The RETINA is the innermost layer of the eyeball located at the posterior region of the eye. Light stimuli in the retina are captured and transformed into nervous impulse. Photoreceptor cells (rods and cones cells) have an important role in this process. The nervous impulse is transmitted to the brain (occipital lobe) through (right and left) optic nerves where it is converted into visual image.

The MACULA is the central area of ​​the retina with the maximum density of photoreceptor cells. Macula ensures quality (reading and writing) vision.

The vitreous body has the consistency of a gel and occupies the posterior 2/3 of the eyeball being attached to the surface of the retina.

DIABETIC RETINOPATHY is caused by diabetic microangiopathy. Retinal vascular changes occur in the walls of capillaries leading to increased vascular permeability. Structural changes of retinal capillaries affect all parts of the vascular wall (e.g. pericytes, basement membrane, endothelium). The association of rheological changes (blood flow) with increasing viscosity and platelet aggregation produce vascular occlusions.

INCREASED VASCULAR PERMEABILITY and VASCULAR OCCLUSION are the main pathological changes of diabetic retinopathy.

As a result of increased capillary vascular permeability red blood cells, fat and liquid clinically expressed by retinal haemorrhages, hard exudates and retinal oedema pass to retinal extracellular space.

Vascular occlusions cause areas of unperfused - ischemic retina (retina where blood does not reach). The hypoxia (lack of oxygen) and retinal ischemia triggers local production of vascular growth stimulants, trying to alleviate hypoxia and ischemia in unperfused areas by forming new vessels. The neovessels cannot alleviate retinal perfusion but produce major ocular complications: preretinal and vitreous bleeding. These haemorrhages cause decreased visual acuity by vitreous haemorrhage, fibrous proliferation, retinal traction with retinal detachment and neovascular glaucoma.

The vision loss caused by diabetic retinopathy is caused by the appearance of neovessels and diabetic maculopathy (damage to the retina centre).

The neovessels can grow at the level of the optic nerve head and / or retina.

The diabetic maculopathy is caused by macular oedema (retinal thickness increase) as a result of the fluid accumulation, haemorrhages, microaneurysms (dilation of capillaries), and macular ischemia.

The diabetic maculopathy can be focal (better prognosis) or diffuse. The diabetic maculopathy may be oedematous and / or ischemic (worse prognosis). The diabetic maculopathy can also be caused by the existence of macula-driven pre-macular membranes.

The stages of the diabetic retinopathy are, as follows:

• Non-proliferative diabetic retinopathy (early, medium and highly-severe)
• Proliferative diabetic retinopathy (NVD and / or NVE)
• Advanced diabetic eye disease (preretinal haemorrhage, vitreous haemorrhage, fibrous proliferation, fibrovascular membranes, retinal detachment, Rubeosis iridis, neovascular glaucoma).

DIABETIC RETINOPATHY is the leading cause of blindness in civilized countries in population aged between 20 and 65.

he risk of diabetic retinopathy increases with diabetes duration. The longer the development of diabetes is, the more frequent and more severe ocular complications are.

Across the globe live about 382 million diabetics and it is estimated that in 2035 the number will reach 592 million. About 46% of them are undiagnosed.

In Romania there are approximately 800,000 people diagnosed with diabetes. The actual number is closer to 1 million with undiagnosed patients.

The analysis of the results of 35 studies carried out in the period from 1980 to 2008 on a total of 22,896 diabetics showed a prevalence of 34.6% of diabetic retinopathy. Proliferative diabetic retinopathy prevalence was 6.96% and 6.81% for macular oedema.

The diabetic retinopathy is influenced by age and type of diabetes.

The patients with type 1 diabetes mellitus developed diabetic retinopathy within the first 5 years from the diagnostic. Diagnosing diabetes coincides with the onset of the disease.

• after 10-15 years from onset  of the disease 25-50% have retinopathy
• after 15 years from onset of the disease 75-95% have retinopathy.

The patients with type 2 diabetes mellitus may have diabetic retinopathy at the time of the diagnosis.

The onset of diabetes is often long before the diagnostic.

• after 11-13 years from the disease onset, 23% of the patients have retinopathy
• after 14-16 years from the disease onset, 41% of the patients have retinopathy
• after 16 years from the disease onset, 60% of the patients have retinopathy

The main causes that produce diabetic retinopathy are hyperglycaemia (high blood glucose) and diabetes duration. Glucose level variations and the fast decrease in high blood sugar levels lead to the worsening of retinopathy.

The longer the diabetes evolves, the higher the risk of retinopathy.

The diabetes is properly monitored by daily glycaemic control and by measuring the glycated haemoglobin (HbA1c) every 3-4 months.

Type 1 diabetes mellitus is treated with insulin and type 2 diabetes mellitus is treated with oral antidiabetic agents and/or insulin.

The drug treatment is not effective unless the diet is controlled (reduction in the intake of carbohydrates).

Smoking and physical inactivity associated with obesity increase the risk of ocular complications.

Risk factors that aggravate the diabetic retinopathy progression are: high blood pressure, dyslipidaemia (high blood cholesterol and triglycerides), impaired kidney function.

The haemodialysis is more frequently associated with retinal and macular lesions aggravation than the peritoneal dialysis and the kidney transplant.

The pregnancy can lead to a worsening of the retinopathy according to blood glucose readings and retinal damage upon its onset. It is very important that the blood sugar levels gradually return to normal for a long period before conception (6 to 8 months). Diabetic women should plan her pregnancy and be monitored by a diabetologist and an ophthalmologist.

Gestational diabetes occurs in pregnant women who do not have diabetes and experience high blood sugar levels during pregnancy. These women have no risk of diabetic retinopathy, but they run an increased risk of developing diabetes in the coming years.

CAUTION! Diabetic retinopathy may be asymptomatic for a long time! This means that the patient may have diabetic retinopathy and does not know it (has no visual symptoms)! This is the best period for diagnosing and treating the diabetic retinopathy. When the visual symptoms appear, the disease is at an advanced stage, and the treatment cannot improve the vision in all cases.

Symptoms of diabetic retinopathy are modifications of vision BUT also red eye and periocular and ocular pain.

Changes in vision caused by diabetic retinopathy are:

• spots or “floaters” in the visual field
• blurred vision and the impression of seeing through a veil or a dirty window
• warp and distorted image
• difficulty in reading and writing
• amputation of the visual field (dark areas in the visual field)
• total loss of vision in one eye
• less frequently, dark or bright spots

CAUTION! ALL THESE CHANGES REQUIRE EMERGENCY EYE CHECK-UP!

Many patients feel they need to change their glasses – THIS IS TOTALLY WRONG AND DANGEROUS for the visual prognosis!

The ophthalmologic examination is complete (the whole eyeball and periocular areas are examined) and required to be made by pupil dilation.

ATTENTION! The patient does not come and go by car to/from the doctor and cannot read and write after the examination for about 2-3 hours!

The eye examination steps are:

• History (type of diabetes, duration of disease, risk factors and other associated diseases, etc.)
• Determining the visual acuity with correction (glasses may NOT be prescribed upon the first examination)
• Slit lamp examination of the anterior segment of the eye
• Measuring the eye pressure
• Pupil dilation (in patients with diabetes it lasts longer)
• Slit lamp examination of the anterior segment after dilation
• Slit lamp examination of the posterior segment (macula, optic nerve head, retina, blood vessels and vitreous body changes are seen)
• In some cases the doctor chooses gonioscopy (before dilation) and / or indirect ophthalmoscopy.

After examining the posterior segment (fundus), the doctor may recommend:

• retinal photography
• macular tomography (OCT)
• retinal fluorescein angiography
• ocular ultrasound

The complete eye examination allows detection of all ocular complications of diabetes (cataract).

CAUTION! The diabetic patient may experience double vision (diplopia) as a result of the eye muscles being affected in diabetics with diabetic neuropathy and high glycaemic levels. The patient must have an emergency eye examination and the blood sugar level must be balanced. The visual prognosis is good and the diplopia resolves in 2-3 months with no visual impairment.

THE EYE EXAMINATION OF A DIABETIC TAKES APPROXIMATELY 1 HOUR!

Early diagnosis of diabetic retinopathy is very important in order to detect and treat retinal lesions and can be done only through EYE EXAMINATION.

Periodic ophthalmologic exam - even in the absence of visual symptoms - is called diabetic retinopathy screening and has certain effectiveness in preventing blindness by diabetic retinopathy.

ALL PATIENTS WITH DIABETES SHOULD PERFORM EYE EXAMINATIONS!

The screening program is based on the type of diabetes and diabetic retinopathy stage.

Patients with diabetes without diabetic retinopathy should have eye exam performed once a year.

Patients with type 1 diabetes can have an eye examination every 3 to 5 years after the diabetes onset.

Patients with type 2 diabetes should have an eye examination upon the diabetes diagnostic.

Patients with diabetes type 1 and 2 have the following screening program, depending on the stage of diabetic retinopathy:

• non-proliferative diabetic retinopathy, early and medium stage - eye examination every 6 months
• advanced non-proliferative diabetic retinopathy - eye examination every 3 to 4 months

At these stages, the diabetic retinopathy does not require an eye treatment.

The association of diabetic maculopathy, which can occur at any stage of diabetic retinopathy, changes the screening program and eye treatment.

The proliferative diabetic retinopathy and advanced diabetic eye disease require emergency eye treatment.

The screening program may be modified by the doctor depending on the association with risk factors (high blood pressure, impaired kidney function) and other general (hepatitis, etc.) and eye (glaucoma, etc.) disease.

Women with diabetes need to plan their pregnancy and the eye check-up is performed at various intervals, depending on the stage of the retinopathy.

Proliferative diabetic retinopathy is treated with laser retinal panphotocoagulation. The laser is made with pupil dilation and do not require hospitalization. Several laser sessions are performed and their number and the laser time frame are determined by the doctor depending on the particular case. Usually there are 4 sessions in 1 month. The laser is clinically proven to stop the emergence and growth of neovessels.

Sometimes the doctor may decide to start laser therapy in advanced non-proliferative diabetic retinopathy stage.

The diabetic maculopathy is treated with laser and / or intravitreal injections. Laser sessions are carried out at greater intervals than the retinal panphotocoagulation. The laser therapy is often associated with intravitreal injections. Intravitreal injections are performed to reduce the macular oedema and anti-inflammatory substances (triamcinolone, etc.) and / or VEGF inhibitory substances (bevacizumab, etc.) are used. Intravitreal injections and laser therapy sessions can be repeated when necessary.

The diabetic maculopathy with traction component is operated for traction removal (vitrectomy).

The macula tomography (OCT) is very useful in order to diagnose and monitor the diabetic maculopathy.

The advanced diabetic eye disease is treated through a surgical intervention called vitrectomy.

The vitrectomy cleans the blood and fibrovascular membranes in the eye and repositions the detached retina. The vitrectomy is associated with laser and intravitreal injections.

The neovascular glaucoma is a medical and surgical emergency and the treatment consists of local and general ocular hypotensive therapy, intravitreal injections with anti-VEGF substances, retinal laser and, in some cases, vitrectomy and anti-glaucomatous surgery (ocular drainage devices).

The eye treatments cannot cure the diabetic retinopathy but they can prevent, delay, reduce, and sometimes even stop the vision loss. Most of the times, even if the vision quality is not improved, the ophthalmologist can stop the retinopathy and the vision from worsening.

The visual prognosis is better in patients with diabetic retinopathy who start therapy with good vision quality and closely observe the treatment for diabetes. The patients with diabetes are monitored through regular eye examinations throughout their lives. Every eye examination, the patient is reminded the importance of keeping the diabetes balanced and treating the associated conditions (e.g. high blood pressure, dyslipidaemia, etc.).

THE BLINDNESS CAUSED BY DIABETIC RETINOPATHY IS PREVENTED THROUGH PERIODIC EYE EXAMINATIONS (the only way to diagnose and treat diabetic retinopathy before the vision is impaired) and THROUGH A CORRECT TREATMENT OF THE DIABETES AND ASSOCIATED RISK FACTORS.