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Diabetic Retinopathy




DRis the disease of the retina that affects patients having diabetesmellitus. Consequently it is the major cause of blindness inindividuals in the age gap 20-64. Thus, it is important to take areview because of its commonality and in essence, it affects about3.4 percent of the population. For all the people with diabetesretinopathy, nearly 25 percent of them has a vision related diseases.The cases of people with DR are increasing every day. The cases areestimated to rise with cases of retinopathy. DR is classified aseither proliferative diabetic retinopathy (PDR) coupled with growthof new blood vessels and non-proliferative diabetic retinopathy(NPDR) and proliferative diabetic retinopathy (PDR). NPDR is dividedfurther into mild, moderate, and severe stages which may or may notinvolve macula diabetic macular oedema (DMO) involvement. The causesof visual impairments that are severe are DMO and PDR. Nearly all thepatients having type 1 diabetes and at least 60 percent of type 2diabetes patients are required to have retinopathy during the firstphase of diabetes incidence (Johnstone&amp Veves, 2005).

Pathophysiologyof Diabetes Retinopathy

Globally,diabetes has been regarded as an epidemic that needs attention, witha clear prediction of diabetes cases to increase to more than 380million by 2025, there is a need to come up with ways of reducinginstances of getting the disease. Consequentially, approximately 4million people between 20 and 74 years in the world will lose theirsight as a result of Diabetes Retinopathy. The progression anddevelopment risk of DR is associated closely with the duration anddiabetes, blood sugar, blood pressure, blood glucose, and possiblylipids. Though the existing landmark cross-sectional studies haveindicated a strong link between progression and development of DR andchronic hyperglycemia, the mechanism underlying the sole reason as tohow hyperglycemia results into retinal microvascular remains amirage. Further research has focussed on comprehending the mechanismof pathogenic with the goal to prevent chances of diabetesretinopathy (Johnstone&amp Veves, 2005).

HowDiabetes Cause Retinopathy

Themain mechanism in which diabetes causes retinopathy is very unclear.In fact, retinopathy and microvascular diabetes complicationsmulti-factorial, is attributed to chronic hyperglycemia, edema,vascular leakage damage, capillary basement neovascularization,membrane thickening, ischemia, and hemorrhage(Johnstone&amp Veves, 2005)..

Levelsof glucose that increases are estimated to cause damage to thefunctional and structural integrity of the capillaries of the retina.Increase in glucose of the blood switches the pathway of normalglucose (though aldose reductase activation) resulting to conversionof sugar into alcohol (example glucose into sorbitol). Furthermore,increased levels of sorbitol causes damage to the intramuralpericytes of the capillaries of the retina, thus resulting toweakness and at the long run eventual saccular outpouching of thewalls of the capillary, and further loss of capillaries of the retinaprimary function and autoregulation. The selective loss of pericytesin the retina capillaries is an aspect that occurs early during thecause Diabetes retinopathy (Ruderman,Neil, John, Stephen, &amp Andrea, 2002.).

Varioushematologic abnormalities have been seen in Diabetes (decreasedderfomabilty of blood cells, increased erythrocyte aggregation,adhesion and platelet aggregation) to sluggish blood circulation,focal capillary occlusion and endothelial damage. This results intoretinal ischemia that influences DR development.

AsDR develops, there is an eventual closure of capillaries leading tohypoxia. A more extensive hypoxia ignites compensatory mechanisms inthe eye to give enough oxygen to the tissues (e.g. venous caliberabnormalities). Continuous increase of ischemia in the retina ignitesproduction of vaso-proliferative aspects that stimulate the formationof new vessels (Ruderman,Neil, John, Stephen, &amp Andrea, 2002.).

Neovascularizationis seen mostly at perfused and non-per fused borders of the retina,and along arcades of the vascular and at optic nerve head. Newvessels break and grow along the surface and into scaffold of thehyaloid face. These vessels rarely cause visual impairments, but theyare highly permeable and delicate. In addition, they are easilydisrupted by traction of vitreous leading to hemorrhage in thepre-retinal space and vitreous cavity. The newer vessels areassociated initially with a little amount of fibroglial tissueformation that increases as the density of the neovascular frontincreases. During the later stages, the blood vessels may regressleaving a contact of avascular fibrous tissue adherent to posteriorhyaloid face and retina. Contraction of vitreous may exert tractionalforces on the retina through fibroglial connections. The traction mayfinally cause edema of the retina, tractional retinal detachmentretinal heterotrophic and retina tear formation(Ruderman, Neil, John, Stephen, &amp Andrea, 2002.)

Effectsof Diabetes Retinopathy

Diabetespatients have higher chances of contracting visual problems and therelated effects on the eyes. For example, patients with diabetes havehigher chances of contracting glaucoma and cataracts, but the mainresult of the disease is felt on the eye. Most patients usuallydevelop eye problems from the age of 20 years. The effect of thediabetes on the eyes is called diabetes retinopathy. As timeprogress, it affects retinal circulatory systems. The initial phaseis referred to as background diabetes retinopathy. During this phase,the arteries of the retina become very weak and begin to leak,forming dot like small hemorrhages.&nbspThe leaking vessels lead toedema or the swelling in the retina and decrease vision (Ruderman,Neil, John, Stephen, &amp Andrea, 2002.).

Thenext stage known as proliferative retinopathy is a stage where bloodcirculation problems cause the areas surrounding the retina to bevoid of oxygen (ischemic). Newer fragile vessels develop as the bloodcirculatory system tries to maintain an adequate supply of oxygenwithin the confines of the retina. As a result, blood may leak in theretina causing floaters or spots alongside decreased vision. Duringthe later phases of the disease, there is a continued abnormal growthof vessels and scar tissue may result to more severe problems such asglaucoma and retinal detachment (Ruderman,Neil, John, Stephen, &amp Andrea, 2002.).

Postoperativehemorrhage occurs immediately and resolves after several weeks.Delayed postoperative hemorrhage happens in one out of 10 eyes withdiabetes and this is in connection with neo-vascular proliferationthe base of vitreous, in most cases at vitrectomy entry points.Anterior cry therapy to the oral serrate may minimize the risk offibrovascular ingrowths and recurrent hemorrhage. Ultrasoundexamination time to time with no fundal view is made to reduce thedetachment of the retina. Rhegmatogenous detachment of retinal aftervitrectomy is as a result of unrecognized retinal breaks and thusneeds urgent surgery to prevent development proliferativevitreoretinopathy and rubeosis iridis(Joslin &amp Kahn, 2005).


DRis an eye disease that affects patients with diabetes mellitus. Ithas been estimated to be the major cause of blindness between peoplebetween 20 and 64 years.Earlydetection of DR can help in reducing cases. For example, timely tightblood glucose control, lipids and blood pressure detection may beworthwhile nevertheless, it is very difficult to achieve clinically.Vasectomy and laser photocoagulation are needed to treat sightthreatening DR. Thus there is an urgent need to comprehend howdiabetes damages the blood vessels of the eyes to drive thedevelopment of better drugs of the DR treatment.


Johnstone,T., M., &amp Veves, A. (2005). Diabetesand Cardiovascular Disease. Totowa,: NJ: Humana.

Joslin,P., E., &amp Kahn, C. R. (2005). Joslin`s Diabetes Mellitus. Philadelphia,PA: Lippincott Williams &amp Willkins.

Ruderman,Neil, John, T. D., Stephen, H. S., &amp Andrea, M. K. (2002).Handbookof Exercise in Diabetes. Alexandria,VA: : American Diabetes Association.