REFERAT

Diabetic Retinopathy

SUPERVISOR:

dr. Dijah Halimi, Sp.M

dr. Shanti Sri Agustina, Sp.M, Mkes

Arranged by :

Shofa Muminah

1102012275

FACULTY OF MEDICINE, YARSI UNIVERSITY

MINISTRY OF THE EYE DEPARTMENT OF DR. DRADJAT PRAWIRANEGARA

Hospital

MAY 2017
 FOREWORD
With praise and gratitude for the presence of Allah SWT for all his gifts, so that the
writing of a referral entitled "Diabetic Retinopathy" can be well structured and completed.
The purpose of writing this referat is to fulfill one of the secretarial duties of eye health
science. Apart from that, another goal is to serve as a source of knowledge for readers.
The author expresses his deepest gratitude to all those who have helped, especially to dr.
Dijah Halimi, Sp.M and dr. Shanti Sri Agustina, Sp.M, Mkes for giving direction and guidance.
The author realizes that there are still many shortcomings in the preparation of this
referat. Therefore, the authors accept constructive criticism and suggestions as improvements.
The author hopes that this referral can be of benefit to all parties concerned.

Serang, May 2017

Author

PIG
 PRELIMINARY

Diabetic retinopathy is the most common cause of blindness in adulthood, where diabetes
patients are 25 times more likely to develop congenitalia than non-diabetics. Diabetes mellitus
(DM) is a group of metabolic diseases characterized by hyperglycemia that occurs due to
abnormalities in insulin secretion, insulin action or both. Chronic hyperglycemia in diabetes is
associated with long-term damage, dysfunction or failure of several organs of the body,
especially the eyes, kidneys, nerves, heart and blood vessels. Diabetes mellitus can cause
changes in most of the ocular tissue. These changes include corneal abnormalities, glaucoma,
extraocular muscle palsy, optic nerve neuropathy and retinopathy. Among the changes that occur
in the ocular structure, the most frequent complication of blindness is diabetic retinopathy.
Nearly 100% of patients with type 1 diabetes and more than 60% of patients with type 2 diabetes
develop diabetic retinopathy during the first two decades of diabetes. Various attempts have been
made to prevent or delay the onset of compilation of vision loss in diabetic retinopathy patients.
Control of blood sugar and blood pressure as determined by the Diabetes Control and
Complications Trial (DCCT) and the Early Treatment DiabeticRetinopathy Study (ETDRS) can
prevent the incidence and progression of diabetic retinopathy. Nearly 100% of patients with type
1 diabetes and more than 60% of patients with type 2 diabetes develop diabetic retinopathy
during the first two decades of diabetes. Various attempts have been made to prevent or delay the
onset of compilation of vision loss in diabetic retinopathy patients. Control of blood sugar and
blood pressure as determined by the Diabetes Control and Complications Trial (DCCT) and the
Early Treatment DiabeticRetinopathy Study (ETDRS) can prevent the incidence and progression
of diabetic retinopathy. Nearly 100% of patients with type 1 diabetes and more than 60% of
patients with type 2 diabetes develop diabetic retinopathy during the first two decades of
diabetes. Various attempts have been made to prevent or delay the onset of compilation of vision
loss in diabetic retinopathy patients. Control of blood sugar and blood pressure as determined by
the Diabetes Control and Complications Trial (DCCT) and the Early Treatment
DiabeticRetinopathy Study (ETDRS) can prevent the incidence and progression of diabetic
retinopathy.

The role of general practitioners in the management of DM retinopathy is to control risk

factors, namely abnormal sugar levels, lipid levels, and blood pressure. Control of these three
factors has been shown to reduce risk and slow the progression of DM retinopathy.9 The optimal
target that must be achieved is HbA1c levels <7%, low-density lipoprotein (LDL) levels <100
mg / dL, high-density lipoprotein levels> 50 mg / dL, triglyceride levels <150 mg / dL and blood
pressure <130/80 mmHg.

Education by general practitioners about DM and retinopathy complications will increase

awareness and compliance with DM sufferers undergoing routine eye examinations. Thus
referral to an ophthalmologist can be made at the right time. This will reduce the rate of
blindness due to DM retinopathy.
1.2. Aim
1.2.1. General purpose
To know and understand the definition, anatomy, physiology, risk factors, pathogenesis,
clinical manifestations, diagnosis, investigations, management, complications, and prognosis of
diabetic retinopathy.
1.2.2. Special purpose
To fulfill one of the duties at the Clerk of the Clinic of Eye Diseases at Dr. Drajat
Prawiranegara Serang and as one of the requirements in taking the exam at the Registrar's Office
of Eye Disease Clinic at Dr. Dradjat Prawiranegara Serang.
 CHAPTER II
LITERATURE REVIEW
2.1 Anatomy
The eye is an organ of vision located in the orbital cavity with a spherical structure with a
diameter of 2.5 cm filled with fluid covered by three layers. From the outside to the inside, the
layers are: (1) sclera / cornea, (2) choroid / ciliary body / iris, and (3) retina. Most of the eye is
covered by a strong, protective connective tissue on the outside, the sclera, which forms the
white part of the eye. Anteriorly (towards the front), the outer layer consists of a transparent
cornea through which rays of light pass into the interior of the eye. The middle layer under the
sclera is the choroid which is highly pigmented and contains blood vessels to feed the retina. The
innermost layer under the choroid is the retina, which consists of a highly pigmented layer on the
outside and a nerve layer on the inside.
Retina
The retina is a thin, semitransparent, multilayer sheet of nerve tissue that lines the interior
two-thirds of the posterior wall of the eyeball. The retina extends forward almost as far as the
ciliary body, and ends at the edges of the ora serata.
The retina is formed from the neuroectoderma layer during embryology. The retina
originates from the forebrain diverticulum (proencephalon). First the optical vesicles are formed
and then invaginated to form a double-walled cup structure, which is called the optical cup.
During its development, the outer wall will form the pigment epithelium while the inner wall will
form the other nine retinal layers. The retina will continue to be attached to the proencephalon
throughout life through a structure called the retinohypothalamic tract.
 Figure 1: Retina Coating
The retina or mesh membrane is the part of the eye that contains receptors that receive
light stimulation. The retina is bordered by the choroid and retinal pigment epithelial cells. The
retina consists of 2 main layers, namely the outer layer which is pigmented and the inner layer
which is the nerve layer. The nervous layer has 2 types of photoreceptor cells, namely stem cells
that are useful for seeing low-intensity light, unable to see color, for peripheral vision and room
orientation, while cone cells are useful for seeing color, high-intensity light and central vision.
The retina has many blood vessels that supply nutrients and oxygen to retinal cells.
Retinal layers from outside to inside:
1. Retinal pigment epithelium.
2. The photoreceptor layer consists of stem cells that have a slender shape and cone cells are
photosensitive cells.
3. External limiting membrane which is the illusionary membrane.
4. Outer nuclear layer, is the arrangement of the nucleus layers of the cone and rod.
5. The outer plexiform layer, namely the acellular layer which is the site of the
photoreceptor synapses with bipolar and horizontal cells.
6. The inner nucleus layer is the body of bipolar cells, horizontal cells, and Muller cells.
This layer gets metabolism from the central retinal artery.
7. The deep plexiform layer is the acellular layer where the synapses of bipolar cells,
amacrine cells and ganglion cells.
 8. Ganglion cell layer which is the layer of the cell body of the second neuron.
9. The layer of nerve fibers is the axon layer of the ganglion cells leading to the optic nerve.
Within this layer are most of the retinal blood vessels.
10. The internal limitan membrane, is a hyaline membrane between the retina and the glass
body.

Retinal Vascularization
The retina receives blood from two sources, namely the central retinal artery which is a
branch of the ophthalmic artery and the choriocapillary artery which lies just outside the Bruch
membrane. The central retinal artery vascularizes the inner two-thirds of the retinal layer
(internal boundary membrane to the inner core layer), while the outer third of the retinal layer
(outer plexiform layer to the retinal pigment epithelium) is nourished by blood vessels in the
choroid. The central retinal artery enters the retina via the optic nerve and branches to the inner
surface of the retina. The branches of this artery are the terminal arteries without anastomose.
The outer layer of the retina does not contain capillaries so that nutrients are obtained by
diffusion, which primarily comes from the rich vascular layer of the choroid.
The retinal vessels have a non-perforated endothelial layer, forming the retinal blood barrier.
The endothelial lining of the choroid vessels is permeable. The outer retinal blood barrier lies at
the level of the epithelial layer of the retinal pigment. The central fovea is an avascular region
and is entirely dependent on diffusion of the choroidal circulation for nutrition. If the retina is
ablated until it hits the fovea, irreversible damage will occur.
Innervation of the Retina
The neurosensory of the retina does not provide a sensible supply. Abnormalities that occur
in the retina are painless due to the absence of sensory nerves in the retina. To see retinal
function, a subjective retina examination is performed, such as: sharp vision, color vision, and
field of view. The objective examinations are an electroretinogram (ERG), electro-oculogram
(EOG), and visual evoked response (VER). One of the tests performed to determine the integrity
of the retina is a funduscopic examination.

2.2 Definitions
 Diabetic retinopathy is a retinal disorder (retinopathy) found in people with diabetes mellitus.
This retinopathy is not caused by an inflammatory process. Retinopathy due to old diabetes
mellitus in the form of aneurysms, dilated veins, bleeding and fat exudate. The earliest
pathologic abnormality is thickening of the basal capillary endothelial membrane and decreased
number of pericits.
2.3 Epidemiology

Diabetes is a common disease in developed countries and is the biggest problem worldwide.
The incidence of diabetes has increased dramatically in the last decade and is expected to double
in the next decade. The increasing prevalence of diabetes leads to increased long-term
complications of diabetes such as retinopathy, nephropathy and neuropathy, which have a major
impact on both patients and society.
Diabetic retinopathy is the most common cause of blindness in adults between 20 and 74
years of age. Diabetic patients are 25 times more likely to develop blindness than nondiabetics.
The risk of developing retinopathy in diabetic patients increases with the length of diabetes. At
the time of diagnosis of type I diabetes, diabetic retinopathy was found in <5% of patients. After
10 years, the prevalence increases to 40-50% and after 20 years more than 90% of patients
already suffer from diabetic rhinopathy. In type 2 diabetes when the diagnosis is made, about
25% already have non-proliferative diabetic retinopathy. After 20 years, the prevalence of
diabetic retinopathy has increased to over 60% in varying degrees. In North America, 3.6% of
patients with type 1 and type 1 diabetes, 6% of patients with type 2 diabetes are completely
blind. In England and Wales, about 1000 diabetic patients are recorded as having partial or total
blindness each year.
2.4 Etiology and Pathogenesis
Although the cause of diabetic retinopathy is not known with certainty, hyperglycemic
conditions have long been considered a major risk factor. Prolonged exposure to hyperglycemic
causes physiological and biochemical changes that ultimately lead to changes in vascular
endothelial damage. Changes in most hematologic and biochemical abnormalities have been
associated with the prevalence and severity of retinopathy, including: 1) increased platelet
adhesion, 2) increased erythrocyte aggregation, 3) serum lipid abnormalities, 4) imperfect
fibrinolysis, 4) serum abnormalities and viscosity blood.
 The retina is a double layered structure of photoreceptors and nerve cells. Retinal health and
metabolic activity are highly dependent on the retinal capillary network. Retinal capillaries form
a network that spreads across the surface of the retina except for an area called the fovea. The
basic defect of many forms of diabetic retinopathy lies in the capillaries of the retina. The retinal
capillary wall consists of three layers from the outside to the inside, namely pericite cells, basal
membrane and endothelial cells. Pericite cells and endothelial cells are connected by pores
contained in the cell membrane located between them. Under normal circumstances, the ratio of
the number of pericite cells and retinal endothelial cells is 1: 1, while in other peripheral
capillaries the ratio reaches 20: 1. Perisit cells function to maintain capillary structure, regulate
contractility, help maintain barrier function and capillary transport and control endothelial
proliferation. Basal membrane functions as a barrier by maintaining capillary permeability to
prevent leakage. Endothelial cells are tightly bound to each other and together with the
extracellular matrix of the basement membrane forms a barrier that is selective against several
types of proteins and small molecules including fluorescent contrast materials used for the
diagnosis of retinal capillary disease.
Retinal capillary histopathological changes in diabetic retinopathy starting from thickening of
the basement membrane, loss of pericits and endothelial proliferation, where in the advanced
state, the ratio between endothelial cells and pericite cells reaches 10: 1. The pathophysiology of
diabetic retinopathy involves five basic processes that occur at the capillary level, namely (1)
formation of microaneurysms, (2) increased vascular permeability, (3) blockage of blood vessels,
(4) proliferation of new blood vessels (neovascular) and fibrous tissue in the retina, (5)
contraction of capillary fibrous tissue and vitreous tissue. Blockage and loss of perfusion causes
retinal ischemia whereas leakage can occur in all blood components.
Diabetic retinopathy is an ocular microangiopathy due to metabolic disorders that affects
three biochemical processes associated with hyperglycemia, namely the polyol pathway, non-
enzymatic glycation and protein kinase C.
 Polyol Line
Hyperglycemic that lasts a long time will cause overproduction and accumulation of polyol, a
sugar and alcohol compound, in the tissues including the lens and optic nerve. One of the
characteristics of polyol compounds is that they cannot pass through the basement membrane so
 that they will be buried in large quantities in cells. Polyol compounds cause an increase in cell
osmotic pressure and cause cell morphological and functional disorders.
 Nonenzimatic Glycation
Non-enzymatic glycation of protein and deoxyribonucleic acid (DNA) that occurs during
hyperglycemia can inhibit enzyme activity and DNA integrity. Glycosylated proteins form free
radicals and will cause changes in cell function.
 Protein Kinase C
Protein Kinase C is known to have an effect on vascular permeability, contractility, basement
membrane synthesis and vascular cell proliferation. In hyperglycemic conditions, PKC activity
in the retina and endothelial cells increases due to increased de novo synthesis of diacylglycerol,
a PKC regulator, from glucose.

Figure 2: Microvascular Occlusion in Diabetic Retinopathy

As a result of these microvascular changes, microvascular occlusion results in retinal

hypoxia. Loss of perfusion (nonperfussion) due to occlusion and accumulation of leukocytes
then causes retinal ischemia while leakage can occur in all blood components. This causes a
large area of nonperfusion and leakage of blood or plasma through the damaged endothelium.
The hallmark of this stage is a cotton wool spot. The effect of retinal hypoxia is an arteriovenous
shunt. AV shunt is associated with capillary occlusion of arterioles and venules. This is what is
called Intraretinal microvascular abnormalities (IRMA). In addition, you can find hemorrhage
nipples and veins that are like beads.
Figure 3: Effects of Retinal Ischemia in Diabetic Retinopathy
Loss of pericite cells in hyperglycemia causes, among others, disruption of barrier
function, weakness of capillary walls and increased intraluminal capillary pressure. Physical
weakness of the capillary walls causes saccular formation in the walls of blood vessels known as
microaneurysms which can then cause leakage or become a thrombus. The consequence of
increased vascular permeability This is a breakdown of the blood-retinal barrier resulting in
leakage of plasma into the retina which causes macular edema. This edema can be diffuse or
local. This edema appears as a thickened and cloudy retina accompanied by microaneurysms and
intraretinal exudate to form a yellow exudate zone rich in fat, round shape (hard exudates)
around the microaneurysm and most often centered on the temporal part of the macula.
Bleeding can occur in all layers of the retina and is in the form of a flame because of its
location within the horizontally oriented layer of nerve fibers. Meanwhile, dot hemorrhage or
spotting is located in the deeper layer of the retina where the axon cells are vertically oriented.
Bleeding occurs due to erythrocyte leakage, exudate occurs due to leakage and plasma
lipoprotein deposition, while edema occurs due to leakage of plasma fluid.

Figure 4: Effects of Increased Vascular Permeability in Diabetic Retinopathy

In an ischemic retina, angiogenic factors such as vascular endothelial growth factor
(VEGF) and insulin-like growth factor-1 (IGF-1) are produced. These factors cause the
 formation of new blood vessels in the preretina and optic nerve (PDR) area and the iris. (rubeosis
iridis). Neovascularization can occur in the disc (NVD) or anywhere (NVE).
The new blood vessels that are formed consist of only one layer of endothelial cells
without pericite cells and the basement membrane so they are very fragile and easily bleed.
These new blood vessels are very dangerous because they grow abnormally out of the retina and
extend into the vitreus, causing bleeding there and leading to blindness. Bleeding into the
vitreous blocks the transmission of light into the eye and gives the field of vision a red, gray, or
black appearance. If the bleeding continues to recur, fibrosis or scarring may occur in the retina.
Because the retina is only a thin layer consisting of several layers of cells, the scars and fibrosis
that occur can pull the retina apart, causing retinal detachment.
2.5 Clinical Symptoms
Diabetic retinopathy is usually asymptomatic for a long period of time. Only in the late
stages in the presence of macular involvement or vitreous hemorrhages will the patient suffer
visual failure and sudden blindness. The clinical symptoms of proliferative diabetic retinopathy
can be divided into two, namely subjective symptoms and objective symptoms.
Subjective Symptoms that can be felt:
 Difficulty reading
 Blurred vision is caused due to macular edema
 Double vision
 Vision suddenly decreases in one eye
 Seeing halos if there has been vitreous hemorrhage
 See dark spots & twinkling light
The objective symptoms of the retina that can be seen are:
 Microaneurysms, are the protrusion of the capillary walls, especially the venous area in the
form of small red spots located near blood vessels, especially the posterior poles.
Microaneurysms are located in the inner nuclear layer and are early lesions that can be
detected clinically. Microaneurysms are small, round red dots initially visible at the temporal
of the fovea. Bleeding can be in the form of dots, lines and spots that are usually located near
the posterior dipole microaneurysm.
 Figure 5: Microaneurysms and hemorrhages in backround diabetic retinopathy
 Changes in blood vessels in the form of dilated blood vessels with irregular lumen and
winding like a sausage-like.

Figure 6: Vein Dilation

 Hard exudaterepresents the infiltration of lipids into the retina. The picture is special, namely
irregular, yellowish. At the outset the punctate exudate enlarges and merges. This exudate
can appear and disappear within a few weeks.

Figure 7: Hard Exudates

  Soft exudateoften called cotton wool patches is retinal ischemia. On ophthalmoscopy
examination will be seen diffuse yellow spots and white. It is usually located at the periphery
of the non-irrigated area and is associated with retinal ischaemia.
 Retinal edema with a sign of loss of retinal image, especially the macular area (macular
edema), so it is very disturbing visual acuity. Retinal edema initially occurs between the
outer plexiform layer and the inner nuclear layer.
 New blood vessels (neovascularization) in the retina are usually located on the surface of the
tissue. They appear as meandering, deep, clustered and irregular vessels. Initially located in
the retinal tissue, then progressing to the preretinal area and then to the body of the glass.
Rupture of neovascularization in these areas can cause retinal hemorrhage, subhialoid
(preretinal) hemorrhage or glass body hemorrhage.
Difference between NPDR and PDR
NPDR PDR
Microaneurism (+) Microaneurism (+)
Intraretina bleeding (+) Intraretina bleeding (+)
Hard exudate (+) Hard exudate (+)
Retinal edema (+) Retinal edema (+)
Cotton Wool Spots (+) Cotton Wool Spots (+)
IRMA (+) IRMA (+)
Neovascularization (-) Neovascularization (+)
Vitreous Bleeding (-) Vitreous Bleeding (+)
Tractionary detachment of the Tractionary detachment of the
retina (-) retina (+)

2.6 Diagnosis and Classification of Diabetic Retinopathy

The diagnosis of diabetic retinopathy is based on the results of a funduscopic examination.
Fundal fluorescein angiography (FFA) is the most reliable method of diagnosis. However, in the
clinic, examination by ophthalmoscopy can still be used for screening. There are many
classifications of diabetic retinopathy made by experts. In general, the classification is based on
the severity of the retinal microvascular changes and or the absence of new blood vessel
formation in the retina.
Table 1: Classification of Diabetic Retinopathy
Step Description
No retinopathy No abnormal signs were found on the retina. Normal vision.
Maculopathy Exudate and bleeding within the macular area, and / or evidence
 of retinal edema, and / or evidence of retinal ischemia. Vision may
be reduced; sight threatening.
Preproliferative Evidence of occlusion (cotton wool spot). Veins become irregular
and may appear to form a circle. Normal vision.
Proliferative Changes in the occlusion cause release of vasoproliferative
substances from the retina which causes the growth of new blood
vessels in the optic plate (NVD) or elsewhere on the retina (NVE).
Normal vision, vision threatening.
Step Description
Continue Proliferative changes can cause bleeding into the vitreus or
between the vitreus and retina. The retina can also be pulled from
the underlying pigment epithelium by fibrous proliferation
associated with the growth of new blood vessels. Vision is
reduced, often acutely with vitreous hemorrhage; sight
threatening.

Early Treatment Diabetic Retinopathy Study Research Group (ETDRS) divides diabetic
retinopathy into nonproliferative and proliferative. Diabetic retinopathy is classified as non-
proliferative diabetic retinopathy (RDNP) if only microvascular changes are found in the
retina.Neovascular is a characteristic sign of proliferative diabetic retinopathy.
Table 2: Classification of Diabetic Retinopathy by ETDRS
Non-proliferative Diabetic Retinopathy
1. Minimal nonproliferative retinopathy: there is ≥ 1 sign of dilated veins,
microaneurysms, small intraretinal bleeding or hard exudate.
2. Mild to moderate nonproliferative retinopathy: there is ≥ 1 sign of mild venous
dilation, bleeding, hard exudation, soft exudate or IRMA.
3. Severe nonproliferative retinopathy: there is ≥ 1 sign of bleeding and
microaneurysms in 4 quadrants of the retina, dilation of veins in 2 quadrants,
or IRMA in 1 quadrant.
4. Very severe nonproliferative retinopathy: ≥ 2 signs of severe nonproliferative
retinopathy are found.
Proliferative Diabetic Retinopathy
 1. Mild proliferative retinopathy (without high risk): if there is minimal
neovascular presence of the disc (NVD) covering <1/4 of the disc area without
preretinal or vitreous bleeding, or neovascular anywhere in the retina (NVE)
without preretinal or vitreous bleeding .
2. High risk proliferative retinopathy: if 3 or 4 of the following risk factors are
found, a) new blood vessels are found anywhere in the retina, b) new blood
vessels are found on or near the optic disc, c) new blood vessels that are
classified as moderate or severe includes> disc area, d) vitreous hemorrhage.
The presence of new, clear blood vessels in the optic disc, or each new vessel
accompanied by bleeding, are the two most common features of high-risk
proliferative retinopathy.

Diagnosis
Diabetic retinopathy and its various stages are diagnosed based on stereoscopic
examination of the fundus with dilated pupils. Ophthalmoscopy and fundoscopic radiograph are
the gold standard for this disease. Fluorescence angiography (FA) is used to determine if laser
treatment is indicated. FA is given by injecting fluorescent substance intravenously and then the
substance through the blood vessels will reach the fundus.
2.7 Management
The main principle of management of diabetic retinopathy is prevention. This can be
achieved by taking into account the factors that can affect the progression of nonproliferative
diabetic retinopathy to proliferative.
1. Routine examination by an ophthalmologist
Patients with type I diabetes mellitus retinopathy rarely develop up to five years after
diagnosis. Whereas most people with type II diabetes mellitus have suffered from
retinopathy when diagnosed with diabetes for the first time. These patients should have an
eye examination when the diagnosis is made. Female patients are at high risk of worsening
diabetic retinopathy during pregnancy. General examination is recommended for pregnant
patients in the first semester and thereafter depending on the optometrist's discretion.
2. Blood Glucose Control and Hypertension
To determine blood glucose control for diabetic retinopathy, the Diabetic Control and
Application Trial (DCCT) conducted a study of 1441 patients with Type I diabetes who had
not been accompanied by retinopathy and who already had RDNP. The result was that
patients without retinopathy and who received intensive therapy for 36 months had a 76%
reduced risk of developing retinopathy while patients with RDNP were able to prevent the
risk of worsening retinopathy by 54%. In a study conducted by the United Kingdom
Prospective Diabetes Study (UKPDS) in patients with Type II diabetes with intensive
therapy, it was shown that every 1% reduction in HbA1c would be followed by a 35%
reduction in the risk of microvascular complications. The results of the DCCT and UKPDS
studies show that although intensive blood glucose control cannot completely prevent
diabetic retinopathy, it can reduce the risk of developing diabetic retinopathy and worsening
existing diabetic retinopathy. Clinically, good blood glucose control can protect vision and
reduce possible risk of undergoing photocoagulation therapy with laser light. The UKPDS
shows that hypertension control is also beneficial in reducing progression of retinopathy and
vision loss. good blood glucose control can protect vision and reduce the risk of undergoing
photocoagulation therapy with laser light. The UKPDS shows that hypertension control is
also beneficial in reducing progression of retinopathy and vision loss. good blood glucose
control can protect vision and reduce the risk of undergoing photocoagulation therapy with
laser light. The UKPDS shows that hypertension control is also beneficial in reducing
progression of retinopathy and vision loss.
3. Photocoagulation
Neovascular development plays an important role in the progression of diabetic
retinopathy. The complications of proliferative diabetic retinopathy can lead to severe vision
loss if untreated. Timely, it is very effective for patients with proliferative diabetic
retinopathy and macular edema to prevent loss of vision due to vitreous hemorrhage and
retinal detachment. Indications for photocoagulation therapy are proliferative diabetic
retinopathy, macular edema and neovascularization located at the angle of the anterior
chamber.
4. Anti VEGF injection
 Bevacizumab (Avastin) is a human recombinant anti-VEGF. A study recently proposed
using intravitreus bevacizum for age-related macular degeneration. In this case, 24 hours
after treatment we saw a dramatic reduction of neovascularization of the iris, and no relapse
within 10 days of follow-up. Treatment with bevacizumab appears to have a rapid and
powerful effect on pathological neovascularization. Avastin is an anti-angiogenic which not
only inhibits and prevents the proliferation of vascular endothelial cells but also causes
vascular regression due to increased endothelial cell death. For ocular use, avastin is given
via intra vitreal injection into the vitreous through the pars plana at a dose of 0.1 mL.
5. Vitrectomy
Early vitrectomy is necessary in patients who have vitreous opacity and who have active
neovascularization. Vitrectomy may also be helpful for patients with extensive
neovascularization or those with fibrovascular proliferation. In addition, vitrectomy is also
indicated for patients who have retinal detachment, vitreous bleeding after photocoagulation,
severe RDP, and vitreous bleeding that does not improve.
Diabetic Retinopathy Vitrectomy Study (DVRS) conducted a clinical trial in patients with
severe proliferative diabetic retinopathy. DRVS evaluated the benefits of rapid vitrectomy
(1–6 months after vitreous hemorrhage) and late (after 1 year) with severe vitreous bleeding
and vision loss (<5/200). Patients with type 1 diabetes clearly show an advantage for early
vitrectomy, but not in type 2. DRSV also shows an advantage of early vitrectomy compared
to conventional management of eyes with very severe proliferative diabetic retinopathy.

2.8 Complications
a) Progressive rubeosis iridis
This disease is the most frequent complication of the anterior segment.
Neovascularization of the iris (rubeosis iridis) is a response to the presence of hypoxia and
retinal ischemia due to various diseases, both in the eye and outside the eye, the most common
being diabetic retinopathy. Neovascularization of the iris initially occurs at the edge of the pupil
as a small branching, then grows and forms a fibrovascular membrane on the surface of the iris
radially to the corner, extends from the root of the iris through the ciliary body and the sclera
spur reaches the trabecular net, thus inhibiting the removal of aquous with the result that the intra
ocular pressure increases. and the state of the corner is still open. One time this fibrovascular
membrane contracted pulling the peripheral iris causing a peripheral anterior synekia (PAS) so
that the front chamber angle was closed and the intraocular pressure increased so high that an
intraocular inflammatory reaction occurred. One-third of patients with rubeosis iridis were found
in people with diabetic retinopathy. The frequency of occurrence of rubeosis in diabetic
retinopathy patients is influenced by surgery. The incidence of rubeosis iridis is reported to be
25-42% after vitrectomy, while the incidence of neovascular glaucoma is around 10-23% which
occurs in the first 6 months after surgery. The frequency of occurrence of rubeosis in diabetic
retinopathy patients is influenced by surgery. The incidence of rubeosis iridis is reported to be
25-42% after vitrectomy, while the incidence of neovascular glaucoma is around 10-23% which
occurs in the first 6 months after surgery. The frequency of occurrence of rubeosis in diabetic
retinopathy patients is influenced by surgery. The incidence of rubeosis iridis is reported to be
25-42% after vitrectomy, while the incidence of neovascular glaucoma is around 10-23% which
occurs in the first 6 months after surgery.
b) Neovascular glaucoma
Neovascular glaucoma is a secondary closed angle glaucoma that occurs due to the
growth of fibrovascular tissue on the surface of the iris and the trabecular webbing, which causes
distraction of aquous flow and can increase intraocular pressure. Other names for this
neovascular glaucoma are hemorrhagic glaucoma, congestive glaucoma, thrombotic glaucoma
and rubeotic glaucoma. The etiology is usually neovascular to the iris (rubeosis iridis).
Neovascularization of the iris (rubeosis iridis) is a response to the presence of retinal hypoxia
and ischemia due to various diseases, both in the eye and outside the eye, most commonly
diabetic retinopathy. Neovascularization of the iris initially occurs at the edge of the pupil as a
small branching,
c) Recurrent vitreous hemorrhage
Vitreous hemorrhage is common in proliferative diabetic retinopathy. Vitreous
hemorrhage occurs due to the formation of neovascularization on the retina to the vitreous
cavity. New blood vessels that do not have a strong structure and are easily brittle so that they
easily cause bleeding. Vitreous hemorrhage suggests pre-retinal hemorrhage(sub-hyaloid) or
intragel. Intragellar hemorrhage includes anterior, middle, posterior, or the entire vitreous body.
The symptom is the sudden development of floaters which occurs when the vitreous
hemorrhage is still small. In massive glass body bleeding, patients usually complain of sudden
 vision loss. Remote direct ophthalmoscopy will show a black shadow as opposed to a red light in
the vitreous hemorrhage that is still small and no red light if the vitreous hemorrhage is profuse.
Direct and indirect ophthalmoscopy shows the presence of blood in the vitreous space. Bscan
ultrasound helps to diagnose glass body bleeding.
d) Retinal detachment
It is a condition where the retinal neurosensory layer is released from the epithelium
pigment layer.Retinal detachment is painless, but it can cause hovering irregular shapes or
flashes of light and cause blurred vision.

2.9 Differential Diagnosis

The differential diagnosis must exclude other retinal vascular diseases, namely
hypertensive retinopathy. Hypertensive retinopathy is a condition characterized by changes in
retinal vascularization in a hypertensive population. This disorder was first noted by Marcus
Gunn in the 19th period in a group of people with hypertension and kidney disease. The signs on
the retina that were observed were generalized and focal arteriolar narrowing, arteriovenous
adhesions or "nicking", flame-shaped and blot-shaped retinal hemorrhages, cotton-wool spots,
and papilla edema. In 1939, Keith et al. Demonstrated that these retinopathy signs could be used
to predict mortality in hypertensive patients.
Modification of the Scheie classification by the American Academy of Ophtalmology

Stadium Characteristics
Stage 0 There is no change, a: v = 2: 3
Stage I Nearly undetectable narrowing of the arteriolar.
Stage II Obvious narrowing with focal abnormalities :, Copper wire
arteries, Silver wire arteries, Banking sign, Salus sign
Stage III Stage II + retinal hemorrhage and / or exudate
Stage IV Stage III + papilledema

2.10 Prognosis
Optimum control of blood glucose (HbA1c <7%) can maintain or delay retinopathy.
Additional arterial hypertension should also be treated (with adjusted blood pressure <140/85
mmHg). Without treatment, retinal tractional detachment and macular edema can cause severe
visual failure or blindness. However, diabetic retinopathy can occur despite optimal therapy.
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