Download Diabetic Retinopathy and Diabetic Macular Edema

A CME-certified supplement to
Release date: August 15, 2014
Expiration date: August 15, 2015
Estimated time to complete activity:
30 minutes
Target Audience: This educational activity is
designed for physicians who treat patients with
diabetes at risk for diabetic macular edema.
Statement of Need: Diabetes is the leading
cause of blindness among adults in the United
States. Diabetic retinopathy (DR), a consequence
of long-term exposure to excess blood glucose in
the microvasculature of the eye, is a significant
contributor to impaired vision and blindness in
patients with diabetes. Diabetic macular edema
(DME), which involves retinal thickening, can
develop at any stage of retinopathy and is a
principal cause of vision loss in diabetes. Although
the American Diabetes Association recommends
an annual dilated eye examination in patients
with diabetes, 30% to 40% of patients do
not receive this preventive measure. Adequate
control of hyperglycemia and hypertension are
also paramount to decreasing risks for DR and
DME. In the last decade, improved understanding
of the multifactorial pathophysiology of DME
has resulted in novel approaches to suppress
angiogenesis and edema, such as anti-VEGF
therapies. This activity will review strategies for
recognizing and managing DME.
Learning Objectives: Upon completion of this
activity, participants will be able to:
•Outline data supporting primary prevention
strategies for DR and DME in patients with
diabetes
•Identify patients with DR and DME who require
treatment early in disease progression to
minimize vision loss
•Discuss therapies for DME, including laser
photocoagulation, anti-VEGF therapies, and
corticosteroids
•Evaluate data on combination therapies and
dosing paradigms in DME management to
improve outcomes and reduce treatment
burden for patients.
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Education to provide continuing medical
education for physicians.
Credit Designation: Indiana University School
of Medicine designates this enduring material
for a maximum of 0.5 AMA PRA Category
1 Credit™. Physicians should claim only the
credit commensurate with the extent of their
participation in the activity.
While it offers CME/CE credits, this activity is
not intended to provide extensive training or
certification in the field.
How to Receive Credit: To receive credit,
participants are required to review the supplement,
relate the content material to the learning objectives,
achieve at least 70% on the self-assessment, and
complete an evaluation form online.
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directed to ACHL at (877) 444-8435, ext. 203.
Recognizing Eye Complications in Diabetes:
Diabetic Retinopathy and
Diabetic Macular Edema
Jennifer I. Lim, MD, FARVO
Professor of Ophthalmology
Marion H. Schenk, Esq., Chair in Ophthalmology for Research of the Aging Eye
Director of the Retina Service
Illinois Eye and Ear Infirmary
UIC Department of Ophthalmology and Visual Sciences
University of Illinois at Chicago
Chicago, Illinois
Prevention of Diabetic Retinopathy
Visual loss from diabetes remains a major
cause of blindness in the world. Untreated, diabetes affects not only the lens (cataracts), but more importantly, the retina.
Fortunately, there are treatments available
to mitigate, and sometimes reverse, visual
loss from diabetic retinopathy (DR). Diabetes is a growing health problem in the
United States; its prevalence is expected
to rise to 21% of adults in 2050 from the
estimated 11.3% of the US population in
2010.1,2 In the United States, it is the seventh leading cause of death.2
In the prevention and treatment of DR,
systemic factors are very important. Numerous epidemiologic studies and trials
have documented the importance of glycemic and blood pressure control in patients
with diabetes. The Diabetes Control and
Complications Trial (DCCT, 1982-1993)
compared intensive with conventional
control for onset and progression of DR
in type 1 diabetics.3 The Epidemiology
of Diabetes Interventions and Complications study (1994-present) followed the
DCCT cohort. At baseline in the DCCT,
726 of the 1,441 participants had no DR
(primary prevention cohort) while 715 had
mild DR (secondary intervention cohort).
Participants were followed for a mean of
6.5 years. The median HbA1c was 7% for
the intensive control group compared with
9% for the conventional control group.
The intensive control showed a 76% reduction in the adjusted mean risk for the
development of DR compared with the
conventional control group. In addition,
intensive control slowed progression of
DR by 54% compared with conventional
control. Although subsequent HbA1c levels in the original intensive and conventional groups converged to approximately
8% for both groups by year 8, initial assignment to intensive therapy continued
to significantly lower the incidence of
further DR progression (hazard reduction
53%-56%).3 Thus, earlier optimization of
glycemic levels continues to have effects
many years later on the progression of DR.
Other studies, such as the United Kingdom Prospective Diabetes Study, which
studied type 2 diabetics, the Wisconsin
Epidemiology Study of Diabetic Retinopathy,4 and the Early Treatment of Diabetic Retinopathy Study (ETDRS),5 also
support the importance of glucose control
in reducing the incidence and progression of DR. In addition, these studies also
showed the importance of control of blood
pressure, lipids, renal function, and body
weight on the incidence and progression of
DR. Thus, systemic diabetes control significantly impacts patients’ eyes. Approximately one third of patients with diabetes
has DR.6
The American Academy of Ophthalmology and the American Diabetes Association recommend that a dilated eye exam
be performed within 3 to 5 years for type
1 diabetics and at the time of diagnosis for
type 2 diabetics.7,8 Yearly dilated eye exams
are recommended thereafter for both types.
Unfortunately, studies have shown that patients do not get regular eye exams and they
are unaware of the existence of sight-threat-
This activity is co-provided by:
Our acknowledgement to Regeneron Pharmaceuticals, Inc.
for an educational grant in support of this activity.
Claim your credits at www.ACHLcme.org • www.globalacademycme.com
Disclosure of Conflicts of Interest: Indiana
University School of Medicine requires that
the faculty participating in a CME/CE activity
disclose all affiliations or other financial
relationships (1) with the manufacturers of any
commercial product(s) and/or provider(s) of
commercial services discussed in an educational
presentation and (2) with any commercial
supporters of the activity. All conflicts of
interest have been resolved prior to this
CME/CE activity. Indiana University School of
Medicine also requires participating faculty to
disclose when unapproved/unlabeled uses of a
product are discussed in a CME/CE activity.
This CME/CE activity might describe the
off-label, investigational, or experimental
use of medications that may exceed their
FDA-approved labeling. Physicians should
consult the current manufacturers’ prescribing
information for these products. Indiana
University School of Medicine requires the
speaker to disclose that a product is not labeled
for the use under discussion.
The following disclosure information has been
provided:
Jennifer I. Lim, MD, FARVO
Sources of Funding Research: Genentech
and Regeneron
Consulting Agreements, Speaker’s Bureau,
and Honorarium Agreements: Genentech,
Regeneron, and Santen
Discussion of Off-Label, Investigational,
or Experimental Drug/Device Use: Use of
aflibercept for diabetic macular edema
All Indiana University School of Medicine and
Academy for Continued Healthcare Learning
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ening retinopathy. In a study of 2,798 patients at the Joslin Diabetes Center, 83% of
those with DR and 78% with advanced DR
were unaware of their disease at their first
visit (personal communication, Lloyd Paul
Aiello, MD, PhD). Patients should also
be followed more closely during onset of
tight glucose control as acceleration of DR
is frequently seen, although it is transient.
During puberty and pregnancy, more frequent exams are also warranted as DR can
rapidly accelerate.
Diagnosis and Treatment of Diabetic
Retinopathy
Levels of Diabetic Retinopathy
Diabetic retinopathy can be classified by
the level of DR and also by the presence or
absence of diabetic macular edema (DME),
swelling in the area within the vascular arcades, temporal edge of the optic nerve head,
and the equivalent area temporal to the foveal center. Diabetic retinopathy is generally divided into non-proliferative (NPDR)
and proliferative (PDR) DR. NPDR has
three stages: mild, moderate, and severe.
These levels, defined by ETDRS, refer to
the severity of the disease and have associated prognostic implications for acceleration
of disease. A patient with mild NPDR may
be seen yearly, whereas a patient with severe
NPDR may need to be seen as often as every
3 months. In NPDR, microaneurysms are
present. Depending upon the severity of the
disease, retinal hemorrhages, cotton wool
spots, venous beading, and intraretinal microvascular anomalies may be seen. There is
typically none to minimal visual loss. However, if there is concomitant DME, there
may be significant visual acuity loss.
In eyes with PDR, neovascular vessels
sprout from the retinal venous circulation. These vessels are immature and prone
to bleeding, which can result not only in
preretinal hemorrhages but also vitreous
hemorrhages with significant loss of vision.
Depending on the location of the neovascularization and presence/type of hemorrhage, the PDR may be graded as high risk
for visual acuity loss. PDR on the nerve
head or within 1 disc diameter of the nerve
head is termed neovascularization of the
disc (NVD); neovascularization elsewhere
is termed NVE. NVD and NVE will continue to progress over time. Fibrosis and
scarring can occur, and these can result in
retinal detachment. Fortunately, panretinal
laser photocoagulation (PRP) is highly effective in curbing the growth of these blood
vessels and can help prevent visual loss. In
fact, in the Diabetic Retinopathy Study,
2
panretinal laser photocoagulation resulted
in a 50% reduction of severe visual loss.9
In the ETDRS, prompt laser was again associated with reduction in progression and
visual loss even in less severe levels of retinopathy.10 It is thus important for the patient to receive prompt care.
Fibrosis and scarring associated with
progressive neovascularization can lead to
tractional retinal detachments. Continued
traction on the retina may result in retinal holes, which may cause elevation of
the retina and hence a rhegmatogenous
retinal detachment. When the detachment
threatens the macula or involves the macular areas, pars plana vitrectomy surgery
(PPV) is needed. During PPV, the vitreous
is removed, the membranes and vitreous
attachment are carefully dissected off the
retinal surface, and laser is applied. An
injection of intraocular gas (or sometimes
a longer tamponade such as silicone oil,
which requires a second surgical procedure
for removal) is needed if there are associated retinal holes.
In some eyes with significant ischemia,
neovascular vessels may develop on the iris
(rubeosis). These fragile vessels can result
in a hyphema (anterior chamber bleed) as
well as glaucoma (neovascular or rubeotic
glaucoma). Unmitigated growth will cause
the anterior chamber angle to scar. These
patients will present with painful eyes and
elevated eye pressure. Glaucoma eyedrops
and treatment to cause regression of the
neovascularization is urgently needed. Depending upon the view to the retina, PRP
may be performed. An anti-vascular endothelial growth factor (VEGF) drug is also
frequently injected into the eye to help
cause regression of the neovascular vessels.
In cases in which no view of the retina is
possible, vitrectomy surgery with PRP is
urgently needed to prevent blindness.
Diabetic Macular Edema
DME occurs in 13% of DR eyes. The
presence of DME has been found to be
associated with higher risks of myocardial infarction (2.5X) and stroke/cerebral
vascular accident (2X) than in patients
without DME. If the central foveal area is
involved, visual acuity loss may be severe.
The term clinically significant macular
edema (CSDME) is used specifically to refer to the subtype of DME with high risk
for severe, and perhaps permanent, visual
acuity loss, if not treated. There are three
types of CSDME as defined in the ETDRS:
1. Edema involving the foveal center or
within 500 microns of the fovea; 2. Edema
www.globalacademycme.com • Recognizing Eye Complications in Diabetes
within 1 disc diameter of the fovea and at
least 1 disc diameter in size; and 3. Edema
associated with any exudate that is within
500 microns of the foveal center.11
CSDME is typically detected through
the use of clinical examination with either a
contact lens on the patient’s eye or through
a non-contact lens. Ancillary tests are helpful to document the presence and extent of
DR or CSDME. Objective measurements of
the degree of thickening are made with the
use of optical coherence tomography (OCT),
a quick, noninvasive, in-office procedure.
Using OCT, the amount of thickening in
various regions of the macula is measured
(microns) (see Figure). These measurements
are very helpful in following a patient’s response to therapy. OCT is frequently repeated during treatment of CSDME.
At the time of CSDME diagnosis, a
fluorescein angiogram (FA), in which a
vegetable-based dye is injected through a
peripheral vein and special filters are used
that allow the retinal vasculature to be imaged, is helpful to determine the presence
and extent of ischemia. Sometimes, edema
may result from ischemia in the absence
of active vascular leakage and this affects
the treatment plan. A FA is also helpful to
detect areas of retinal neovascularization
(leaks profusely). However, a good clinical
exam alone is often all that is needed to
make a diagnosis of CSDME or PDR.
Treatment options for CSDME include
laser, intravitreal steroid, and intravitreal
injection of anti-VEGF drugs. The ETDRS
showed that focal or grid laser of CSDME
reduced the risk of moderate visual loss
(3 lines) by approximately 50%.12 Focal laser treatment may need to be repeated at
4-month intervals until a response or complete treatment is achieved.
Recent Clinical Trial Results:
Advancements in Therapy for DME
Most recently, treatments other than laser or
in combination with laser have been shown
to be efficacious for treatment of DMEassociated edema. These include corticosteroids and anti-VEGF therapies. Corticosteroids stabilize the blood-retinal barrier. The
use of VEGF as a target was predicated by
findings that increased levels of VEGF have
been well documented in eyes with DME
or DR.13,14 In general, the more severe the
DME and the higher the level of DR, the
higher the VEGF level.15 The efficacy of
intravitreal injections of anti-VEGF has
been well documented in numerous clinical trials. Most noteworthy are the DRCR
Protocol I results16 and the RIDE/RISE17
and VISTA/VIVID18 studies. These phase
3 clinical trials led to the approval of the
anti-VEGF drugs ranibizumab and aflibercept. The DRCR presented an alternative
dosing regimen to the monthly injections
used in RISE and RIDE for ranibizumab.
The VISTA and VIVID studies showed
that aflibercept was superior to laser treatment but was not compared directly to
ranibizumab.18 The use of bevacizumab is
off-label for DME, but is often used due to
its lower cost and evidence of efficacy.19 At
present, a large, randomized DRCR study
is comparing the effects of ranibizumab,
ters (RIDE control) and 2.9 letters (RISE
control) at 24 months. After 24 months,
the sham group was allowed to receive ranibizumab 0.5 mg monthly. At the end of
3 years, the visual acuity improved 10.5 to
11.4 letters (RIDE) and 11 to 14.2 letters
(RISE) versus 4.7 (RIDE/ sham/ranibizumab) and 4.3 (RIDE sham/ranibizumab).17
In the eyes that received 0.3 mg ranibizumab monthly, 39% to 36% received
rescue laser by 24 months in the RIDE/
RISE studies.17 In contrast, 70% (RIDE)
or 74% (RISE) of the sham group received
laser treatment. Furthermore, it was rare
(1.6% RIDE and
0% RISE) for ranibizumab 0.3 mg
treated eyes to
require PRP as
compared with the
sham-treated eyes
(12.3% RIDE and
Image courtesy of Dr. Jennifer Lim 11% RISE). In fact,
OCT image of the left eye of a patient with marked macular
the overall retinopedema. The dark circular spaces represent macular edema cyst
athy severity of the
within the retina. The bright white dots represent lipids. The
an-ti-VEGFtreated
dome-shaped area centrally represents subretinal fluid.
eyes improved in
aflibercept, and bevacizumab in the treat- over one third of the ranibizumab-treated
ment of CSDME eyes.
eyes versus only 4% (RIDE) to 7% (RISE) of
Adverse events associated with anti-VEGF sham-treated eyes.17 It is unclear at this time
therapies include local adverse events and whether the effects will persist or wane over
potential systemic risks in patients with di- time after frequent therapy is decreased or
abetes, such as the ocular potential for infec- stopped.
tion or damage to ocular structures during
In the DRCR study, anti-VEGF was given
the intravitreal injection itself. The risk of at baseline and monthly for a total of 3 indamage to ocular structures is extremely jections. If the visual acuity was not 20/20,
low in trained hands, and the risk of en- or if the OCT still showed edema, 2 more
dophthalmitis is about 1 in 1000. Potential injections spaced monthly were given.16 A
systemic adverse events include Antiplate- computerized algorithm was used to deterlet Trialists’ Collaboration (APTC)-defined mine the need for further treatments. Using
arterial thromboembolic events. There was this method, a total of approximately 9 to 10
a trend for the higher dose of ranibizumab injections were given in the first year, 3 to 4
(0.5 mg) to be associated with more APTC in the second year, and 1 to 2 in the third year
events than the lower dose of ranibizum- of the study. Thus, it appears that continuous
ab (0.3 mg).17 Because of this potential, therapy is not required to achieve sustained
the lower (0.3 mg) dose was approved for visual acuity improvement. The timing of
use in diabetes instead of the 0.5 mg dose. laser therapy immediately with the first anHowever, one should remember that these ti-VEGF treatment was compared to deferred
studies were not powered to detect a differ- laser therapy (6 months) in the DRCR study.
ence in systemic risks between anti-VEGF– The results were similar. In fact, it was found
treated eyes and control (laser-treated) eyes. that 70% of the deferred eyes never required
The dosing regimen used in RIDE and laser. Many questions about the timing of
RISE was monthly intravitreal injections of laser therapy remain to be answered: whetheither 0.3 mg or 0.5 mg ranibizumab versus er to add, when to add, and what long-term
a sham injection.17 Patients were followed benefit occurs with combined anti-VEGF and
monthly, and OCT was performed at each laser in the treatment of DME.
visit. Laser photocoagulation was allowed
Most recently, the VISTA and VIVID
beginning at month 3, and could be given results have been reported. In these multievery 3 months. Using this regimen, the vi- center, randomized studies, eyes with CSDsual acuity improved 11 to 12 letters (RIDE) ME were randomized to laser therapy (as
and 12 to 13 letters (RISE) versus 2.3 let- needed every 12 weeks) versus aflibercept
Recognizing Eye Complications in Diabetes • www.globalacademycme.com
3
2 mg monthly versus aflibercept 2 mg
monthly for 3 doses and then every 8 weeks.18
In VIVID, aflibercept eyes improved 10.5
letters (2 mg monthly) and 10.7 letters
(2 mg q 8) versus laser eyes, which improved
1.2 letters. In VISTA, aflibercept eyes improved 12.5 letters (2 mg monthly) and 10.7
letters (2 mg q 8) versus laser eyes, which improved 0.2 letters. More aflibercept-treated
eyes improved 2 steps in the severity of DR
than sham-treated eyes (33 to 27% vs 7.5%
VIVID; 33.8%-29% vs 14.3% VISTA).
Results were maintained at 100 weeks.
The use of corticosteroids is usually restricted to pseudophakic or phakic eyes,
due to risk of cataract formation. In fact,
in the DRCR studies, corticosteroids given
every 4 months decreased macular edema,
but visual acuity decreased later due to cataract formation.16 When a subgroup of pseudophakic eyes was studied, no subsequent
secondary drop in visual acuity occurred.
In fact, the visual acuity improvement in
these eyes receiving laser with corticosteroid injected intravitreally was similar to
that seen in eyes given anti-VEGF intravitreally with or without prompt laser.
Sustained release implants have been
studied in the treatment of DME. In the
dexamethasone implant study, eyes with
DME of at least 90 days duration were
randomized to either 350 µg or 700 µg
dexamethasone implant.20 The primary
endpoint, a 10 or more letter increase at
day 90, was seen in 33.3% of the 700 µg
and 21.1% of the 350 µg group versus
12.3% in the observation group (P=0.007
for 700 µg). At day 180, a 10 or more letter increase was seen in 30% of the 700 µg
and 19% of the 350 µg group, and 23%
in the observation group (P>0.4 for treated
vs observed eyes). Greater improvements
in central retinal thickness and fluorescein leakage were found in treated eyes than
observed eyes (P=0.03; day 90). The dexamethasone implant was well tolerated.
Another steroid, fluocinolone, has also
been studied in eyes with DME. In the
FAME study, more eyes gained visual acuity
in either the 0.2 µg/day (28.7%) or the 0.5
µg/day (27.8%) fluocinolone implant groups
compared with control (18.9%) (P=0.018).21
In a preplanned subgroup analysis, there was
a doubling of benefit compared with sham
injections in patients who reported a duration
of DME for ≥3 years at baseline; ≥15 gain at
month 36 was 34.0% (low dose; P<0.001) or
28.8% (high dose; P=0.002) compared with
13.4% (sham). In addition, an improvement
≥2 steps in the ETDRS retinopathy scale
occurred in 13.7% (low dose) and 10.1%
(high dose) compared with 8.9% in the sham
group. Complications included cataract in
almost all phakic patients, but their visual
benefit after cataract surgery was similar to
that in pseudophakic patients.22
One must remember that intraocular
infection is a real risk with all intravitreal treatments. Therefore, if the edema does
not involve the center and the visual acuity is better than 20/40, one should consider focal laser treatment. The timing of
focal laser with anti-VEGF therapies and
the treatment of chronic DME is not yet
established. For eyes with chronic edema,
intraocular steroids may be more beneficial
than anti-VEGF drugs.
References
9. The Diabetic Retinopathy Study (DRS) Research
Group: Preliminary report on the effects of photocoagulation therapy: DRS Report No. 1. Am J
Ophthalmol. 1976;81:383-396.
10. Early Treatment of Diabetic Retinopathy Study
Group. Early Photocoagulation Study Group.
Techniques for scatter and local photocoagulation
treatment of diabetic retinopathy: The Early Treatment of Diabetic Retinopathy Study report no. 3.
Int Ophthalmol Clin. 1987;27:254-264.
11. T reatment techniques and clinical guidelines for photocoagulation of diabetic macular edema. Early Treatment Diabetic Retinopathy Study Report Number 2.
Early Treatment Diabetic Retinopathy Study Research
Group. Ophthalmology. 1987;94(7):761-774.
12. Photocoagulation for diabetic macular edema.
Early Treatment Diabetic Retinopathy Study report
number 1. Early Treatment Diabetic Retinopathy Study research group. Arch Ophthalmol.
1985;103(12):1796-1806.
13. Aiello LP, Avery RL, Arrigg PG, et al. Vascular endothelial growth factor in ocular fluid of patients with
diabetic retinopathy and other retinal disorders.
N Engl J Med. 1994;331(22):1480-1487.
14. Funatsu H, Yamashita H, Noma H, Mimura T,
Yamashita T, Hori S. Increased levels of vascular
endothelial growth factor and interleukin-6 in the
aqueous humor of diabetics with macular edema.
Am J Ophthalmol. 2002;133(1):70-77.
15. Funatsu H, Yamashita H, Ikeda T, et al. Vitreous
levels of interleukin-6 and vascular endothelial
growth factor are related to diabetic macular edema. Ophthalmology. 2003;110(9):1690-1696.
16. Diabetic Retinopathy Clinical Research Network,
Elman MJ, Aiello LP, et al. Randomized trial evaluating ranibizumab plus prompt or deferred laser or
triamcinolone plus prompt laser for diabetic macular
edema. Ophthalmology. 2010;117(6):1064-1077.
17. B
rown DM, Nguyen QD, Marcus DM, et al. Longterm outcomes of ranibizumab therapy for diabetic
macular edema: The 36-month results from two
phase III trials: RISE and RIDE. Ophthalmology.
2013;120(10):2013-2022.
18. D
o DV. Intravitreal afliberept injection (IAI) for
diabetic macular edema (DME): 12-month results
of VISTA-DME and VIVID-DME. Paper presented
at: the 2013 Annual Meeting of the American
Academy of Ophthalmology; November 16-19,
2013; New Orleans, LA.
19. Michaelides M, Kaines A, Hamilton RD, et al. A prospective randomized trial of intravitreal bevacizumab
or laser therapy in the management of diabetic
macular edema (BOLT study) 12-month data: Report
2. Ophthalmology. 2010;117(6):1078-1086.
20. H
aller JA, Kuppermann BD, Blumenkranz MS, et
al. Randomized controlled trial of an intravitreous
dexamethasone drug delivery system in patients
with diabetic macular edema. Arch Ophthalmol.
2010;128(3):289-296.
21. C
ampochiaro PA, Brown DM, Pearson A, et al.
Long-term benefit of sustained-delivery fluocinolone acetonide vitreous inserts for diabetic macular
edema. Ophthalmology. 2011;118(4):626-635.
22. Campochiaro PA, Brown DM, Pearson A, et al.
Sustained delivery fluocinolone acetonide vitreous
inserts provide benefit for at least 3 years in patients
with diabetic macular edema. Ophthalmology.
2012;119(10):2125-2132.
1. Boyle JP, Thompson TJ, Gregg EW, Barker LE,
Williamson DF. Projection of the year 2050 burden
of diabetes in the US adult population: Dynamic
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National Diabetes Fact Sheet, 2011. http://www.cdc.
gov/diabetes/pubs/factsheet11.htm. Accessed May
16, 2014.
3. Aiello LP. Diabetic retinopathy and other ocular findings in the diabetes control and complications trial/
epidemiology of diabetes interventions and complications study. Diabetes Care. 2014;37(1):17-23.
4. Klein R, Knudtson MD, Lee KE, Gangnon R, Klein
BE. The Wisconsin Epidemiologic Study of Diabetic
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of retinopathy in persons with type 1 diabetes.
Ophthalmology. 2008;115(11):1859-1868.
5. Fong DS, Ferris FL 3rd, Davis MD, Chew EY. Causes
of severe visual loss in the early treatment diabetic
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Am J Ophthalmol. 1999;127(2):137-141.
6. Zhang X, Saaddine JB, Chou CF, et al. Prevalence
of diabetic retinopathy in the United States, 20052008. JAMA. 2010;304(6):649-656.
7. American Academy of Ophthalmology Retina Panel.
Preferred Practice Pattern Guidelines. http://one.
aao.org/preferred-practice-pattern/diabetic-retinopathy-ppp--september-2008-4th-print. Accessed May
16, 2014.
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4
Summary
Novel treatments in development include
drugs that inhibit pericytes and those that
affect non-VEGF pathways. At present, we
are fortunate that there are several drugs that
can reduce the edema and cause regression
of DR. For eyes in which DME does not involve the center of the fovea, laser remains
an important treatment. Laser is also the
main treatment for eyes with PDR. Studies
are ongoing to determine the benefit of anti-VEGF and laser combination therapy in
eyes with CSDME as well as eyes with PDR.
However, with all of these treatments, one
needs to remember that earlier stages of disease are more readily treated and have better
potential outcome. Prompt diagnosis and
treatment of retinopathy combined with
concomitant systemic glycemic, blood pressure, lipid, and weight control will result in
lower rates of morbidity from DR.
www.globalacademycme.com • Recognizing Eye Complications in Diabetes