diabetes consultation. If you have not had an eye examination within the recommended period of time, you will be referred to a specialist for examination. If you have not had an eye examination, make sure you mention this to your doctor during your next consultation.
When you are diagnosed with diabetes or when you attend a new doctor for treatment, they will need to enquire about your diabetes and general health, as well as any eye symptoms you might be experiencing, in order to determine the best course of management to prevent vision loss from diabetic retinopathy. In particular, the doctor is likely to enquire about your:

  • General health;
  • Diabetes duration;
  • Blood sugar levels, past and current;
  • The medications you use to treat diabetes;
  • Other conditions, such as hypertension, cholesterol, obesity and kidney disorders;
  • Pregnancy; and
  • Ocular symptoms, past and current.

If you are experiencing eye symptoms, the doctor will also need to rule out other eye disorders that may produce similar symptoms to diabetic retinopathy.

Clinical Examination of Diabetic Eye Disease: Proliferative Diabetic Retinopathy

Clinical examination of an individual for diabetic retinopathy focuses on assessment of the eyes. It usually includes:

  • A visual acuity test, for example using a Snellen chart in which you are asked to read out lines of progressively smaller letters;
  • Examination of the eyes for signs of vessel damage using a special lamp. Eye drops are often used to widen the pupils before the examination. There are a range of different ways the eye can be examined, depending on the extent of disease and which structures in the eye are affected (e.g. the retina or vitreous fluid). If you live in a remote area, the doctor may take photos of your eye to be sent away for examination by a specialist.

Both eyes should be examined and the severity of retinopathy should be graded according to the standard system used in Australia. According to this system, diabetic retinopathy can be classified as:

  • No disease;
  • Non-proliferative (mild);
  • Non-proliferative (moderate);
  • Non-proliferative (severe); or
  • Proliferative (may be high-risk or advanced).

Each of the four disease states may occur with or without macula oedema.
The eye examination is often conducted by a specialist such as an ophthalmologist. It is important to ensure that the doctor who treats your diabetes is aware of the test results. The ophthalmologist will probably send the results to your doctor, but it is still a good idea to take your test results to your next appointment.
If you are diagnosed by an ophthalmologist but have not been diagnosed with diabetes or do not have a regular doctor who treats your diabetes, go to a general practitioner for diabetes assessment. If they are unable to provide diabetes treatment, they can refer you to another doctor who can.
The doctor may also perform tests to assess your diabetes control. For example, they may measure your blood sugar levels or blood pressure.

How is Diabetic Eye Disease: Proliferative Diabetic Retinopathy Diagnosed?

Proliferative diabetic retinopathy is diagnosed on the basis of eye examination results, when abnormal blood vessels are found growing in the retina.

Prognosis of Diabetic Eye Disease: Proliferative Diabetic Retinopathy

Proliferative diabetic retinopathy leads to vision loss unless treated. Timely treatment with laser surgery or other treatments reduces progression of the disease and the risk of vision loss. However, treatment cannot restore eyesight that has already been lost.

How is Diabetic Eye Disease: Proliferative Diabetic Retinopathy Treated?

Proliferative diabetic retinopathy pictureTreatments for all types of diabetic retinopathy can prevent further vision loss. It is important to note that they do not cure the underlying vessel damage that causes the conditions, and so will not restore lost vision. Early treatment is the most important factor in preventing vision loss. Treatment involves a combination of managing diabetes and treating the eyes affected by neovascularisation.

Diabetes management

Blood sugar control reduces the risk of retinopathy and its progression, and is an important component of treatment.
Lowering blood pressure using medications (beta blockers or ACE inhibitors) has been shown to reduce the progression of diabetic retinopathy.
Lowering cholesterol levels may also decrease the risk of visual loss from diabetic retinopathy.

Scatter (panretinal) laser photocoagulation

Scatter or panretinal laser photocoagulation is a treatment used in the early stages of proliferative diabetic retinopathy when abnormal blood vessels have commenced growth but have not started to bleed into the retina and vitreous fluid. It is at least 50% effective in preventing severe vision loss.
The surgery involves directing laser beams into the eye and placing microscopic burns into the affected area of the retina. Treatment typically involves 1,000–2,000 laser burns, and two or more sessions are often required to complete the treatment. The laser beams achieve photocoagulation (closure of the blood vessels as a result of the laser burns) and prevents further neovascularisation by reducing oxygen demand in affected areas of the eye. In some cases, scatter laser photocoagulation can lead to regression of existing abnormal vessels. The treatment is most effective at closing newly formed blood vessels (in the early stages of proliferative retinopathy).
Scatter laser photocoagulation may improve vision in individuals with established neovascularisation who are already experiencing vision loss due to bleeding. When bleeding is present, smaller microscopic burns (1/2–1/5 the width of the burns used in early neovascularisation) are placed around the bleeding vessels.
Following scatter laser therapy, it is important to return for a review so that the doctor can determine whether or not the abnormal blood vessels have regressed and if there is any new abnormal growth. Failure of vessels to regress or their redevelopment usually indicates further treatment is required.
Like all surgical procedures there are risks associated with scatter laser photocoagulation, which include:

  • Central vision loss as a result of the surgery worsening macular oedema;
  • Loss of peripheral vision;
  • Poor dark adaptation; or
  • Bleeding into the vitreous.

Who requires early treatment?

Early treatment is warranted for pregnant women with neovascularisation and other risk factors for the development of proliferative disease (diabetes duration > 15 years, poor glycaemic or blood pressure control). In these cases, treatment aims to prevent irreversible vision loss during pregnancy.


Vitrectomy, a procedure that involves removing blood from the vitreous fluid, is indicated in cases of severe proliferative retinopathy characterised by bleeding in the retina or vitreous. It may be particularly useful in people who have also developed macular oedema.
Early vitrectomy is a cost-effective treatment that leads to visual acuity improvements or stabilisation in 90% of people treated. It is most effective when performed within 3 months of the onset of retinal or vitreous bleeding. It appears to be more effective in patients with type 1 diabetes compared to those with type 2 diabetes.
People who may be treated using vitrectomy include those with:

  • Type 1 diabetes and severe proliferative retinopathy causing bleeding in the vitreous;
  • Severe proliferative disease that fails to regress after extensive treatment with photocoagulation surgery;
  • Risk of macular detachment; and
  • Severe macular oedema, when other treatments fail.

Vitrectomy should only be instituted after as much laser photocoagulation has been performed as possible. This reduces complications following the surgery. Recurrent bleeding in the vitreous is the most common complication of vitrectomy. The risk of recurrent bleeding appears to be reduced when pre-treated (1 week before vitrectomy) with intravitreal bevacizumab injection.

Injection into the eye of anti-VEGF

Anti-vascular endothelial growth factor (anti-VEGF) drugs, including pegaptanib, ranibizumab and bevacizumab, are emerging as promising methods of treating proliferative retinopathy. The drugs do not damage the eyes, but repeat injections are usually necessary and there is some concern regarding the systemic effects (effects on other body systems) of bevacizumab, which is the most frequently used drug.
VEGFs are produced naturally by the body and mediate the growth of blood vessels. Increased production of VEGFs (as occurs in the retina in diabetic retinopathy) causes abnormal formation of new blood vessels. Anti-VEGFs impair the activity of VEGFs and reduce neovascularisation. They are a new form of treatment and further research is required to demonstrate the extent to which they reduce vision loss. However, early studies into the use of anti-VEGFs have produced promising results (e.g. improved visual acuity in treated patients) and these medicines have been approved for the treatment of diabetic retinopathy in Australia.

Support services available for people with deteriorated vision

Individuals who have experienced irreversible visual loss may find it difficult to cope with day-to-day activities. If your vision is affected by diabetic retinopathy, ask your doctor for a referral to support services (e.g. rehabilitation, support, counselling) for vision impaired or blind people. Coping with vision loss is difficult and it is important to seek help.
If your vision deteriorates significantly, you may be able to register as legally blind, which may make it easier for you to access support services.

More Information

Diabetes For more information on diabetes, including different types of diabetes, blood glucose and dietary control, and long-term complications, as well as some useful videos, see Diabetes.


Diabetic Eye Disease: Proliferative Diabetic Retinopathy Prevention

Preventative screening

Proliferative diabetic retinopathy pictureVision loss due to retinopathy can be prevented through frequent eye examination and timely treatment when proliferative retinopathy or macular oedema is diagnosed. This is the key preventative measure. However, at least 22% of Australian diabetics are not screened as often as recommended by the National Health and Medical Research Council (NHMRC), making them at risk of delayed diagnosis and vision loss.
Diabetics should have regular, comprehensive eye examinations by an eye specialist. Preventative screening and timely treatment where appropriate have been shown to be highly cost-effective. Treatment reduces the risk of vision loss from retinopathy by 95%.
Non-compliance with screening and post-diagnosis treatment reduces the efficacy of this prevention strategy. In addition, non-specialists (e.g. general practitioners) are less able to identify retinopathy than specialists during screening. Examination by an eye specialist is therefore recommended.
An eye examination should be performed at the time your diabetes is diagnosed, and at least once every 2 years thereafter. Some diabetics have a higher risk of vision loss and should have more regular eye examinations. These people include:

  • Indigenous Australians;
  • Australians from a non-English speaking background;
  • Those who have had diabetes for a longer period of time, as risk of retinopathy and vision loss increases with increasing duration of diabetes; and
  • Those with poorly controlled blood sugar, blood pressure or cholesterol.

Children with diabetes onset should have their eyes re-examined at the onset of puberty. Diabetic women who become pregnant should also have their eyes assessed when the pregnancy is diagnosed. If there is evidence of retinopathy, these women need close monitoring throughout pregnancy. Monitoring is not required in cases of gestational diabetes, unless diabetes persists post-pregnancy.

Emergency referral

Emergency (same day) referral to a specialist is recommended if a person has severe symptoms, including sudden visual loss or symptoms of retinal detachment (e.g. floating spots in the vision). If new blood vessels, bleeding into the vitreous fluid or rubeosis iridis (new blood vessel growth on the iris) are detected, immediate referral (within 1 week) to a specialist is required.
If proliferative retinopathy or macular oedema is suspected, prompt referral to a specialist (within 4 weeks) who can treat the condition is essential. You should also see your general practitioner or an eye specialist if you experience:

  • Reduced night vision;
  • Blurred vision;
  • Vision blocked by patches or streaks; or
  • Sudden vision loss.

Diabetes management

Adequate control of blood sugar, blood pressure and cholesterol in diabetics minimises the chance that retinopathy will develop. Data show that with optimal diabetes treatment, a person is 29% less likely to require laser surgery to prevent vision loss and 16% less likely to be declared legally blind after 10 years, compared to those who receive normal diabetes management.
If you have diabetes or poorly controlled blood sugar (e.g. as in metabolic syndrome) improving your diabetes treatment through a range of dietary, lifestyle and medication changes can reduce your chance of vision loss from diabetic retinopathy. Make sure you are fully informed about the role of obesity and metabolic abnormalities in diabetic retinopathy, and about the importance of adhering to a diabetic diet and exercising regularly.
It’s also important to avoid alcohol. While alcohol consumption alone is not associated with diabetic retinopathy, the consumption of empty calories from alcohol makes adhering to a restricted calorie diet very difficult.

Diabetic Eye Disease: Proliferative Diabetic Retinopathy References

  1. Chapter 9: Management of proliferative diabetic retinopathy. In: Wu G. Diabetic Retinopathy: The essentials. Philadelphia, PA: Lippincott Williams & Wilkins; 2010: 122-37. [Book]
  2. Guidelines for the management of diabetic retinopathy [online]. Canberra, ACT: National Health and Medical Research Council; 2008 [cited 28 February 2011]. Available from: URL link
  3. Classification of diabetic retinopathy. In: Tabandeh H, Goldberg M. The Retina in Systemic Disease: A color manual of ophthalmoscopy. New York, NY: Thieme Medical Publishers; 2009: 91-108. [Book]
  4. Trad MJ. Diabetic retinopathy. In: Onofrey BE, Skorin L, Holdeman NR. Ocular Therapeutics Handbook: A clinical manual (2nd edition). Philadelphia, PA: Lippincott Williams & Wilkins; 2005: 520-6.[Book]
  5. Spurling G, Askew D, Jackson C. Retinopathy: Screening recommendations. Aust Fam Physician. 2009;38(10):780-3. [Abstract | Full text]
  6. Diabetic retinopathy [online]. San Francisco, CA: American Academy of Ophthalmology; 2008 [cited 28 February 2011]. Available from: URL link
  7. Facts about diabetic retinopathy [online]. Bethesda, MD: National Eye Institute; October2009 [cited 22 February 2011]. Available from: URL link
  8. Lee CC, Stolk RP, Adler AI,et al. Association between alcohol consumption and diabetic retinopathy and visual acuity: The AdRem Study. Diabet Med. 2010;27(10):1130-7. [Abstract]
  9. Zhang X, Saaddine JB, Chou C, et al. Prevalence of diabetic retinopathy in the United States, 2005-2008. [Abstract | Full text]
  10. Watkins PJ. Retinopathy. BMJ. 2003;326(7395):924-6. [Abstract | Full text]
  11. Fong DS, Aiello L, Gardner T, et al. Diabetic retinopathy. Diabetes Care. 2003;26(Suppl 1):S99-102. [Abstract | Full text]
  12. Ockrim Z, Yorston D. Managing diabetic retinopathy. BMJ. 2010;341:c5400. [Abstract]
  13. Stewart MW. Chapter 1: Pathophysiology of diabetic retinopathy. In:Browning DJ (ed). Diabetic Retinopathy: Evidence-based management. New York: Springer;2010: 1-31. [Book]
  14. Diabetic retinopathy: Symptoms [online]. London: National Health Service; 16 December 2009 [cited 16 June 2011]. Availbale from: URL link
  15. Diabetic retinopathy: Initial and follow-up evaluation [online]. San Francisco, CA: International Council of Ophthalmology; 3 January 2011 [cited 22 February 2011]. Available from: URL link
  16. Viswanath K, McGavin DD.Diabetic retinopathy: Clinical findings and management.Community Eye Health. 2003;16(46):21-4. [Full text]

Drugs/Products Used in the Treatment of This Disease:

All content and media on the HealthEngine Blog is created and published online for informational purposes only. It is not intended to be a substitute for professional medical advice and should not be relied on as health or personal advice. Always seek the guidance of your doctor or other qualified health professional with any questions you may have regarding your health or a medical condition. Never disregard the advice of a medical professional, or delay in seeking it because of something you have read on this Website. If you think you may have a medical emergency, call your doctor, go to the nearest hospital emergency department, or call the emergency services immediately.