14th Annual Diabetes Report
Contemporary Care Protocols for DR and DME
New treatment paradigms for diabetic eye disease are enabling our patients to enjoy improved visual function and sustained visual acuity gains.
Release Date: August 2012
Expiration Date: August 1, 2015
Diabetic retinopathy (DR) is the leading cause of blindness in the working-aged population of the western world. As the number of people living with type 2 diabetes mellitus continues to rise, eye care providers are seeing more cases of DR than ever before. Traditional treatment of DR still is an effective management approach. But, with newer, more effective options, such as MPLT and pharmacotherapy, the outcome profile for affected patients is changing for the better.
Carlo J. Pelino, O.D., and Joseph J. Pizzimenti, O.D.
This course is COPE-approved for 2 hours of CE credit. COPE ID is 35278-PS. Please check your state licensing board to see if this approval counts toward your CE requirement for relicensure.
This continuing education course is joint-sponsored by the Pennsylvania College of Optometry.
Drs. Pelino and Pizzimenti have no relationships to disclose.
Diabetic retinopathy (DR) is
the leading cause of blindness in the working-age
population of the western
world. As the number of people
living with type 2 diabetes mellitus
(DM) continues to rise, eye care
providers are seeing more cases of
DR than ever before. In general,
lethargy and obesity in children,
adolescents and adults have widely
contributed to this increased prevalence in type 2 DM.
DR is a microvascular disease.
Proliferative DR is characterized
by new vessel formation in the
retina and optic disc as a result of
hypoxia, microangiopathy and capillary occlusion. Tractional retinal
detachment, diabetic macula edema
(DME) and neovascular glaucoma
are associated complications that
may result in severe vision loss.
In 2005, we experienced a sea
change in the preferred treatment
of exudative age-related macular
degeneration (AMD)—a shift
from ablative therapy to pharmacotherapy. Now, another sweeping transition is occurring in the
treatment of DR and DME, with
thousands of patients achieving
improved visual outcomes with
The Burden of Disease
People with DM are at an
increased risk for a multitude of
ocular complications. Common
ocular symptoms in patients with
DM include blurred or fluctuating
vision, diplopia and ocular surface
dryness. These individuals are 40%
more likely to develop glaucoma
and 60% more likely to develop
cataracts than those without DM,
according to the American Diabetes Association (ADA).1 More
specifically, cataracts develop earlier and progress faster in patients
with DM, and the risk of glaucoma
increases with advanced age and
longer disease duration.2,3
Other ocular anomalies associated with DM include decreased
corneal sensitivity, iris neovascularization, pupillary abnormalities
secondary to autonomic neuropathy, fluctuating refractive error
associated with sorbitol in the lens, a "snowflake" cataract in patients
with type 1 DM, optic nerve abnormalities and other cranial nerve
Both the prevalence and the economic burden of DM and DR are
on the rise.6 Patients with DR represent a large and growing segment
of the American population with
vision impairment. The Centers for
Disease Control and Prevention
estimates that DR causes 12,000 to
24,000 new cases of blindness each
year.6 In fact, patients with DM
are 29 times more likely to become
blind than individuals of similar
age and gender without diabetes.7,8
A loss of fine detail in central
vision typically is one of the first
and most common symptoms in
patients with DR. Night vision
problems, flashes and floaters are
other, less common complaints.
Severe and moderate levels of
vision loss secondary to DR often
are preventable with timely detection and treatment.9-14
Patients with DM may not
understand the importance of
dilated retinal examinations or recognize the benefits of early disease
detection. Survey data published by
the National Eye Institute indicated
that just about half of all patients
with DM obtained an annual dilated retinal exam.15
Pathophysiology of DR
Most individuals with DM ultimately develop some degree of
retinopathy.13,16 DR results from an
alteration in retinal blood flow that
degrades the retina's performance.
DR affects the retinal capillaries
before it impacts the larger vessels.17-19 However, the exact cause
of microvascular complications in
DM is unknown.17,18
An early finding in DR is the loss
of pericytes, which may cause leakage and dysfunction of capillary
endothelial cells.17,18 Pericytes are
the modified smooth muscle cells
of capillaries that regulate retinal
vascular flow via dilation and contraction. These mural cells provide
structural support for the capillaries' endothelium and help constitute the inner blood-retinal barrier.
Excess glucose within the retinal
capillary is thought to stimulate
production of vascular endothelial
growth factor (VEGF), protein
kinase C and advanced glycation
end-product.17,20 These biochemicals alter the capillary pericyte
integrity. Over time, non-perfusion
weakens the capillary walls, resulting in bulging, leaking or scarring.
Outpouchings of the capillaries
(microaneurysms) frequently are
the earliest clinically detectable
sign of DR. With tissue ischemia,
angiogenic growth factors (such
as VEGF) are upregulated and
released, causing neovascularization and increased vascular permeability—both of which lead to
Leakage from the perifoveal vessels may cause DME, which manifests as swelling or thickening of
the central retina. DME continues
to be a common cause of central
vision loss and decreased quality of
life in working-aged Americans.23,24 Results from the Wisconsin Epi-demiologic Study of Diabetic
Retinopathy indicated that, after
15 years of known diabetes, the
prevalence of DME is approximately 20% in patients with type
1 DM, 25% in patients with
type 2 DM who take insulin and
14% in patients with type 2 DM
who do not take insulin.25 In the
United States, the incidence of DME
approaches 30% in adults who have
had DM for 20 years or more.
Also of note: The prevalence
of DME in mild non-proliferative
diabetic retinopathy (NPDR) is
just 3%. However, this statistic
balloons to 38% in eyes with
moderate to severe NPDR, and
71% in eyes with proliferative reti-nopathy (PDR).25
DME occurs as a consequence
of both vascular abnormalities and
inflammatory processes. Both components interact with each other
to promote disease progression.
The vascular abnormalities stimulate the inflammatory processes
that eventually lead to further
vascular compromise and leakage.
Hypoxia, altered blood flow, ischemia, toxicity and inflammation
are processes that cause macular
edema formation. Compromise
to the inner blood-retinal barrier
causes increased vascular permeability as well as extravasation of
lipoproteins and other macromolecules. Over time, accumulation of
intraretinal fluid in combination
with macular thickening causes
decreased visual acuity.19
Much more is now understood
about the origins of diabetic
inflammation. Leukocytes are
recruited to the retinal vasculature
after the retinal tissue has been
stressed. Intracellular adhesion
molecules eventually are expressed
on the luminal surface of the vascular endothelial cells, which
allows the adhesion of leukocytes
and possible blockage of the capillary (known as leukostasis). In
DR, the white blood cells no longer
flow freely within the retinal vessels. Eventually, they damage and
kill the cells that line the blood
vessel wall. After adhesion occurs,
several chemotactic molecules, such
as monocyte chemo-attractive protein-1 (MCP-1), are secreted by the
vascular lumen. MCP-1 influences
the migration of leukocytes into the
Once the leukocyte is inside
the retina, a variety of inflammatory cytokine mediators, such as
interleukin-1 beta, interleukin-6,
tumor necrosis factor-alpha (TNF-alpha), insulin-like growth factor
1, stromal-cell derived factor-1
and VEGF-A, are secreted and
propagate the vascular permeability process.19
Also, the insulin-sensitizing
agents Avandia (rosiglitazone,
GlaxoSmithKline) and Actos
(pioglitazone, Takeda Pharmaceuticals) may increase the risk of
DME in patients with type 2 DM
who experience peripheral edema
and weight gain.26 So, if your
patients are using either agent, you
may wish to switch them to an
entirely different category of diabetes medications.
Clinical Features and
Classification of DR
The classic clinical features
of NPDR include dot- and blot-shaped hemorrhages, microaneu-rysms, intraretinal microvascular
abnormalities (IRMA), venous
beading, hard exudates (lipid), cotton-wool spots and retinal edema
Cotton-wool spots represent
focal infarcts of the retinal nerve
fiber layer (figure 2). IRMA are
dilated and tortuous capillaries,
and are good indicators of progressive DR. Venous beading is a focal
irregularity in the caliber of retinal
veins that serves as a strong predictor for the development of neovas-cularization.27
leaking capillaries and IRMA may
result in intraretinal hemorrhages.
The ophthalmoscopic appearance
of these hemorrhages is consistent
with the retinal level in which
Hemorrhages in the retinal nerve
fiber layer have a flame-shaped
appearance that is consistent with
the layer's structure. (Also, note
that flame-shaped hemorrhages
typically occur in patients with
located deeper in the retina assume
a pinpoint, blot or dot shape and
are more characteristic of DR.
While NPDR is characterized by
a microangiopathy that involves
intraluminal, intramural and
extravascular damage, PDR is an
entirely different disease entity.
The hallmark of PDR is the formation of new blood vessels at the
vitreoretinal interface and in the
vitreous itself. Fibrovascular tissue
proliferates on the surface of the
retina, optic nerve and/or iris. After
15 to 20 years of DM, this proliferative form affects about 50% of
patients with type 1 DM; 5% to
10% of patients with non-insulin-
dependent type 2 DM; and 30%
of patients with insulin-dependent
type 2 DM.28
For an eye to be classified as
having PDR, it must exhibit one or
more of the following characteristics: neovascularization of the optic
nerve head or disc (NVD); neovas-cularization elsewhere (NVE); or
vitreous or pre-retinal hemorrhage
associated with NVE (figure 3).29
Leakage from perifoveal vessels
causes DME, which could result in
permanent central vision loss if left
untreated. This edema can occur at
any stage of retinopathy, whether
proliferative or non-proliferative.
For macular edema to be classified
as clinically significant (CSME), an
eye must exhibit one or more of the
following characteristics: thickening of the retina within 500µm
of the center of the macula; hard
exudates within 500µm of the center of the macula with associated
thickening of the adjacent retina;
or at least one zone of retinal thickening that is greater than one optic
disc diameter in size.27,29
Is "tomographically significant"
macular edema—visible on OCT
but not on fundoscopy—changing
the definition of what constitutes
CSME? Clinical evidence certainly
suggests so, because OCT yields
both qualitative and quantitative
information about retinal thickness
Thus, OCT can be helpful, in a
non-invasive manner, to support
a diagnosis of CSME or to rule it
out. On OCT, CSME is represented by increased retinal thickening
due to intraretinal fluid leakage,
which appears as hyporeflective
(dark) areas on the cross-sectional
image (figure 4). Additionally,
OCT is valuable in monitoring the
eye's response to treatment.30
Further, there is now evidence
that OCT plays a defining role in
determining DME treatment criteria. Researchers from the Diabetic Retinopathy Clinical Research
Network (DRCR.net) have recommended OCT-measured central
retinal thickness values greater than
or equal to 250µm as an eligibility criterion for at least 11 study
protocols. In the RISE and RIDE
studies, which investigated the efficacy of intravitreal ranibizumab in
treating DME, an OCT-measured
central subfield thickness greater
than or equal to 275µm was used
as one of the two eligibility criteria
for treatment.30 Subsequently, the
Safety and Efficacy of Ranibizumab
in Diabetic Macular Edema With
Center Involvement (RESOLVE)
trial used an OCT-measured central retinal thickness of greater than
or equal to 300µm, as well as with
visual acuity parameters, as eligibility criteria for the treatment of
DME with ranibizumab.30
As these studies indicate, OCT
imaging could enable closer monitoring, more intensive systemic diabetes management and more timely
treatment of DME.30
Management of Concomitant
Proper management of associated systemic disorders ultimately
influences the onset, progression
and visual outcome of DR.
* Hypertension. Systemic
hypertension is an established risk
factor for the development and
progression of retinopathy. In the
third U.S. National Health and
Nutritional Examination Survey,
hypertension was documented
in up to 75% of adults with
diabetes.31 Research has shown
that individuals with DM and
hypertension are more likely to
develop DR, and likely experience
more rapid disease progression
compared to DM patients without
hypertension.9 Additionally, DM
patients with concomitant hyper
tension are up to three times more
likely to develop DME.
Fortunately, reduced blood pressure levels have been shown to
decrease the risk of DR progression.9 Several antihypertensive
agents have been evaluated for
their therapeutic effect on DR.
(ACE) inhibitors and angiotensin
receptor blockers have been shown
to reduce DR progression in nor-motensive patients with type 1 DM
and mild DR.32 In multiple trials,
aggressive blood pressure treatment
was accompanied by improved
outcomes in both retinopathy and
nephropathy. As a result, the Joint
British Diabetes Societies have
recommended that both type 1
and type 2 DM patients should be
aggressively treated to blood pressure levels of less than 130mm Hg
systolic and 80mm Hg diastolic.31
If any degree of proteinuria is present, the diastolic blood pressure
should be lower than 75mm Hg.
This research also indicated that
any individual with DM should
have a diastolic blood pressure
lower than 75mm Hg if there is any
evidence of retinopathy.31
* Kidney disease. Because DR is
also associated with renal disease
patients with renal dysfunction
should be monitored closely for
progressive retinopathy. Also, any
patient with rapidly progressing
DR should be evaluated for possible nephropathy.9 Further, most
patients with type 1 DM should
receive ACE inhibitors to reduce
the risk of progression from micro-albuminuria to macroalbuminuria.
* Elevated cholesterol. Dyslipidemia may also play a role in the
progression of DR and DME—
although there is conflicting evidence. Some studies have linked
elevated HDL and total cholesterol
levels with a higher incidence of
DR.9 A cross-sectional analysis
from the Wisconsin Epidemiology Study of Diabetic Retinopathy
trial, however, showed no association between elevated cholesterol
levels and the severity of DME in
either type 1 or type 2 diabetes
Nonetheless, lipid-lowering medications should be considered for any
diabetes patients with high cholesterol.9 Studies of fenofibrate mono-therapy have indicated that the drug
may slow DME progression.34
* Anemia. Anemia is a common
finding in patients with DM due to
the high systemic burden of chronic
kidney disease. Reduced hemoglobin levels independently help to
identify DM patients who are at
an increased risk for microvascular
complications (including retinopathy), cardiovascular disease and
Anemia often accompanies
diabetic kidney disease. When
glomerular filtration rates are
less than 60mL/minute, the most
common cause of the anemia is a
relative erythropoietin deficiency
that reduces hemoglobin levels
to less than 11g/dL.31 An ETDRS
analysis found that low hematocrit was a risk factor for the development of high-risk DR. A separate
cross-sectional study uncovered
an increased risk of retinopathy
in patients with hemoglobin levels
lower than 12g/dl.9
|Diabetes Affects All Retinal Cell Types64
Altered tight junctions; endothelial cell and pericyte death.
|| Altered contacts with vessels; release inflammatory
mediators; impaired glutamate metabolism.
|| Increased number; release inflammatory mediators.
|| Death of ganglion cells; inner nuclear layer; axonal atrophy.
* Sleep apnea. Obstructive sleep
apnea (OSA) is a common disorder that often coexists with DM.36 The consequences of OSA include
cardiovascular morbidity (coronary artery disease/myocardial
ischemia), cerebrovascular accident
and overall mortality.36
Obesity, a well-known risk factor for type 2 DM, is also a risk
factor for OSA. Patients with OSA
often have a body mass index
greater than 25kg/m2 and a neck
circumference larger than 17 inches
in men and 16 inches in women.36 Several studies also have found a
link between OSA and hypertension.36-39 OSA may aggravate DR
secondary to nocturnal hypertension and hypoxemia.
* Tobacco use. The role of
smoking in DR has not been
clearly established. Some studies
have shown a definitive association, while others have shown no
relationship when controlling for
additional risk factors, such as age
of onset and duration of diabetes
and/or associated hypertension.31 Smoking increases circulating leukocytes and platelet activation.
Nicotine in tobacco smoke causes
severe retinal vasoconstriction.
Smokers often exhibit higher levels
of LDL and lower levels of HDL.
Because the link between cigarette
smoking and cardiovascular disease is well established—especially
among patients with DM—it is
essential that doctors encourage
their patients to stop smoking.31
Treatment of DR
* Treatment of NPDR (without CSME). NPDR is significant
because of its potential to progress to PDR. The current stage
of NPDR at the initial diagnosis
dictates the patient's follow-up
Mild NPDR carries a 5% chance
of progression to PDR in one year,
and a 15% chance of progression to high-risk PDR within five
years.27,40,41 Moderate NPDR has a
12% to 27% chance of progressing to PDR in one year, and a 33%
chance of progressing to high-risk
PDR within five years.27,40,41 Finally, severe NPDR has a 52% chance
of progressing to PDR in one year,
and a 60% chance of progressing to high-risk PDR within five
Both the Diabetes Control and
Complications Trial (DCCT) and
the United Kingdom Prospective
Diabetes Study showed the therapeutic benefit of intensive glycemic
control in patients with type 1
and type 2 DM. Improved glucose
control significantly reduced the
likelihood of vitreous hemorrhage,
retinopathy that required laser pho-tocoagulation and renal failure.10,42
Management of NPDR centers
on stabilizing the condition and
arresting the progression to PDR.
The DCCT showed that intensive
glycemic control involving multiple daily blood sugar measurements, nutritional counseling, and
both medical and glycosylated
hemoglobin evaluations every
three months decreased the risk of
the development and progression
The ADA recommends an
interdisciplinary approach to
management of DM and its complications, with close monitoring
of blood pressure, blood glucose
and cholesterol, as well as smoking
avoidan/ROExams/cessation, exercise and
weight control.1,43 Further, proper
instruction from a certified diabetes
educator regarding self-management techniques is a mainstay of
any interdisciplinary treatment
* Treatment of PDR (without
CSME). In cases of PDR, retinal
imaging with fluorescein angiog-raphy is needed to determine if/
when the patient has reached any
treatment landmarks, as well as to
document any leakage patterns.17,29 Treatment of PDR usually involves
laser surgery to seal leaking vessels (indirectly) and prevent further
development of neovascularization.
New, weaker blood vessels can
rupture, scar and cause retinal tissue necrosis.
The Diabetic Retinopathy Study
(DRS) and the Early Treatment
of Diabetic Retinopathy Study
(ETDRS) provided evidence that
laser photocoagulation significantly
reduced the risk of severe vision
loss in patients with DR. Results of
the DRS indicated that panretinal
photocoagulation reduced the risk
of severe vision loss in most (60%)
patients with PDR.44 Earlier and
more adequate treatment is effective
in more than 90% of cases.11,45-47
The inherent retinal tissue scarring associated with thermal laser
photocoagulation may cause
reduced contrast sensitivity, poor dark adaptation and visual field
loss. Intravitreal injections of anti-VEGF agents have been shown
to be effective as individual and/
or combination treatments for
PDR. Several studies are still being
conducted to assess the safety of
repeated intravitreal injections,
which frequently are needed to
achieve optimum benefit.48
Because thickened posterior vitreous cortex is one of the main factors in the development of disease
proliferation in patients with PDR,
a consequent shrinkage of the posterior vitreous cortex often leads to
hemorrhages and tractional retinal
detachments. In this instance, the
new vessels use the posterior vitreous face as a scaffold. Therefore,
some clinicians believe that PDR
should be called "proliferative diabetic vitreoretinopathy."49
In some cases of PDR, vitrectomy surgery can be beneficial.
Indications for vitrectomy include
vitreous hemorrhage that blocks
the view of the retina, dense
premacular hemorrhage, complicated retinal detachment and severe
neovascular proliferation that does
not respond to laser treatment. The
Diabetic Retinopathy Vitrectomy
Study results showed that early vitrectomy was beneficial in restoring
and preserving vision in patients
with PDR with or without associated vitreous hemorrhage.49
So-called pharmacologic vitreolysis has been suggested as
another important consideration
for future management. Diabetes
induces significant biochemical and
structural changes within the vitreous. Because a diabetic vitreous is
different from a normal vitreous,
pharmacologic vitreolysis of a normal vitreous may fail to uncover
an agent that is effective for pathologic conditions.
This may explain why Vitrase
(hyaluronidase, Bausch + Lomb)
failed in phase III FDA clinical
trials for treatment of vitreous
hemorrhage in patients with DR.
Hyaluronidase is a vitreous lique-factant, not a vitreous interfactant.
Thus, the agent will liquefy the gel
vitreous, but will not induce vitreoretinal dehiscence. In PDR, this
results in persistent traction on the
neovascularization, which may lead
to possible recurrent vitreous hemorrhage and vision loss.
It is worth noting that Ocriplasmin (microplasmin, ThromboGenics) likely will be the first drug
approved for clinical pharmacologic
vitreolysis in cases of symptomatic
vitreomacular adhesion. Biologically, Ocriplasmin serves as both a
liquefactant and an interfactant.50
Treatment of DR (With CSME)
Although PDR is more likely to
cause severe vision loss (20/200 or
worse) than NPDR, the most common cause of functional visual loss
(worse than 20/40) in patients with
DR is DME (specifically CSME).
With more than 25 million people
estimated to have DM in the United States, the morbidity of CSME
has a significant impact on public
health.33 So, CSME needs to be
treated early—before chronic disease leads to irreversible functional
* Conventional laser treatment.
Laser photocoagulation is the standard of care in the treatment of
CSME. Focal or grid laser photo-coagulation reduces macular edema
by inducing coagulation necrosis.
Focal laser treatment is intended to
close leaky microaneurysms, while
grid laser is used to treat more diffuse edema.46
The goal of laser treatment for
CSME is not to improve vision, but
to slow or prevent central visual
loss as a result of chronic edema
and secondary tissue damage. The
ETDRS indicated that focal or grid
laser photocoagulation reduced the
risk of moderate visual loss due to
CSME by 50%.51
As previously mentioned, the
anatomical and visual benefits of
laser photocoagulation have been
shown to be effective over the long
term; however, the treatment of
DME is associated with risks and
side effects caused by iatrogenic
damage of retinal tissue.
* Micropulse laser treatment.
Micropulse laser technology
(MPLT) has been shown to be as
effective as conventional argon
laser for DME.52 Micropulse technology with 810nm and 577nm
lasers is used to produce a therapeutic effect without inducing collateral retinal damage during or
after treatment.53 With MPLT,
the induced temperature increase
in the targeted tissue remains
sublethal, and no visible lesion is
Micropulse power as low as 25%
of the visible threshold intensity has been shown to be have a
therapeutic effect, while sparing
neurosensory retinal tissue.53
MPLT is less destructive to
tissue, yet achieves the desired
therapeutic effect. For instance, one
study showed that MPLT appears
to be as effective as laser photo-coagulation for the treatment of
DME, but causes far less damage
to the retinal pigment epithelium.54
|The Optometrist's Role in DM and DR Management
| • Educate—Eduate patients about proper nutrition and healthy lifestyle.
• Evaluation—Perform a comprehensive ophthalmic workup and annual dilated fundus
• Early detection––Conduct regular monitoring of reported ocular complications.
• Comanagement—Provide timely consultation and appropriate referral.
• Rehabilitation—Offer or arrange low vision care for individuals who experience
significant vision loss.
* Pharmaceutical options.
Although laser therapy may slow
visual loss, it is not often accompanied by visual gain. This led to
evaluation of other CSME management options, including potential
pharmacologic therapies that may
be used alone or in combination
with laser therapy.
The anti-inflammatory effect of
intravitreal corticosteroids contributes to a reduction of edema.55 More specifically, intravitreal
triamcinolone has been shown to
reduce macular edema and improve
visual acuity.56,57 However, the
short-term effect of steroids necessitates multiple treatments, which
may increase the risk of adverse
effects, including ocular hypertension, glaucoma, cataract, retinal
detachment, epimacular membrane
Sustained-release devices containing the corticosteroids dexa-methasone and fluocinolone may
provide long-term therapeutic benefits, and are undergoing clinical
trials. However, such devices also
may increase the patient's risk for
the aforementioned adverse effects.
A large, multicenter study that
compared intravitreal triamcinolone with laser photocoagulation
was designed to help elucidate
the therapeutic role of steroids
in CSME management.58 The
researchers determined that, over a
two-year period, focal/grid photo-coagulation was more effective and
had fewer side effects than 1mg
or 4mg doses of preservative-free
intravitreal triamcinolone. These
results also suggest that focal/grid
photocoagulation should remain
the benchmark against which other
CSME treatments are compared in
future clinical studies.58
Recently, several studies have
evaluated the therapeutic effect of
anti-VEGF agents on CSME.59,60 It
appears that pan-VEGF-A inhibitors (which block uptake of all
VEGF-A isoforms) exhibit better
bioactivity than selective VEGF-A
inhibitors in patients with CSME.48
Eylea (aflibercept, Regeneron
Pharmaceuticals) is a recombinant fusion protein that inhibits
the function of both VEGF-1 and
VEGF-2 receptors. The DA VINCI
study showed that aflibercept, compared to macular laser photoc-agulation, produced a statistically
significant and clinically relevant
visual acuity improvement in
patients with DME.60
DRCR.net conducted a randomized controlled trial to assess
whether an intravitreal injection
of Lucentis (ranibizumab, Genen-tech/Roche) combined with either
prompt or deferred laser or intra-vitreal triamcinolone acetonide
combined with prompt laser could
improve visual acuity outcomes for
patients with DME when compared
to focal/grid photocoagulation.61 This Phase III study clearly showed
that intravitreal Lucentis, with
either prompt or deferred laser,
provided superior anatomic and
functional outcomes in individuals with DME through two years
of follow-up compared to laser
* Surgical intervention. Vitrectomy also may aid in the resolution
of DME. The initial rationale for
use of vitrectomy was justified by
evidence from early epidemiologic
studies. Researchers observed a
lower incidence of complete posterior vitreous detachment in patients
with DME than in those without
evidence of edema.62 This finding
suggested that a partially attached
vitreous is a risk factor for DME,
and that vitrectomy will remove the
tractional forces at the retinal surface, reduce oxygen consumption
of the vitreous and reduce hypoxia
at the retina.62
On the basis of currently available data, we don't know yet
if prolonged ocular treatment
with anti-VEGF agents will yield
increased systemic side effects, such
as hypertension and cardiovascular
or thromboembolic events. The
probable need for repeated injections also elevates the risk of visually devastating ocular side effects,
such as endophthalmitis.63
Combination therapy comprised
of laser and pharmacologic agents
potentially can yield additional
benefits, including improved visual
outcome and less frequent re-treatments—which, in turn, can reduce
the risk of adverse events.
The longer a patient has been living with diabetes, the more likely it
is that he or she will develop DR.
Diabetic retinopathy is a significant
public health problem, especially
among blacks and Hispanics. Fortunately, however, DR is a treatable condition.
Traditional treatment of DR
still is an effective management
approach. But, with newer, more
effective options, such as MPLT
and pharmacotherapy, the outcome profile for affected patients is
changing for the better.
Dr. Pelino is an assistant professor at Pennsylvania College of
Optometry at Salus University in
Elkins Park, Pa. Dr. Pizzimenti
is an associate professor at Nova
Southeastern University College
of Optometry in Fort Lauderdale,
Fla. Together, they co-author our
"Review of Systems" column.
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- Chopra V, Varma R, Francis BA, et al. Type 2 diabetes mellitus and
the risk of open-angle glaucoma the Los Angeles Latino Eye Study.
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- Leske MC, Wu SY, Hennis A, et al. Diabetes, hypertension, and
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- Negi A, Vernon SA. An overview of the eye in diabetes. J R Soc
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- Rogell GD. Corneal hypesthesia and retinopathy in diabetes mel-litus. Ophthalmology. 1980 Mar;87(3):229-33.
- The U.S. Centers for Disease Control and Prevention. Department
of Health and Human Services. National diabetes fact sheet: general
information and national estimates on diabetes in the United States,
2005. Available at: www.cdc.gov/diabetes/pubs/pdf/ndfs_2005.pdf (accessed July 27, 2012).
- Baker RS, Bazargan M, Bazargan-Hejazi S, Calderón JL. Access to
vision care in an urban low-income multiethnic population. Ophthalmic Epidemiol. 2005 Feb;12(1):1-12.
- Klein R, Klein BE. Vision disorders in diabetes. In: Diabetes in
America, 2nd ed. Bethesda, M.D.; National Institutes of Health;
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