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THE CORRELATION BETWEEN DIABETES
MELLITUS AND RETINOPATHY
Composed by:
Aditya Angga Dharma
030.06.010
Supervised by:
dr. Husnun , SpM
Fakultas Kedokteran
Universitas Trisakti
Jakarta
2010
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PREFACE
Firstly, I would like to praise and thank The Lord for His grace and mercy so I can
finally finish this paper on time.
Secondly, I would like to thank both of my parents, my sister and brother for all
support that they have been given to me during this paper was been composed.
Last but not least, I would like to commit my greatest thanks to Dr. Hj. Martiem
Mawie, MS as my lecturer and supervisor. Under his guidance, I could explore and
create more fresh ideas to compose this paper.
This paper was firstly made to accomplish my final English task before graduating
from Trisakti Medical Faculty. The subject that I explore is currently one of major
concern in medical world due to its frequently outbreak. Diabetes mellitus (DM) is a
major medical problem throughout the world. Diabetes causes an array of long-term
systemic complications, which have considerable impact on both the patient and the
society because it typically affects individuals in their most productive years.
Ophthalmic complications of diabetes include corneal abnormalities, glaucoma, iris
neovascularization, cataracts, and neuropathies. However, the most common and
potentially most blinding of these complications is diabetic retinopathy.
Finally, I realize that this paper is far from excellent. Therefore I would like to
apologize if there are mistakes or lack of information in this paper. Critics and
suggestions will be truly admired and welcomed.
Writer,
Aditya Angga Dharma
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CONTENT
Preface.. 2
Content. 3
Abstract 4
I. Introduction. 5
II. Diabetes Mellitus 6
a. Definition....... 6
b. Clasification .. 6
c. Diagnosis. 7
e. Complication 11
III. Diabetes mellitus and Nephropathy.......................................... 12
a. Definition.. 12
b. Risk factors 13
c. Patofisiology ..... 13
d. Pathogenesis ... 14
e. Diagnosis 15
f. Treatment. 18
g. Prevention... 20
h. Evaluation. 22
IV. Conclusion. 24
V. Reference 25
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ABSTRACT
Diabetic retinopathy is a common complication of diabetes affecting the blood
vessels in the retina (the thin light-sensitive membrane that covers the back of the
eye). If untreated, it may lead to blindness. If diagnosed and treated promptly,
blindness is usually preventable.
Patients with type 2 diabetes should have an initial dilated and comprehensive
eye examination by an ophthalmologist or optometristshortly after diabetes diagnosis.
Subsequent examinations for both type 1 and type 2 diabetic patients should be
repeated annually by an ophthalmologist or optometrist who is knowledgeable and
experienced in diagnosing the presence of diabetic retinopathy and is aware of its
management. Less frequent exams (every 2-3 years) may be considered with the
advice of an eye care professionalin the setting ofa normal eye exam. Examinations
will be requiredmore frequentlyif retinopathy is progressing. This follow-upinterval
is recommendedrecognizing that there are limited dataaddressing this issue.
Patients who experience vision loss from diabetes should be encouraged to
pursue visual rehabilitation with an ophthalmologistor optometristwho is trained or
experienced in low-vision care.
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INTRODUCTION
Over 135 million individuals are afflicted with diabetes across the world. In the U.S.,
diabetes affects over 18.2 million people(or 6.3% of the total population) and 800,000
new cases of type 2 diabetes are diagnosed each year(1)(2). Retinopathy is the most
common microvascular complication of diabetes, resulting inblindness for over
10,000 people with diabetes per year. Epidemiological studies have described the
natural history of and treatmentfor diabetic retinopathy. During thefirst two decades
of disease, nearly all patients with type1 diabetes and >60% of patients with type 2
diabetes have retinopathy. In the Wisconsin Epidemiologic Study of Diabetic
Retinopathy (WESDR), 3.6% of younger-onset patients (type 1 diabetes) and 1.6% of
older-onset patients (type 2 diabetes)were legally blind. In the younger-onset group,
86% of blindnesswas attributable to diabetic retinopathy. In the older-onsetgroup, in
which other eye diseases were common, one-third ofthe cases of legal blindness were
due to diabetic retinopathy. There is evidence that retinopathybegins to develop at
least 7 years before the clinical diagnosis of type 2 diabetes. Clinical trials have
demonstrated the effectiveness of photocoagulation, vitrectomy, and control of
hyperglycemia and hypertension for diabetic retinopathy.
DIABETES MELLITUS
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A. Definition
Diabetes is a chronic disease that occurs when the pancreas does not produce enough
insulin, or alternatively, when the body cannot effectively use the insulin it produces.
Insulin is a hormone that regulates blood sugar. Hyperglycaemia, or raised blood
sugar, is a common effect of uncontrolled diabetes and over time leads to serious
damage to many of the body's systems, especially the nerves and blood vessels.(1,10)
B. The clasification of diabetes mellitus may include :
1. Type 1 diabetes (previously known as insulin-dependent or childhood-onset)
is characterized by a lack of insulin production. Without daily administration
of insulin, Type 1 diabetes is rapidly fatal.(1,2,10)
o Symptoms include excessive excretion of urine (polyuria), thirst
(polydipsia), constant hunger, weight loss, vision changes and fatigue.
These symptoms may occur suddenly.
2. Type 2 diabetes (formerly called non-insulin-dependent or adult-onset)
results from the bodys ineffective use of insulin. Type 2 diabetes comprises
90% of people with diabetes around the world, and is largely the result of
excess body weight and physical inactivity.(1,2,10)
o Symptoms may be similar to those of Type 1 diabetes, but are often
less marked. As a result, the disease may be diagnosed several years
after onset, once complications have already arisen.
o Until recently, this type of diabetes was seen only in adults but it is
now also occurring in obese children.
3. Gestational diabetes is Gestational diabetes starts when your body is not able
to make and use all the insulin it needs for pregnancy. Without enough insulin,
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glucose cannot leave the blood and be changed to energy. Glucose builds up in
the blood to high levels. This is called hyperglycemia. (1,2,10)
o Symptoms of gestational diabetes are similar to Type 2 diabetes.
Gestational diabetes is most often diagnosed through prenatal
screening, rather than reported symptoms.
Impaired Glucose Tolerance (IGT) and Impaired Fasting Glycaemia (IFG) are
intermediate conditions in the transition between normality and diabetes. People with
IGT or IFG are at high risk of progressing to type 2 diabetes, although this is not
inevitable. (1,2,3)
C. Diabetes Mellitus Diagnosis
The following tests are used for diagnosis:
A fasting plasma glucose (FPG) test measures blood glucose in a person who
has not eaten anything for at least 8 hours. This test is used to detect diabetes
and pre-diabetes. Diabetes is diagnosed if higher than 126 mg/dL on 2
occasions. (5)
Random Plasma Glucose Test (non-fasting) blood glucose level -- diabetes
is suspected if higher than 200 mg/dL and accompanied by the classic
symptoms of increased thirst, urination, and fatigue (this test must be
confirmed with a fasting blood glucose test). (5)
An oral glucose tolerance test (OGTT) measures blood glucose after a
person fasts at least 8 hours and 2 hours after the person drinks a glucose-
containing beverage. This test can be used to diagnose diabetes and pre-
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diabetes. Diabetes is diagnosed if glucose level is higher than 200 mg/dL after
2 hours. (5)
Test results indicating that a person has diabetes should be confirmed with a second
test on a different day.
FPG Test
The FPG test is the preferred test for diagnosing diabetes because of its convenience
and low cost. However, it will miss some diabetes or pre-diabetes that can be found
with the OGTT. The FPG test is most reliable when done in the morning. Results and
their meaning are shown in Table 1. People with a fasting glucose level of 100 to 125
milligrams per deciliter (mg/dL) have a form of pre-diabetes called impaired fasting
glucose (IFG). Having IFG means a person has an increased risk of developing type 2
diabetes but does not have it yet. A level of 126 mg/dL or above, confirmed by
repeating the test on another day, means a person has diabetes.
Table 1. FPG test
Plasma Glucose Result (mg/dL) Diagnosis
99 or below Normal
100 to 125
Pre-diabetes
(impaired fasting glucose)
126 or above Diabetes*
*Confirmed by repeating the test on a different day. (1,2,10)
OGTT
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Research has shown that the OGTT is more sensitive than the FPG test for diagnosing
pre-diabetes, but it is less convenient to administer. The OGTT requires fasting for at
least 8 hours before the test. The plasma glucose level is measured immediately
before and 2 hours after a person drinks a liquid containing 75 grams of glucose
dissolved in water. Results and their meaning are shown in Table 2. If the blood
glucose level is between 140 and 199 mg/dL 2 hours after drinking the liquid, the
person has a form of pre-diabetes called impaired glucose tolerance (IGT). Having
IGT, like having IFG, means a person has an increased risk of developing type 2
diabetes but does not have it yet. A 2-hour glucose level of 200 mg/dL or above,
confirmed by repeating the test on another day, means a person has diabetes.
Table 2. OGTT
2-Hour Plasma Glucose Result (mg/dL) Diagnosis
139 and below Normal
140 to 199Pre-diabetes
(impaired glucose tolerance)
200 and above Diabetes*
*Confirmed by repeating the test on a different day. (1,2,10)
Gestational diabetes is also diagnosed based on plasma glucose values measured
during the OGTT, preferably by using 100 grams of glucose in liquid for the test.
Blood glucose levels are checked four times during the test. If blood glucose levels
are above normal at least twice during the test, the woman has gestational diabetes.
Table 3 shows the above-normal results for the OGTT for gestational diabetes. (1,2,10)
Table 3. Gestational diabetes: Above-normal
results for the OGTT*
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When Plasma Glucose Result (mg/dL)
Fasting 95 or higher
At 1 hour 180 or higher
At 2 hours 155 or higher
At 3 hours 140 or higher
Note: Some laboratories use other numbers for this test.
*These numbers are for a test using a drink with 100 grams of glucose. (1,2,10)
Random Plasma Glucose Test ( non fasting )
A random, or casual, blood glucose level of 200 mg/dL or higher, plus the presence of
the following symptoms, can mean a person has diabetes:
increased urination
increased thirst
unexplained weight loss
Other symptoms can include fatigue, blurred vision, increased hunger, and sores that
do not heal. The doctor will check the persons blood glucose level on another day
using the FPG test or the OGTT to confirm the diagnosis. (1,2,10)
D. The complications
Over time, diabetes can damage the heart, blood vessels, eyes, kidneys, and nerves.
Diabetic retinopathy is an important cause of blindness, and occurs as
a result of long-term accumulated damage to the small blood vessels in
the retina. After 15 years of diabetes, approximately 2% of people
become blind, and about 10% develop severe visual impairment.
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Diabetic neuropathy is damage to the nerves as a result of diabetes,
and affects up to 50% of people with diabetes. Although many
different problems can occur as a result of diabetic neuropathy,
common symptoms are tingling, pain, numbness, or weakness in the
feet and hands.
Combined with reduced blood flow, neuropathy in the feet increases
the chance offoot ulcers and eventual limb amputation.
Diabetes is among the leading causes of kidney failure. 10-20% of
people with diabetes die ofkidney failure.
Diabetes increases the risk ofheart disease and stroke. 50% of people
with diabetes die of cardiovascular disease (primarily heart disease and
stroke).
The overall risk of dying among people with diabetes is at least double
the risk of their peers without diabetes. (1,3,5,7)
RETINOPATHY IN DIABETES MELLITUS
A. Natural History of Diabetic Retinopathy
Diabetic retinopathy progresses from mild nonproliferative abnormalities,
characterized by increased vascular permeability, to moderate and severe
nonproliferative diabetic retinopathy (NPDR), characterizedby vascular closure, to
proliferative diabetic retinopathy (PDR), characterized by the growth of new blood
vessels on the retina and posterior surface of the vitreous. Macular edema,
characterized by retinal thickening from leaky blood vessels, can develop at all stages
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of retinopathy. Pregnancy, puberty, blood glucosecontrol, hypertension, and cataract
surgery can accelerate thesechanges.(1,3,5)
Vision-threatening retinopathy is rare in type 1 diabetic patients in the first 3-5 years
of diabetes or before puberty. During the next two decades, nearly all type 1 diabetic
patients develop retinopathy. Up to 21% of patients with type 2 diabetes have
retinopathy at the time of first diagnosis of diabetes, and most develop some degree of
retinopathy over time. Vision loss due to diabetic retinopathy results from several
mechanisms. Central vision may be impaired by macular edema or capillary
nonperfusion. New blood vessels of PDR and contraction of the accompanying
fibrous tissue can distort the retina and lead to tractional retinal detachment, producing
severe and oftenirreversible vision loss. In addition, the new blood vesselsmay bleed,
adding the further complication of preretinal or vitreous hemorrhage. Finally,
neovascular glaucoma associatedwith PDR can be a cause of visual loss.(5)
B. Risk Factor
The duration of diabetes is probably the strongest predictor for development and
progression of retinopathy. Among younger-onset patients with diabetes in the
WESDR (Wisconsin Epidemiologic Study of Diabetic Retinopathy), the prevalence of
any retinopathywas 8% at 3 years, 25% at 5 years, 60% at 10 years, and 80% at 15
years. The prevalence of PDR was 0% at 3 years and increased to 25% at 15 years.
The incidence of retinopathy also increased with increasing duration. The 4-year
incidence of developing proliferative retinopathy in the WESDR (Wisconsin
Epidemiologic Study of Diabetic Retinopathy) younger-onset group increased from
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0% during the first 5 years to 27.9% during years 13-14 of diabetes. After 15 years,
the incidence of developing PDRremained stable.(5)
C. Patophysiologi
Several biochemical pathways have been proposed to link hyperglycemia and
microvascular complications. These include polyol accumulation, formation of
advanced glycation end products (AGEs), oxidative stress, and activation of protein
kinase C (PKC). These processesare thought to modulate the disease process through
effectson cellular metabolism, signaling, and growth factors.(3,5)
Polyol accumulation
Accumulation of polyol occurs in experimental hyperglycemia, which in rats and
dogs is associated with the development ofbasement thickening, pericyte loss, and
microaneurysm formation. High concentrations of glucose increase flux throughthe
polyol pathway with the enzymatic activity of aldose reductase, leading to an
elevation of intracellular sorbitol concentrations. This rise in intracellular sorbitol
accumulation has been hypothesizedto cause osmotic damage to vascular cells. (3,5)
AGEs
Another well-characterized pathway is damage resulting from accumulation of
AGEs. High serum glucose can lead to nonenzymaticbinding of glucose to protein
side chains, resulting in theformation of compounds termed AGEs. After 26 weeks
of induced hyperglycemia, the retinal capillaries of diabetic rats have marked
accumulation of AGEs as well as a loss of pericytes.(3,5)
Oxidative damage
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Diabetes and hyperglycemia can also lead to oxidative stress and formation of
reactive oxygen species (ROS), leading to vasculardamage. (3,5)
D. Pathogenesis
Diabetic retinopathy is result of microvascular retinal changes. Hyperglycemia-
induced pericyte death and thickening of the basement membrane lead to
incompetence of the vascular walls. These damage change the formation ofblood
retinal barrier and also make retinal blood vessel become more permiable.
Small blood vessels such as those in the eye are especially vulnerable to poor
blood glucose control. An overaccumulation ofglucose and/orfructose damages the
tiny blood vessels in the retina. During the initial stage, called nonproliferative
diabetic retinopathy (NPDR), most people do not notice any changes 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.
As the disease progresses, severe nonproliferative diabetic retinopathy enters an
advanced, or proliferative, stage. The lack ofoxygen in the retina causes fragile, new,
blood vessels to grow along the retina and in the clear, gel-like vitreous 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
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retinopathy (PDR) can remain asymptomatic for a very long time, and so should be
monitored closely with regular checkups.(4)
E. Diagnosis
Many techniques are used in the detection of diabetic retinopathy, including direct
and indirect ophthalmoscopy, fluorescein angiography,stereoscopic digital and color
filmbased fundus photography, and mydriatic or nonmydriatic digital color or
monochromaticsingle-field photography.(4)
Ophthalmoscopy is the most commonly used technique to monitor for
diabetic retinopathy. However, undilated ophthalmoscopy,especially by non
eye care providers has poor sensitivitycompared with stereoscopic seven-field
color photography .Under typical clinical conditions, direct ophthalmoscopy
by
nonophthalmologists has a sensitivity of 50% for the detection
of
proliferative retinopathy.(4)
Ocular Coherence Tomography or OCT: This is a scan similar to an
ultrasound which is used to measure the thickness of the retina. It produces a
cross section of the retina and can determine if there is any swelling or
leakage.
(4)
Tonometry: A standard test that determines the fluid pressure (intraocular
pressure) inside the eye. Elevated pressure is a possible sign ofglaucoma,
another common eye problem in people with diabetes.(4)
Slit Lamp Biomicroscopy Retinal Screening Programs: Systematic programs
for the early detection of diabetic retinopathy using slit-lamp biomicroscopy.
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These exist either as a standalone scheme or as part of the Digital program
(above) where the digital photograph was considered to lack enough clarity for
detection and/or diagnosis of any retinal abnormality. (4)
The Inoveon Diabetic Retinopathy system compared SSF photographsof 290
diabetic patients recorded on 35-mm film and on theirproprietary system. The
sensitivity and specificity of the digital system in detecting threshold events
were 98.2 and 89.7%, respectively.Although Inoveons diabetic retinopathy-
3DT system provideshighly accurate diabetic retinopathy referral decisions,
the requirement for dilation and the cost both reduce its usefulness as a
screening tool.(4)
The DigiScope is a semiautomated instrument that acquires fundus images,
evaluates visual acuity, and transmits the data to a remote reading center
through telephone lines. A pilot study in normal eyes of normal volunteers and
17 consecutivediabetic patients showed that the visualization of many retinal
lesions present in diabetic retinopathy can be visualized by the DigiScope.
Further studies are needed to evaluate the test characteristics of this
technology.(4)
The use of single-field fundus photography has also been usedas a detection tool for
diabetic retinopathy.
Table 2International Clinical Diabetic Retinopathy Disease Severity Scale.(6)
Proposed disease severity
level Findings observable upon dilated ophthalmoscopy
No apparent retinopathy No abnormalities
Mild NPDR Microaneurysms onlyModerate NPDR More than just microaneurysms but less than severe
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NPDR
Severe NPDR Any of the following:
>20 intraretinal hemorrhages in each of 4 quadrants
Definite venous beading in 2+ quadrants
Prominent intraretinal microvascular abnormalities in
1+ quadrant
And no signs of proliferative retinopathy
PDR One or more of the following:
Neovascularization
Vitreous/preretinal hemorrhage
F. Management
There are three major treatments for diabetic retinopathy, which are very
effective in reducing vision loss from this disease. In fact, even people with
advanced retinopathy have a 90 percent chance of keeping their vision when they
get treatment before the retina is severely damaged. Still, the best way of
addressing diabetic retinopathy is to monitor it vigilantly and ensure that it does
not happen in the first place by careful blood glucose control and limitation of
dietary fructose.
These three treatments are laser surgery, injection of triamcinolone into the
eye and vitrectomy. It is important to note that although these treatments are very
successful, they do not cure diabetic retinopathy. Caution should be exercised in
treatment with laser surgery since it causes a loss of retinal tissue. It is often more
prudent to inject triamcinolone. In some patients it results in a marked increase of
vision, especially if there is an edema of the macula.
Avoiding tobacco use and correction of associated hypertension are important
therapeutic measures in the management of diabetic retinopathy. (3,4,5,6)
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The many kind of theraphy diabetes retinopathy among other :
1. Laser surgery
A type of laser surgery called panretinal photocoagulation, or PRP, is used to treat
severe macular edema and proliferative retinopathy. The goal is to create 1 000 - 2
000 burns in the retina with the hope of reducing the retina's oxygen demand, and
hence the possibility of ischemia. In treating advanced diabetic retinopathy, the burns
are used to destroy the abnormal blood vessels that form at the back of the eye.
Before the surgery, the ophthalmologist dilates the pupil and applies anesthetic drops
to numb the eye. In some cases, the doctor also may numb the area behind the eye to
prevent any discomfort. The lights in the office are also dimmed to aid in dilating the
pupil. The patient sits facing the laser machine while the doctor holds a special lens to
the eye. During the procedure, the patient may see flashes oflight. These flashes may
eventually create an uncomfortable stinging sensation for the patient. After the laser
treatment, patients should be advised not to drive for a few hours while the pupils are
still dilated. Vision may remain a little blurry for the rest of the day, though there
should not be much pain in the eye. (4)
2. Scatter laser treatment
Rather than focus the light on a single spot, the eye care professional may make
hundreds of small laser burns away from the center of the retina, a procedure called
scatter laser treatmentorpanretinal photocoagulation. The treatment shrinks the
abnormal blood vessels. Patients may lose some of their peripheral vision after this
surgery, but the procedure saves the rest of the patient's sight. Laser surgery may also
slightly reduce colour and night vision.
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A person with proliferative retinopathy will always be at risk for new bleeding as well
as glaucoma, a complication from the new blood vessels. This means that multiple
treatments may be required to protect vision. (4)
3. Vitrectomy
Instead of laser surgery, some people need an eye operation called a vitrectomy to
restore vision. A vitrectomy is performed when there is a lot of blood in the vitreous.
It involves removing the cloudy vitreous and replacing it with a saline solution made
up ofsalt and water. Because the vitreous is mostly water, there should be no change
between the saline solution and the normal vitreous.
Studies show that people who have a vitrectomy soon after a large hemorrhage are
more likely to protect their vision than someone who waits to have the operation.
Early vitrectomy is especially effective in people with insulin-dependent diabetes,
who may be at greater risk of blindness from a hemorrhage into the eye.
Vitrectomy is often done under local anesthesia. The doctor makes a tiny incision in
the sclera, or white of the eye. Next, a small instrument is placed into the eye to
remove the vitreous and insert the saline solution into the eye.
Patients may be able to return home soon after the vitrectomy, or may be asked to stay
in the hospital overnight. After the operation, the eye will be red and sensitive, and
patients usually need to wear an eyepatch for a few days or weeks to protect the eye.
Medicated eye drops are also prescribed to protect. (4)
G. Prevention
The prevention can do with any method include :
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1. Glycemic Control
The Diabetes Control and Complications Trial (DCCT) investigated the effect of
hyperglycemia in type 1 diabetic patients, as well as the incidence of diabetic
retinopathy, nephropathy,and neuropathy. A total of 1,441 patients who had either no
retinopathy at baseline (primary prevention cohort) or minimal-to-moderateNPDR
(secondary progression cohort) were treated by either conventionaltreatment (one or
two daily injections of insulin) or intensivediabetes management with three or more
daily insulin injectionsor a continuous subcutaneous insulin infusion. In the primary
prevention cohort, the cumulative incidence of progression in retinopathy over the
first 36 months was quite similar between the two groups. After that time, there was a
persistent decreasein the intensive group. Intensive therapy reduced the mean riskof
retinopathy by 76%. In the secondary intervention cohort, the intensive group had a
higher cumulativeincidence of sustained progression during the first year. However,
by 36 months, the intensive group had lower risks of progression. Intensive therapy
reduced the risk of progression by 54%.(5)
The protective effect of glycemic control has also been for confirmed patients with
type 2 diabetes. The U.K. Prospective Diabetes Study (UKPDS) demonstrated that
improved blood glucose control reduced the risk of developing retinopathy and
nephropathy and possibly reduces neuropathy. The overall rate of microvascular
complications was decreased by 25% in patients receiving intensive therapy versus
conventional therapy. Epidemiological analysis of the UKPDS data showed a
continuous relationship between the risk of microvascular complications and
glycemia, such thatfor every percentage point decrease in HbA1c (e.g., from 8 to7%),
there was a 35% reduction in the risk of microvascularcomplications.(5)
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2. Blood Pressure Control
The The U.K. ProspectiveDiabetes Study (UKPDS) also investigated the influence of
tight blood pressure control. A total of 1,148 hypertensive patients with type 2
diabetes were randomized to less tight (
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potentially blinding disorders. Detection of these problems adds value to the
examination but is rarely considered in analyses of screening interval. Patient
education also occurs during examinations. Patients know the importance of
controllingtheir blood glucose, blood pressure, and serum lipids, and thisimportance
can be reinforced at a time when patients are particularly aware of the implications of
vision loss. In addition, long intervals between follow-up visits may lead to
difficultiesin maintaining contact with patients. Patients may be unlikely to remember
that they need an eye examination after severalyears have passed.
After considering these issues, and in the absence of empirical data showing
otherwise, persons with diabetes should have an annual eye examination.(3,5)
Table 1Ophthalmologic examination schedule(7)
Patient group Recommended first examination
Minimum routine follow-
up*
Type 1 diabetes Within 35 years after diagnosis of
diabetes once patient is age 10 years
or older
Yearly
Type 2 diabetes At time of diagnosis of diabetes Yearly
Pregnancy in
preexisting diabetes
Prior to conception and during first
trimester
Physician discretion
pending results of first
trimester exam
* Abnormal findings necessitate more frequent follow-up.
Some evidence suggests that the prepubertal duration of diabetes may be important in
the development of microvascular complications; therefore, clinical judgment should
be used when applying these recommendations to individual patients
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CONCLUSIONS
Diabetic retinopathy is still a leading cause of blindness.
However, our understanding
of the pathophysiology of the diseaseis increasing as new biochemical pathways are
identified. Our ability to diagnosis and classify retinopathy is also improving.
Treatment modalities exist that can prevent or delay the onset of diabetic retinopathy,
as well as prevent loss of vision,in a large proportion of patients with diabetes. The
DCCT and the UKPDS established that glycemic, blood pressure and serum lipid
controlcan prevent and delay the progression of diabetic retinopathy in patients with
diabetes. Timely laser photocoagulation therapy can also prevent loss of vision in a
large proportion of patients with severe NPDR and PDR and/or macular edema.
Because a significantnumber of patients with vision-threatening disease may not have
symptoms, ongoing evaluation for retinopathy is a valuable andrequired strategy. In
the near future, clinical trials of several pharmacologic agents may lead to the
introduction of additional treatmentsand reduction in the frequency of visual loss.
.
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REFERENCES
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3. Diabetes Care: Retinopathy in Diabetes. Available from
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January 2009.
4. South-West Vision Center: Diabetic Retinopathy. Available from
http://swvc.net/eye_conditions_swvc.htm. Accessed 3 January 2009.
5. Diabetes Care: Diabetic Retinopathy. Available fromhttp://care.diabetesjournals.org/cgi/content/full/27/10/2540?. Accessed 2
January 2009.
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Available from http://care.diabetesjournals.org/cgi/content-
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January 2009.
8. The Diabetic Retinopathy Study Research Group: A modification of the
Airlie House classification of diabetic retinopathy (DRS report no. 7).Invest
Ophthalmol Vis Sci 21:210226, 1981.
9. Gabbay KH: Hyperglycemia, polyol metabolism, and complications of
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10. World Health Organization (WHO): Diabetes. Available from
http://www.who.int/mediacentre/factsheets/fs312/en/index.html. Accessed 2
January 2009 .
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http://care.diabetesjournals.org/cgi/content/full/27/suppl_1/s84http://swvc.net/eye_conditions_swvc.htmhttp://care.diabetesjournals.org/cgi/content/full/27/10/2540http://care.diabetesjournals.org/cgi/content-nw/full/27/10/2540/T2.%20Accessed%202%20January%202009http://care.diabetesjournals.org/cgi/content-nw/full/27/10/2540/T2.%20Accessed%202%20January%202009http://diabetes.niddk.nih.gov/dm/pubs/diagnosis/http://www.who.int/mediacentre/factsheets/fs312/en/index.htmlhttp://care.diabetesjournals.org/cgi/content/full/27/suppl_1/s84http://swvc.net/eye_conditions_swvc.htmhttp://care.diabetesjournals.org/cgi/content/full/27/10/2540http://care.diabetesjournals.org/cgi/content-nw/full/27/10/2540/T2.%20Accessed%202%20January%202009http://care.diabetesjournals.org/cgi/content-nw/full/27/10/2540/T2.%20Accessed%202%20January%202009http://diabetes.niddk.nih.gov/dm/pubs/diagnosis/http://www.who.int/mediacentre/factsheets/fs312/en/index.html