DIABETIC RETINOPATHY DT.pptx

8/13/2019 DIABETIC RETINOPATHY DT.pptx

1/29

DIABETIC RETINOPATHY


2/29

Definition

Diabetic retinopathy is progressivedysfunction of the retinal vasculaturecaused by chronic hyperglycemia.


3/29

Epidemiology The first 5 years of type 1 diabetes has a very low risk of

retinopathy. However, 27% of those who have had diabetes for510years and 7190% of those who have had diabetes for

longer than 10years have diabetic retinopathy. After 2030years, the incidence rises to 95%, and about 3050% ofthese patients have proliferative diabetic retinopathy (PDR).

Yanko et al. found that the prevalence of retinopathy 1113years after the onset of type 2 diabetes was 23%; after 16 ormore years, it was 60%; and 11 or more years after the onset,3% of the patients had PDR. Klein et al. reported that 10yearsafter the diagnosis of type 2 diabetes, 67% of patients hadretinopathy and 10% had PDR.


4/29

Epidemiology cont.

Thirty-five percent of patients with symptomaticretinopathy have proteinuria, elevated bloodurea nitrogen values, or elevated creatininelevels.

Systemic hypertension appears to be an

independent risk factor for diabetic retinopathy.


5/29

Pathogenesis

Aldose reductase

Vasoproliferative factors

Platelet and blood viscosity


6/29

Aldose Reductase


7/29

lens epithelial cells, retinal pericytes andSchwann cellshigh concentration of aldosereductase

sorbitol cannot easily diffuse out of cells, theirintracellular concentration increases. Osmotic

forces then cause water to diffuse into the cell,resulting in electrolyte imbalance.


8/29

Vasoproliferative Factors

Considerable evidence suggests that VEGF has adirect role in the proliferative retinal vascular

abnormalities that are found in diabetes. Currently intense interest exists in vasoproliferative

factors released by the retina itself, retinal vessels,and the retinal pigment epithelium, which are felt to

induce neovascularization. The concentration of VEGF in aqueous and vitreous

directly correlates with the severity of retinopathy.


9/29

Platelets and Blood Viscosity

It has been postulated that plateletabnormalities or alterations in blood viscosity indiabetics may contribute to diabetic retinopathyby causing focal capillary occlusion and focalareas of ischemia in the retina which, in turn,

contribute to the development of diabeticretinopathy.


10/29

Ocular Manifestations

Early nonproliferative diabetic retinopathy

Advanced nonproliferative diabetic retinopathy

Proliferative diabetic retinopathy


11/29

Early nonproliferative diabeticretinopathy Microaneurysmsseen as small red dots in the

middle retinal layers.

It is very difficult to distinguish a small dothemorrhage from a microaneurysm byophthalmoscopy.

Fluorescein angiography helps to distinguishpatent microaneurysms because they leak dye


12/29


13/29

Macular edema, or retinal thickening, representsthe leading cause of legal blindness in diabetics.

Clinically, macular edema is best detected bybiomicroscopy with a 60-diopter or contactmacular lens.

This decreases the retinas translucency suchthat the normal retinal pigment epithelial andchoroidal background pattern is blurred


14/29

Advanced nonproliferative diabeticretinopathy Signs of increasing inner retinal hypoxia appear,

including multiple retinal hemorrhages, cotton-

wool spots, venous beading and loops,intraretinal microvascular abnormalities(IRMA), and large areas of capillary

nonperfusion depicted on fluoresceinangiography.


15/29


16/29

Cotton-wool spots, also called soft exudates or nervefiber infarcts, result from ischemia, not exudation.

Venous beading is an important sign of sluggishretinal circulation.

IRMA, multiple retinal hemorrhages, venousbeading and loops, widespread capillary

nonperfusion, and widespread leakage onfluorescein angiography were all significant riskfactors for the development of proliferativeretinopathy. Interestingly, cotton-wool spots werenot.


17/29

Proliferative diabetic retinopathy Although the macular edema, exudates, and

capillary occlusions seen in NPDR often cause

legal blindness, affected patients usuallymaintain at least ambulatory vision.

PDR, on the other hand, may result in severevitreous hemorrhage or retinal detachment, with

hand-movements vision or worse. Approximately 50% of patients with very severe

NPDR progress to proliferative retinopathywithin 1 year.


18/29


19/29


20/29

The new vessels usually progress through a stageof further proliferation, with associated

connective tissue formation. As PDR progresses, the fibrous component

becomes more prominent, with the fibrotictissue being either vascular or avascular.

The fibrovascular variety usually is found inassociation with vessels that extend into thevitreous cavity or with abnormal new vessels onthe surface of the retina or disc.


21/29

Vitreous traction is transmitted to the retinaalong these proliferations and may lead to

traction retinal detachment.

As the vitreous contracts, it may pull on the opticdisc, causing traction striae involving the

macular area, or actually drag the macula itself,both of which contribute to decreased visualacuity


22/29

Two types of diabetic retinal detachments occur,those that are caused by traction alone

(nonrhegmatogenous) and those caused byretinal break formation (rhegmatogenous).


23/29


24/29


25/29

Other Ocular Complications ofDiabetes Mellitus Corneal sensitivity is decreased

Corneal abrasions

primary open-angle glaucoma

The risk of cataract is 24 times greater indiabetics than in nondiabetics and may be 1525

times greater in diabetics under 40 years old optic neuropathy

Extraocular muscle palsies


26/29

Diagnosis and Ancillary Testing In nearly all instances, diabetic retinopathy is

diagnosed easily via ophthalmoscopic

examination intravenous fluorescein angiography is a widely

administered ancillary test. Optical coherence tomography (OCT) is a

noninvasive imaging technique that accuratelymeasures retinal thickness, demonstratesmacular edema, and details the architecture ofthe macula and surrounding structures


27/29

Differential Diagnosis Radiation retinopathy Hypertensive retinopathy

Retinal venous obstruction (central retinal veinocclusion (CRVO), branch retinal vein occlusion(BRVO))

The ocular ischemic syndrome

Anemia Leukemia Coats disease Idiopathic juxtafoveal retinal telangiectasia

Sickle cell retinopathy


28/29

Treatment

The mainstay of prevention of progression ofretinopathy is good control of hyperglycemia,

systemic hypertension, andhypercholesterolemia.

Photocoagulationvisus decreased or cause

many complications Vitrectomy


29/29

Thank you

DIABETIC RETINOPATHY DT.pptx

Documents

Transcript of DIABETIC RETINOPATHY DT.pptx