What is Diabetic Retinopathy (diabetic blindness)

Introduction

Retina is the part of the eye that is responsible for receiving images and transmitting them to the brain through optic nerve. Diabetic retinopathy refers to the retinal changes in patients with diabetes mellitus. It is a common complication of diabetes mellitus, which can eventually lead to blindness. It is an ocular manifestation (involves the eye) of systemic disease which affects up to 80% of all patients who have had diabetes for 10 years or more. With the increase in life expectancy of people with diabetes, the incidence of retinoparht is on the rise. It is the leading cause of blindness in the developed nations. Research indicates that at least 90% of these new cases of diabetic retinonathy could be reduced if there was proper and vigilant treatment and monitoring of the eyes.




Diabetic retinopathy can be proliferative (growing) or nonproliferative (not growing), referring to the growth
of abnormal blood vessels in the retina. Nonproliferative retinopathy is much more common and may not require treatment. In proliferative retinopathy, abnormal blood vessels start to grow when the existing blood vessels close off. The proliferative type of retinopathy can lead to impaired vision.

Risk factors-

1) Duration of diabetes

2) Sex=> female sex: male sex= 4:3

3) Poor metabolic control

4) Heredity: autosomal recessive

5) Pregnancy: accelerates the changes

6) Hypertension:  associated hypertension accelerates changes

7) Smoking

8) obesity

9) hyperlipidaemia (increased blood cholesterol)

Symptoms:

Blurring of vision mostly during the daytime is seen in some patients. But in a majority it progresses without any symptoms.

Black spots floating in the visual field. (floaters)

Finally there is complete loss of vision

Blurry vision



On fundoscopic examination, a doctor will see cotton wool spots, flame hemorrhages and dot-blot hemorrhages.

Incidence by age-

Nearly 50% patients develop disease by the end of 10 years. 70% by the end of 20 years and nearly 90 % patients develop the disease by the end of 30 years.

Pathogenesis- 

Diabetic retinopathy is the result of microvascular changes in the retinal blood vessels. Hyperglycemia-induced intramural pericyte death and thickening of the basement membrane lead to incompetence of the vascular walls. These damages change the formation of the blood-retinal barrier and also make the retinal blood vessels become more permeable.
The pericyte death is caused when "hyperglycemia persistently activates protein kinase C-δ (PKC-δ, encoded by Prkcd) and p38 mitogen-activated protein kinase (MAPK) to increase the expression of a previously unknown target of PKC-δ signaling, Src homology-2 domain–containing phosphatase-1 (SHP-1), a protein tyrosine phosphatase. This signaling cascade leads to PDGF receptor- dephosphorylation and a reduction in downstream signaling from this receptor, resulting in pericyte apoptosis."
Small blood vessels – such as those in the eye – are especially vulnerable to poor blood sugar (blood glucose) control. An overaccumulation of glucose and/or fructose damages the tiny blood vessels in the retina. During the initial stage, called nonproliferative diabetic retinopathy (NPDR), most people do not notice any change in their vision.
Some people develop a condition called macular edema. It occurs when the damaged blood vessels leak fluid and lipids onto the macula, the part of the retina that lets us see detail. The fluid makes the macula swell, which blurs vision.
Elevation of blood-glucose levels can also cause edema (swelling) of the crystalline lens (hyperphacosorbitomyopicosis) as a result of sorbitol (sugar alcohol) accumulating in the lens. This edema often causes temporary myopia (nearsightedness). A common sign of hyperphacosorbitomyopicosis is blurring of distance vision while near vision remains adequate.
As the disease progresses, severe nonproliferative diabetic retinopathy enters an advanced, or proliferative, stage when blood vessels proliferate (ie grow). The lack of oxygen in the retina causes fragile, new, blood vessels to grow along the retina and in the clear, gel-like vitreous humour that fills the inside of the eye. Without timely treatment, these new blood vessels can bleed, cloud vision, and destroy the retina. Fibrovascular proliferation can also cause tractional retinal detachment. The new blood vessels can also grow into the angle of the anterior chamber of the eye and cause neovascular glaucoma.
Nonproliferative diabetic retinopathy shows up as cotton wool spots, or microvascular abnormalities or as superficial retinal hemorrhages. Even so, the advanced proliferative diabetic retinopathy (PDR) can remain asymptomatic for a very long time, and so should be monitored closely with regular checkups.

Treatment options include laser photo coagulation, panretinal photocoagulation, intra vitreal triamcinolone, and finally vitrectomy.