Diabetic Retinopathy

J.F. Arévalo, M.D., F.A.C.S.( )

S. Bonafonte-Royo, M.D.

Chief of Vitreoretinal Division, The King Khaled Eye

Department of Ophthalmology, Centro de Oftalmología

Specialist Hospital, Riyadh, Kingdom of Saudi Arabia

Bonafonte, Pasaje Mendez Vigo 6, Barcelona 08009,

Professor of Ophthalmology, Wilmer Eye Institute,

Spain

e-mail: 9640sbr@comb.cat

The Johns Hopkins University, Baltimore, MD, USA

e-mail: arevalojf@jhmi.edu

A.F. Lasave, M.D.

Retina and Vitreous Service, Clinica Oftalmológica

Centro Caracas, Edif. Centro Caracas PH-1, Av. Panteon,

San Bernardino, Caracas, DF, 1010, Venezuela

e-mail: andreslasave@gmail.com

D.G. Zeballos, M.D.

Department of Ophthalmology, Clínica Kennedy

Alborada, Primer piso, Oficina 101, Alborada 12ª Etapa,

Calle Crotos y Av. Rodolfo Baquerizo Nazur, Guayaquil,

Guayas, Ecuador

e-mail: david_zeballos@hotmail.com

J.F. Arévalo (ed.), Retinal and Choroidal Manifestations of Selected Systemic Diseases,

387

DOI 10.1007/978-1-4614-3646-1_21, © Springer Science+Business Media New York 2013

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J.F. Arévalo et al.

diabetes. The prevalence of retinopathy is strongly

Introduction

related to the duration of diabetes. After 20 years

of diabetes, nearly all patients with type 1 diabetes

Diabetes mellitus (DM) is a group of metabolic

and >60% of patients with type 2 diabetes have

diseases characterized by hyperglycemia result-

some degree of retinopathy. Diabetic retinopathy

ing from defects in insulin secretion, insulin

poses a serious threat to vision. In the Wisconsin

action, or both. The chronic hyperglycemia of

Epidemiologic Study of Diabetic Retinopathy

diabetes is associated with long-term damage,

(WESDR), 3.6% of younger-onset patients (aged

dysfunction, and failure of various organs, espe-

<30 years at diagnosis, an operational definition of

cially the eyes, kidneys, nerves, heart, and blood

type 1 diabetes) and 1.6% of older-onset patients

vessels. Several pathogenic processes are involved

(aged³30 years at diagnosis, an operational

in the development of diabetes. These range from

definition of type 2 diabetes) were legally blind. In

autoimmune destruction of the B cells of the pan-

the younger-onset group, 86% of blindness was

creas with consequent insulin deficiency to abnor-

attributable to diabetic retinopathy. In the older-

malities that result in resistance to insulin action.

onset group, where other eye diseases were com-

The basis of the abnormalities in carbohydrate,

mon, one-third of the cases of legal blindness were

fat, and protein metabolism in diabetes is deficient

due to diabetic retinopathy. Overall, diabetic retin-

action of insulin on target tissues. Deficient insu-

opathy is estimated to be the most frequent cause

lin action results from inadequate insulin secre-

of new cases of blindness among adults aged

tion and/or diminished tissue responses to insulin

20–74 years. Diabetic macular edema (DME) is a

at one or more points in the complex pathways of

manifestation of diabetic retinopathy that produces

hormone action [1].

loss of central vision. Macular edema within 1

The vast majority of cases of diabetes fall into

disk diameter of the fovea is present in 9% of the

two etiopathogenetic categories. In one category,

diabetic population [3]. Although visual loss sec-

type 1 diabetes, the cause is an absolute deficiency

ondary to proliferative changes is more common

of insulin secretion. This form of diabetes, insu-

in patients with type 1 diabetes, visual loss in

lin-dependent diabetes or juvenile-onset diabetes,

patients with type 2 diabetes is more commonly

which accounts for only 5–10% of those with

due to macular edema [4].

diabetes, results from a cellular-mediated auto-

The objective of this chapter is to describe the

immune destruction of the B cells of the pancreas.

clinical findings of DR as well as its epidemiol-

For the other category, a much more prevalent

ogy, pathogenesis, risk factors, diagnosis,

category, type 2 diabetes, the cause is a combina-

classification, and current management.

tion of resistance to insulin action and an inade-

quate compensatory insulin secretory response.

Pathogenesis

This form of diabetes, non-insulin-dependent

diabetes or adult-onset diabetes, which accounts

for ~90–95% of those with diabetes, results from

The pathogenesis of diabetic retinopathy begins

an insulin resistance and usually has relative

with prolonged hyperglycemia, which results in

insulin deficiency. At least initially, and often

expression of factors that activates the b(beta)2

throughout their lifetimes, these individuals do

isoform of protein kinase C and stimulates vascu-

not need insulin treatment to survive [1].

lar endothelial proliferation and increases capil-

Currently, there are approximately 13 million

lary permeability. Other mechanisms may also be

Americans with diagnosed diabetes and millions

involved such as increased glucose metabolism

more who remain unaware that they have the dis-

via the polyol pathway (aldose reductase) or the

ease. This number is expected to increase to 29

accumulation of advanced glycation end prod-

million by the year 2050 [2].

ucts. High concentrations of glucose increase

Diabetic retinopathy (DR) is a highly specific

flux through the polyol pathway with the enzy-

vascular complication of both type 1 and type 2

matic activity of aldose reductase, leading to an