C L I N I C A L A N D E X P E R I M E N T A L

Diabetic retinopathy: classification and optometric management Cockburn

OPTOMETRY

Diabetic retinopathy: classification, description

and optometric management

David M Cockburn OAM DSc hc
MScOptom
Department of Optometry and Vision
Sciences
The University of Melbourne
Accepted for publication: 20 April 1999
Background: Diabetes mellitus is an important cause of visual loss, which can be mod-
erated by treatment at specific stages of diabetic retinopathy. Existing monitoring for
retinopathy has been shown to fall short of ideal, resulting in unnecessary visual loss.
Using appropriate guidelines, optometrists should be well-placed to contribute to the
management of patients having diabetic eye disease.
Method: The underlying pathology of diabetic retinopathy is reviewed as a basis for
recognising the various stages of diabetic retinopathy, including macular oedema and
risk of progression of disease. These stages are detailed in terms of classification, preva-
lence and appropriate examination techniques. An illustrated guide summarises these
features and provides a suggested management regimen for continued monitoring,
reporting, referral and ongoing management by optometrists.
Conclusions: The majority of optometrists have the diagnostic skills and the clinical
equipment required for efficient monitoring of diabetic retinopathy. Inclusion of
optometrists in the team providing health services for diabetes is an economic and
practical solution to improving the primary eye care of people having diabetes and
ensuring a significant reduction of unnecessary visual loss caused by diabetic retinopathy.
(Clin Exp Optom 1999; 82: 2–3: 59–73)

Key words: diabetes mellitus, guidelines, maculopathy, optometrists, retinopathy

Diabetic retinopathy (DR) is present in
approximately one-third of all diabetics
and is sight-threatening in approximately
10 to 15 per cent.1 Patients of optometrists
in Australia appear to have approximately
the same prevalence of diabetes and its
ocular complications, according to a re-
port based on an optometry private prac-
tice population.2 These results suggest that
optometric patients are reasonably repre-
sentative of the diabetic community. It
follows that our examination techniques
and screening regimens should conform
to best practice evidence-based guidelines
developed for medical practitioners.
When determining the prevalence of
complications of diabetes, it is important
that care is taken to obtain samples that
are free from selection bias. If a sample is
taken from a specialist diabetic clinic in a
large public hospital, it would be expected
that the sample would be distorted by the
tendency of these clinics to attract a dis-
proportionate number of advanced cases
and therefore have a higher rate of com-
plications. Alternatively, a general practi-
tioner’s list may include only early and
mildly-affected diabetics, chiefly of type 2
diabetes. A survey of an entire community
will be more likely to provide a representa-
tive sample of the problem in the overall
population. There still remains the prob-
lem of avoiding bias due to the demo-
graphics of age or ethnic background in
the area being surveyed and the tech-
niques used to identify eye complications.
For these reasons, there are wide varia-
tions in the published figures for the
prevalence of DR with higher figures
being reported in clinic samples than in
community-based samples. For our pur-
poses, a prevalence of DR obtained in an
Australian community provides the most
useful data on which to plan allocation of
services.

Clinical and Experimental Optometry 82.2–3 March–June 1999

59
Diabetic retinopathy: classification and optometric management Cockburn
The occurrence of diabetic retinopathy
is directly related to the duration of the
diabetes, with more rapid onset of visual
complications in older type 2 diabetics,
who are generally middle aged or older
at the time of diagnosis of diabetes.3 Tight
control of blood glucose levels 4 and blood
pressure 5 has a very significant beneficial
effect on delaying the development and
progression of diabetic retinopathy in type
1 and type 2 diabetics. Other than this con-
trol, there is no effective prophylactic
treatment against the onset of retinopa-
thy.
When diabetic retinopathy develops,
timely treatment at very specific stages of
the condition reduces the risk of severe
visual loss by more than one-third.6 Al-
though the other forms of diabetic retin-
opathy can lead to very severe visual loss,
maculopathy is the most common cause
of visual loss in diabetics, particularly in
the more common type 2 diabetes. Its
effect may be significantly reduced by
prompt treatment.7
The recommendations for optometric
management of diabetic patients pro-
posed in this discussion are based on rec-
ognising threats to vision and implement-
ing proven treatment options. The nature
and timing of this treatment is detailed
in a companion paper on ‘Treatment of
diabetic retinopathy’.8
The monitoring of diabetic patients for
diabetic retinopathy appears to fall short
of being satisfactory, with only 28 per cent
of Australian general practitioners (GPs)
examining all their diabetic patients for
DR and most failing to dilate pupils.9 Only
45 per cent of GPs often or always meas-
ure the visual acuity of their diabetic
patients. Unpublished data from a Victo-
rian population survey suggest that 74 per
cent of optometrists state that they would
perform dilated ophthalmoscopy on their
diabetic patients, 50 per cent would use
slitlamp fundoscopy and 19 per cent
would use indirect ophthalmoscopy. It is
likely that these results could be improved
by providing post-graduate education pro-
grams for medical and optometry gradu-
ates. The Australian optometry under-
graduate courses already address this
issue.
Clinical and Experimental Optometry 82.2–3 March–June 1999
Optometrists are ideally placed to pro-
vide an eye disease screening service for
diabetic patients by virtue of their train-
ing, equipment, accessibility and dedica-
tion to providing full ocular health assess-
ment. Their effectiveness in diagnosing
and assessing diabetic ocular disease is
well established.10-15 It should be relatively
simple to harness the potential of optom-
etrists to monitor diabetic eye disease
within the diabetic care team.
THE UNDERLYING PATHOLOGY OF
DIABETIC RETINOPATHY
A number of processes interact to produce
diabetic retinopathy. These include hor-
monal growth factor abnormalities, bio-
chemical abnormalities of the aldose re-
ductase pathway, non-enzymatic glycation
and haemodynamic changes. The effect
of these factors can be simplified and used
to explain the clinical appearance of dia-
betic retinopathy and its progress. In turn,
this simplifies an understanding of the
classification and assessment of the dia-
betic fundus and the planning of future
monitoring, management or referral.
The principle changes caused by diabe-
tes to the retinal microvascular system and
the blood constituents are: 16,17
1. thickening of the basement membrane
2. proliferation of endothelial cells
3. loss of capillary pericytes
4. increased platelet adhesion
5. changes in red blood cells.
The cumulative effect of this retinal
microangiopathy leads to retinal anoxia
as a result of microvascular occlusions,
breakdown of the blood retinal barrier
causing haemorrhages and oedema in-
cluding intra-retinal lipid exudates (for-
mally known as diabetic hard exudates).
If sufficiently extensive, the retinal anoxia
leads to production of a vaso-proliferative
stimulus, which leads to a growth of new
blood vessels with a supporting fibrous
matrix. These changes and their effects
are listed below.
Basement membrane
Thickening of the basement membrane
reduces the effectiveness of the transfer
of metabolites and waste products to and
60
from the retina. This leads to a variable
degree of anoxia, retention of fluid in the
retina (oedema), which is seen as cystoid
oedema, retinal thickening and/or the
deposition of intra-retinal lipid exudates.
Endothelial cells
Endothelial cell proliferation reduces the
size of the capillary lumen, which has the
effect of restricting the blood flow. This
further contributes to occlusion of retinal
capillaries. Endothelial cells also become
less effective in their role of maintaining
metabolic transfer, further contributing to
the breakdown of the blood retinal barrier.
Pericytes
Pericytes provide structural support for
capillaries. Their loss is associated with for-
mation of the saccular outpouching of
retinal vessels seen as microaneurysms.
Microaneurysms may break down to con-
tribute to the formation of intra-retinal
dot and blot haemorrhages, intra-retinal
lipid exudates and retinal oedema.
Platelets
Platelets are the blood cells responsible
for the process of clotting when there is a
breach in the vascular tree. In diabetes,
these cells become abnormally sticky and
tend to form clots inappropriately; thus
contributing to the process of retinal
microvascular occlusion with its sequelae
of anoxia.
Erythrocytes
Red blood cells are slightly larger in
diameter than the capillaries through
which they must pass. They deform to
traverse the lumen and during their con-
tact with the capillary endothelium, trans-
fer oxygen. In diabetics, the cells have
reduced capacity to deform in this man-
ner which also contributes to capillary
occlusion and retinal anoxia.
The cellular changes associated with dia-
betes interact to cause the signs of diabetic
retinopathy through formation of
microaneurysms, retinal haemorrhages,
intra-retinal lipid exudates, retinal thick-
ening, macular oedema and capillary non-
perfusion. Further progression of DR is
 Diabetic retinopathy: classification and optometric management Cockburn

Changes Effect Clinical signs

Basement membrane Restricted metabolic transport Capillary non-perfusion seen on angiography.

thickening Retinal anoxia
Proliferation of endothelial Reduction of size of capillary lumen.
cells Occlusion of capillaries. Stimulus
to neo-vascularisation
Formation of intra-retinal microvascular
abnormalities (IRMA), venous loops and
beading. Formation of new vessels on the disc,
retina, iris and trabeculae. Pre-retinal and
vitreous haemorrhages

Hypoxic changes affecting the Cotton wool patches

nerve fibre layer

Loss of pericytes Weakening of vessel walls Formation of microaneurysms

Breakdown of blood retinal barrier Microaneurysms, leak causing haemorrhages,
retinal thickening, diffuse and cystoid macular
oedema and accumulation of diabetic intra-
retinal lipid exudates

Increased platelet adhesion Thrombosis of retinal vessels leading Capillary non-perfusion with formation of IRMA,
Loss of deformability of RBCs to retinal hypoxia. venous beading and loops, leading to NVD,
Production of stimulus to NVE, NVI and cotton wool patches
neovascularisation

Table 1. Underlying pathology of diabetic retinopathy, its effect on the retina and the resulting clinical signs

marked by the formation of intra-retinal
microvascular abnormalities (IRMA) and
venous changes in the form of loops and
beading. Cotton wool patches may appear
if the nerve fibre layer is affected by
increasing anoxia. As retinopathy
progresses, retinal anoxia triggers the for-
mation of a stimulus to neovascularisation
which may develop on the disc (NVD), on
the retina (NVE) or in the anterior cham-
ber. These latter events are more fully
described under the heading of prolifera-
tive DR.
These changes, their effect and the
resulting clinical signs of diabetic retin-
opathy are summarised in Table 1.
CLASSIFICATION OF DIABETIC
RETINOPATHY
The Airley House classification of diabetic
retinopathy18 provides a very detailed clas-
sification of retinopathy with a consider-
able number of sub-categories. This clas-
sification is generally adopted as the
standard for research purposes because of
its suitability for precision in descriptive
grading of DR. A simplified Wisconsin ver-
sion, 19 which is adequate for clinical
assessment of treatment planning and
outcome, has been developed for ophthal-
mological use. Both classifications prob-
ably go beyond the needs of clinical op-
tometrists, whose interests are centred on
monitoring the normal diabetic ocular
fundus through to the stage of early and
moderate retinopathy and macular
oedema, with particular emphasis on
detecting the stages, where ophthalmo-
logical treatment might be effective. It is
also important that later, previously un-
detected, stages of retinal disease are man-
aged appropriately should they present to
an optometrist.
The headings used here to describe DR
focus on decision-making in the optomet-
ric monitoring of retinopathy. This mir-
rors the objectives of the World Health
Organization grading system and the
American Diabetes Association recom-
mendations of 1999,20,21 which propose
categories based on sight-threatening and
non-sight-threatening fundus signs and
availability of effective treatment. It also
takes account of the probability that up
to two-thirds of diabetic patients of optom-
etrists will present initially with no detect-
able signs of retinopathy and no visual loss
attributable to the disease. Of those who
do present with retinopathy, only a minor-
ity will require referral for treatment. The
remainder should be monitored at inter-
vals determined by assessment of the risk
of preventable visual loss in the individual
patient and modified by the optometrist’s
proficiency and interest in this field.
The primary classification of DR is into
non-proliferative, formerly termed simple,
or background retinopathy, and prolifera-
tive (PDR) with macular oedema and reti-
nal thickening possibly being present in
either type. Because there are retinal signs
of impending advancement from non-
proliferative retinopathy to the prolifera-
tive stages, it is useful to identify those
signs and particularly those conferring in-
creased likelihood of high risk PDR. It is
equally important to recognise early the

Clinical and Experimental Optometry 82.2–3 March–June 1999

61
Diabetic retinopathy: classification and optometric management Cockburn
often symptomless macular oedema and
retinal thickening before significant visual
loss occurs and at a stage where treatment
is most effective.
Diabetic macular oedema
CLASSIFICATION AND DESCRIPTION
Diabetic macular oedema is defined here
as the presence of intra-retinal exudates
and/or retinal thickening in the macular
area within two disc diameters of the cen-
tre of the fovea, but not involving the cen-
tral 500 microns (1/3 DD). The oedema
may be derived from defective retinal ves-
sels including microaneurysms, deep leak-
age from the choroid through the retinal
pigment epithelium, ischaemia caused by
vascular occlusions or a combination of
any of these. Oral and intra-venous
fluorescein angiography may show the
intra-retinal fluid to be due to diffuse or
focal leakage or a combination of the two.
Focal macular oedema usually takes the
form of cystoid deposits surrounding and
centred on the fovea with the larger cysts
nearest to the central fovea. Figure 1 shows
typical intra-retinal lipid exudates defin-
able as macular oedema.
Practice reference 1
Macular oedema—ophthalmoscopic
and angiographic signs
• Focal exudative serous oedema
• Diffuse exudative serous oedema
• Retinal thickening
• Intra-retinal lipid exudate deposits
• Ischaemic maculopathy
• Combined forms
CLINICALLY SIGNIFICANT MACULAR
OEDEMA
This consists of one or a combination of:
1. thickening of the retina at or within 500
microns (1/3 DD) of the centre of the
fovea
2. lipid exudates at or within 500 microns
of the centre of the fovea
3. any area of retinal thickening equal to
or greater than one disc diameter with
any part within one disc diameter of the
centre of the fovea.
Clinical and Experimental Optometry 82.2–3 March–June 1999
Practice reference 2
Diabetic macular oedema—definitions
Macular oedema—not clinically
significant
Oedema, retinal thickening or lipid
exudates, but not at or within 500 microns
of the fovea
Macular oedema—clinically significant
Oedema, retinal thickening or lipid
exudates on or within 500 microns
(1/3 DD) of the fovea or any thickening
>1 DD having any part within 1 DD of
foveal centre
Central vision is usually intact in the Figure 1. Macular oedema (clinically not
presence of non-significant macular significant). Note lipid exudates superior and
oedema but at the clinically significant temporal to the fovea but not within one disc
stage vision is either seriously threatened diameter of the centre of the fovea. There
or already affected (Figure 2). are several small intra-retinal haemorrhages
and some microaneurysms which are not
PREVALENCE resolved in the photograph. The patient is a
Macular oedema develops at some stage 30-year-old type 1 diabetic of approximately
in approximately nine per cent of all dia- 15 years duration. This patient should be
betic patients, is more common in type 2 referred to an ophthalmologist.
than in type 1 diabetics and is diabetes
duration dependent, rising to a preva-
lence of approximately 25 per cent for
patients with 20 or more years duration
of the disease.22
EXAMINATION TECHNIQUES FOR
MACULAR OEDEMA
Reliable detection of macular oedema
requires ophthalmoscopy through a
dilated pupil. The oedematous, thickened
retina loses its normal sheen, transparency
and colour. It appears thickened and has
a dirty grey colour. The most important
ophthalmoscopic technique involves use
of the slitlamp and a pre-corneal or fun-
dus contact lens. This provides a stere-
oscopic view of the retina within the fine
Figure 2. Clinically significant macular
slit beam, making retinal thickening more
oedema. The lipid exudate deposits are
readily detectable. Subtle retinal thicken-
within 1/3 disc diameter of the centre of the
ing is easily overlooked but in severe cases
fovea. Note also greyish colour of the foveal
the retina may be up to three or four times
area suggesting retinal thickening. This
its normal thickness and the bright bands
patient should have an urgent referral to an
representing the retinal extremities are
ophthalmologist.
well separated. In contrast, intra-retinal
lipid exudates are readily seen by direct
ophthalmoscopy as crisply defined, yellow-
ish deposits of varying size and shape lying
chiefly in the outer plexiform layer and
62

Practice reference 3
Macular oedema examination
techniques
• Dilated pupil direct ophthalmoscopy
with transillumination and indirect
ophthalmoscopy
• Slitlamp with precorneal or fundus
contact lens
• Confirm with fluorescein angiography
oral or IV
• Amsler grid evaluation
• Visual acuity
thus deep to visible retinal vessels. These
lipid exudates may form in a ring, often
around an ischaemic section of the retina
or surrounding the fovea.
Although fluorescein angiography
(intra-venous or oral) is usually necessary
to confirm the diagnosis of macular
oedema and to separate diffuse from focal
oedema, cystoid deposits can sometimes
be seen by using the direct ophthalmo-
scope to transilluminate the retina. A
small bright light source in the ophthal-
moscope or slit should be directed adja-
cent to but not directly onto the portion
of retina being assessed. The cystoid spaces
may then be seen as they are transillum-
inated through the retina. Angiography
may be required to delineate areas of
capillary non-perfusion, which is causing
an ischaemic form of macular oedema.
In addition to causing reduction in
visual acuity, macular oedema may cause
distortion of the normal retinal topogra-
phy, resulting in metamorphopsia. The
Amsler chart provides a subjective means
of confirming the presence of this symp-
tom and for following the course of the
complication. However, some patients
have difficulty in maintaining fixation of
the centre of the chart while assessing the
remainder of the grid and the results are
not always reliable.
MANAGEMENT OF CASES HAVING
MACULAR OEDEMA
Non-significant macular oedema requires
close monitoring because it may progress
to become clinically significant over a rela-
tively short time. Its presence also suggests
that the blood retinal barrier is defective
Clinical and Experimental Optometry 82.2–3 March–June 1999
Diabetic retinopathy: classification and optometric management Cockburn
and further complications could follow
relatively quickly. Referral to an ophthal-
mologist having access to fluorescein an-
giography facilities is usually advisable. In
recognition of the role of the GP as co-
ordinator of management, a report should
be sent to him or her.
Although ophthalmological opinion is
advisable to confirm the diagnosis of clini-
cally non-significant macular oedema, it
may be expedient for an optometrist to
provide follow-up monitoring in co-opera-
tion with an ophthalmologist. If this is the
case, monthly reviews may be in order and
certainly should be carried out at inter-
vals not exceeding three months. The
patient should be provided with Amsler
and acuity charts, be instructed in their
use and advised to use these at weekly, or
shorter intervals.
It is important that deterioration of visual
acuity or metamorphopsia should trigger
an urgent further review and referral.
Treatment of macular oedema that does
not reach the standard of clinically signifi-
cant oedema is generally delayed as there
appears to be no advantage in early treat-
ment.23 However, it is necessary to moni-
tor closely these patients for any worsen-
ing of the condition toward the clinically
significant stage or any documented loss
of visual acuity.
Patients having clinically significant
macular oedema require immediate oph-
thalmological referral regardless of the level
of visual acuity. Photocoagulation of diffuse
and clinically significant macular oedema
is effective over the long term in eyes hav-
ing vision of 6/9 or better at the time of
treatment but contributes little when vision
Practice reference 4
Macular oedema—management
• Clinically non-significant—refer for
confirmation, or monitor closely if mild
• If continuing monitoring, provide acuity
and Amsler charts for patient use at
home
• Review 3 monthly, or more frequently if
progressing, or refer
• Clinically significant, refer urgently (lipid
exudates, retinal thickening or oedema
at or within 1/3 DD of the fovea)
63
is already at the level of 6/20 or worse.24
This underscores the importance of de-
tection and treatment of the early, possi-
bly symptomless, stage of the condition
and hence the need for careful inspection
of the macula as described above.
Minimal non-proliferative
diabetic retinopathy
CLASSIFICATION AND DESCRIPTION
Microaneurysms are usually the first de-
tectable sign of retinopathy and range in
size from invisible by ophthalmoscopy,
through just discernible dark red spots to
saccular outpouchings of between 50 and
100 microns in diameter. Minimal non-
proliferative DR exists where there are a
few microaneurysms only. They are most
commonly found in clusters within the
boundaries of the principle vascular
arcades. Their initial appearance is often
in the region just temporal to the macula.
Microaneurysms may be solitary or in
clusters, red when patent and whitish
when hyaline material occludes the lumen
of older lesions. They tend to resolve in
time to be replaced by others.
Fluorescein angiography detects many
more microaneurysms than are visible
through the ophthalmoscope (Figure 3).
Patent microaneurysms fluoresce early,
remain bright throughout the angiogram
when some will leak late, whereas the
hyalnised lesions remain hypofluorescent
or simply ‘frost’ late.
PREVALENCE
Some degree of DR is present in approxi-
mately one-third of diabetics taking part
in community population studies.25 The
relative prevalence of minimal DR in this
group is difficult to determine, but it prob-
ably represents the largest proportion of
the total population having retinopathy
because the other more serious forms
would have passed through this stage. In
addition, it is very easy to overlook the
presence of one or two microaneurysms
and the smaller lesions can be detected
only by angiography, suggesting that the
true prevalence is probably greater than
generally observed.
In contrast to the relatively benign effect
Diabetic retinopathy: classification and optometric management Cockburn

of minimal DR, sight-threatening involve-

ment, including clinically significant
macular oedema is present in approxi-
mately one-third of all cases of DR or 11
per cent of all diabetics. The presence and
severity of DR is highly correlated with the
duration of the diabetes and tends to
occur at a shorter duration of the disease
in older diabetics than in those with younger
onset. Proliferative retinopathy is more
commonly a cause of visual loss in type 1
but maculopathy is the principal cause of
visual loss in type 2 diabetics.27

Practice reference 5 Figure 3. Fluorescein angiogram (late venous phase) showing

Signs of minimal diabetic retinopathy
• Microaneurysms only
The risk of visual loss in minimal non-
proliferative retinopathy is low, provided
that the microaneurysms are not located
close to the foveal avascular zone. When
they are near the foveal centre they may
leak and cause macular oedema. Exclud-
ing the presence of macular oedema, the
risk of visual loss, due to minimal DR and
transition to more serious proliferative DR
within five years, must be very low.
The eyes of most elderly late-onset type
2 diabetics with relatively short life expect-
ancy remain in this category until death,
with a changing distribution of the
microaneurysms and only minor worsen-
ing of signs, with perhaps an occasional
transient haemorrhage. However, it is
worth noting that the progress of retin-
opathy appears to be more rapid in the
aged than in young diabetics. An increase
in the number of microaneurysms over
time is a good indicator of the degree of
progression of the retinopathy. It must be
kept in mind that macular oedema can
occur concurrently with minimal (or any
other stage) DR.
EXAMINATION TECHNIQUES
The examination should include direct
and indirect ophthalmoscopy through a
dilated pupil. Red-free illumination may
assist in detecting haemorrhages and
microaneurysms. Close inspection of the
macular region with a precorneal or
numerous hyperfluorescent spots due to dye-filled micro-
aneurysms. Many of these microaneurysms would not have been
visible on ophthalmoscopy. The larger hypofluorescent patches
inferior and temporal to the fovea are haemorrhages. This
moderate DR and is best managed by an ophthalmologist.
fundus contact lens and slitlamp is advis- ing into account the patient’s age, blood
able. The patient should be medically pressure and glycaemic control, duration
assessed for all non-retinal ocular compli- of the disease and compliance with treat-
cations of diabetes as described in ‘Dia- ment. Proximity of any microaneurysms
betes mellitus: the general practitioners to the foveal avascular zone is also an
perspective’.28 Any suspicion of associated important factor in establishing the fre-
macular oedema requires either oral or quency of reviews. Where the microaneu-
intra-venous fluorescein angiography rysms are relatively close to the macula,
assessment. but not meeting the definition of macu-
lar oedema, patients should be asked to
OPTOMETRIC MANAGEMENT return if there is any visual change. An acu-
Patients with minimal DR should be ity chart and Amsler grid may be provided
reviewed at yearly or at shorter intervals for weekly self assessments of vision. Figure
depending on the assessment of risk, tak- 4 illustrates minimal diabetic retinopathy.
Practice reference 6
Practice reference 5.1
Optometric management of minimal Signs of mild non-proliferative
non-proliferative diabetic retinopathy diabetic retinopathy
• Report to GP and endocrinologist Microaneurysms plus one or more of:
detailing management plan • Intra-retinal haemorrhages
• Review 6 to 12 months depending on • Intra-retinal lipid exudates
severity
• Cotton wool patches
• Record fundus by text and photogra-
phy or drawing

Clinical and Experimental Optometry 82.2–3 March–June 1999

64

Figure 4. Minimal non-proliferative diabetic
retinopathy in a type 1 diabetic girl aged nine
years. One microaneurysm is just visible in
this photograph. More would be seen on
fluorescein angiography. This patient should
be monitored at yearly intervals with more
frequent monitoring at commencement of
menarche.
Mild non-proliferative diabetic
retinopathy
CLASSIFICATION AND DESCRIPTION
Mild non-proliferative DR is defined as
microaneurysms plus one or more of the
following: cotton wool patches, retinal
haemorrhages or intra-retinal lipid exu-
dates, but not having the characteristics
of moderate retinopathy (see below).
Figures 5a, 5b, 5c illustrate fundi hav-
ing the classification of mild non-prolif-
erative retinopathy. Macular oedema may
also be present at this stage of DR.
PREVALENCE
Diabetics with mild non-proliferative retin-
opathy tend to have long duration of diabe-
tes with a longer duration required for on-
set in younger onset type 1, than in older
onset type 2 diabetes. The Wisconsin popu-
lation-based study of DR found a prevalence
of minimal plus mild retinopathy of 26.9
per cent of all diabetics. The prevalence of
lipid exudates and cotton wool patches in
diabetes by type is shown in Table 2.
Clinical and Experimental Optometry 82.2–3 March–June 1999
Diabetic retinopathy: classification and optometric management Cockburn
Practice reference 7
Optometric management of mild non-
proliferative diabetic retinopathy
• Dilated pupil fundus examination with
direct and indirect ophthalmoscopy –
draw or photograph fundus lesions
• Exclude presence of IRMA or venous
loops and beading
• Slitlamp fundus lens examination for
macular oedema– refer if present or
suspected
• Slitlamp and gonioscopic examination
of the iris and anterior chamber for new
vessels
• Assess severity and arrange review
appointments as indicated, but not less Figure 5a. Mild non-proliferative diabetic
frequently than 6 months retinopathy: cotton wool patches in a type 1
• Provide Amsler chart and acuity chart. diabetic patient having a 20 year duration of
Ensure patient understands their use diabetes
and need to report if changes are noted
• Report to endocrinologist and/or general
practitioner with statement of future
management protocol
• OR refer if progression has been rapid
or patient poorly controlled for blood
pressure or blood glucose levels
EXAMINATION TECHNIQUES
A dilated pupil fundus examination is
necessary, using direct, binocular indirect
and slitlamp ophthalmoscopy with a fun- Figure 5b. Mild non-proliferative diabetic
dus contact lens or pre-corneal lens. A retinopathy: intra-retinal haemorrhages
careful search should be carried out for
IRMA and venous loops or beading, which
would suggest that the next higher grad-
ing of moderate DR is appropriate. The
presence of cotton wool patches should
alert the clinician to a more serious stage
of mild DR and to the need for more care-
ful follow-up.
Macular oedema is more likely to be
present in the mild form than in mini-
mal DR so this should also be sought as
described previously. A slitlamp exami-
nation of the iris and pupil margin seek-
ing new vessels is also necessary and the
anterior chamber angle should be in-
spected by gonioscopy. Any sign of new
vessels on the iris or in the anterior Figure 5c. Mild non-proliferative diabetic
chamber angle is a sign that the grad- retinopathy: lipid exudates. Note that this eye
ing is more advanced than mild or mod- also has clinically significant macular oedema
erate DR. Immediate referral would be and should be referred for treatment of the
required. oedema.
65
Diabetic retinopathy: classification and optometric management Cockburn
MANAGEMENT
The risk of progression from mild non-
proliferative DR to proliferative (but not
high risk PDR) retinopathy in one year is
estimated to be approximately five per
cent and to high risk proliferative retin-
opathy one per cent.23 These low risks,
combined with the absence of any proven
prophylactic treatment at this stage, sug-
gest that three-monthly review is adequate
but with careful attention to the possibil-
ity of development of macular oedema.
Although the presence of cotton wool
patches has been included as part of mild
non-proliferative DR, their presence sug-
gests that the condition is at the more
severe stage of development. Any new
vessels on the optic disc or elsewhere on
the retina should trigger immediate refer-
ral as this indicates a worse stage than the
assumed mild or moderate DR.
Moderate to severe non-
proliferative diabetic retinopathy
CLASSIFICATION AND DESCRIPTION
Moderate to severe non-proliferative DR
is defined as the presence of more exten-
sive haemorrhages, microaneurysms, cot-
ton wool patches and lipid exudates
present in all quadrants and greater than
in mild retinopathy, plus any IRMA,
venous loops or venous beading. Regions
of capillary closure are seen on fluorescein
angiography. Macular oedema is likely to
be found in these eyes and is the most
common cause of any visual loss. Eyes with
moderate to severe non-proliferative DR
are illustrated in Figures 6a and 6b.
Practice reference 8
Signs of moderate to severe non-
proliferative diabetic retinopathy
• Extensive microaneurysms
• Extensive dot and blot haemorrhages
and nerve fibre layer haemorrhages
• Extensive lipid exudates
• Extensive cotton wool patches
• IRMA
• Venous beading or loops
• Large areas of capillary closure seen
on angiography
Clinical and Experimental Optometry 82.2–3 March–June 1999
Type 1 diabetics
(younger age of onset)
Intra-retinal lipid exudates 24%
Cotton wool patches 15%
Table 2. Prevalence of intra-retinal lipid exudates and cotton wool
patches in type 1 and type 2 diabetics. Modified from Klein and
colleagues.26
PREVALENCE
In type 2 diabetics the overall prevalence
of non-proliferative retinopathy is ap-
proximately 28 per cent, with the contri-
bution of moderate to severe non-prolif-
erative retinopathy being approximately
seven per cent of these eyes.1 In type 1
diabetics with onset before 30 years of
age, the moderate to severe stage is rela-
tively more common pro rata, although
it appears after a longer duration of the
underlying disease than in patients hav-
ing older onset of type 2 diabetes. Table
3 shows the estimated prevalence of the
definitive signs of moderate to severe
non-proliferative DR in older type 2 dia-
betic patients which is additional evi-
dence that the more serious stages of
non-proliferative DR (excluding macu-
lar oedema) are relatively uncommon in
these patients.
Type 1 diabetics comprise only approxi-
mately 10 per cent of all diabetics but are
those more likely to have the advanced
stages of non-proliferative DR. Because
the prevalence of the more severe DR is
less common in the other 90 per cent of
type 2 diabetics, it is likely that optom-
etrists only occasionally see patients with
severe non-proliferative DR. An optomet-
ric practice with a patient base of 10,000
patients could expect to have at most, ap-
proximately 20 type 1 diabetics, assuming
that these patients are not tending to self-
select to attend ophthalmologists rather
than optometrists. At a late stage of retin-
opathy, the patient probably has devel-
oped other diabetic complications, which
tend to involve them with hospital diabetic
clinics and associated specialist physicians
66
Type 2 diabetics
(older onset)
Intra-retinal lipid exudates 19%
Cotton wool patches 10%
including ophthalmologists. This can be
expected to significantly reduce the
number of patients, who seek optometric
care with this level of DR.
EXAMINATION TECHNIQUES
As in all ocular fundus examinations of
diabetics, a dilated pupil examination is
necessary and a careful record of the fun-
dus condition should be made, preferably
by fundus photography. For a full evalua-
tion, direct, binocular indirect and
slitlamp inspection using a precorneal or
fundus contact lens is required. Macular
oedema is likely to be present, particularly
if there is loss of visual acuity.
It is necessary to search carefully for evi-
dence of IRMA which consist of small ves-
sels making direct arteriolar-venous
shunts (Figure 6b). As the name suggests,
these vessels lie deep in the retina as dis-
tinct from new vessels which spread over
the retinal surface and invade the pre-reti-
nal space created by vitreous detachment
and possibly the vitreous itself. On angi-
ography, IRMA shunts frost (hyperfluo-
resce along their length) but do not tend
to leak during the later angiogram as do
true new vessels. They probably derive
from pre-existing retinal capillaries which
have enlarged grossly. 17 At the stage
where IRMA is present, there is exten-
sive retinal anoxia and ischaemia, which
is seen on angiography as dark (hypo-
fluorescent) areas usually bounded by reti-
nal vessels.
Venous loops are large (up to 100 mi-
cron) billabong-like extensions usually
seen on the larger veins (Figure 6a). They
probably represent shunts that develop

Figure 6a. Moderate to severe non-
proliferative diabetic retinopathy: venous
loop in the superior temporal vein
Lipid exudates 9.4%
Cotton wool patches 5.4%
IRMA 2.6%
Venous beading 0.9%
Table 3. Type 2 diabetics older than
30 years at diagnosis and not using
insulin. Prevalence of lipid exudates,
cotton wool patches, IRMA or
venous beading. Modified from
Klein and colleagues.26
around thromboses or the result of the
vessel being pulled into a loop by traction
of fibrous tissue.29 Venous beading com-
monly occurs as part of severe DR and
appears as sausage-like dilatations, chiefly
on the larger veins (Figure 6b). They are
associated with capillary closure and there-
fore are a risk sign for development of
proliferative retinopathy.
A very careful search should be made
for subtle NVD or NVE, including the mid-
peripheral retina. Pre-retinal haemor-
rhages (Figure 7) are indications of the
presence of NVD or NVE which may be
obscured by the haemorrhages as they
lie anterior to the retinal features. Oral
or intra-venous fluorescein angiography
Clinical and Experimental Optometry 82.2–3 March–June 1999
Diabetic retinopathy: classification and optometric management Cockburn
6b. Moderate to severe non-proliferative
diabetic retinopathy: venous beading and
intraretinal microvascular abnormality. There
is high risk of development of proliferative
DR and visual loss making referral necessary
at this stage.
is useful for detection of subtle NVD or
NVE.
New vessels on the pupil margin can be
very indistinct and require a dedicated
search. They are bright red in colour and
in this respect differ from normal iris
vessels in their lack of a fibrous and
pigmented coating. Gonioscopy is also
required to seek new vessels in the angle.
These signs of course are indications of
proliferative retinopapthy for which the
patient should be referred as soon as pos-
sible.
Practice reference 9
Management of moderate to severe
diabetic retinopathy
• Refer for ophthalmological opinion
except where special circumstances
apply
• If continuing monitoring because of
special circumstances, inform GP or
endocrinologist of the circumstances
and:
• Review monthly
• Provide acuity and Amsler chart
• Obtain ophthalmological attention
immediately on appearance of new
vessels NVD, NVE or NVI, visual
loss or rapid progress of DR
67
Figure 7. Red-free photograph showing new
vessels on the disc (NVD) and a less obvious
small patch of new vessels elsewhere (NVE)
temporal and slightly inferior to the fovea.
The patient should be referred for evaluation
for laser treatment as a matter of urgency.
MANAGEMENT
Moderate to severe non-proliferative DR
carries a high risk of progressing to pro-
liferative DR. The features which suggest
this high risk are an increase in severity
of the signs, particularly, IRMA, beading
and cotton wool patches. However, the
most important sign is the presence of
large areas of capillary non-perfusion
which can be detected only by fluor-
escein angiography. Patients having this
level of DR should be under the care of
an ophthalmologist. There may be cir-
cumstances where referral to an ophthal-
mologist is not immediately possible due
to other health problems. In this event,
it is important to monitor carefully for
any signs of proliferative DR, which
would then make the referral impera-
tive.
Proliferative diabetic retinopathy
CLASSIFICATION AND DESCRIPTION
Proliferative DR consists of newly-formed
blood vessels on the disc or within one disc
diameter of it which is described as NVD
and/or new vessels elsewhere on the
retina (NVE) (Figure 8). In addition,
there may be new vessels on the iris and
in the anterior chamber angle (NVI)
Diabetic retinopathy: classification and optometric management Cockburn
Figure 8. Bright red new vessels on the iris. These may extend
into the anterior chamber angle and cause secondary glaucoma.
Pan-retinal photocoagulation will lead to resolution of these
vessels.
Practice reference 10
Signs of risk of progression to
proliferative diabetic retinopathy
Presence of :
• Intra-retinal microvascular abnormali-
ties (IRMA)
• Venous beading and venous loops
• Extensive cotton wool patches
• Extensive dot, blot or flame haemor-
rhages
• Vitreous or pre-retinal haemorrhage
(indicates likely NVD or NVE)
• Extensive capillary non-perfusion
seen on angiography
Any NVD or NVE or NVI indicates the
proliferative stage
Macular oedema may be present at any
stage of retinopathy
(Figure 9). It is believed that progressive
retinal ischaemia caused by capillary non-
perfusion, stimulates the production of vas-
cular growth factors which in turn stimulate
the production of the new vessels.30
An important characteristic of new
intraocular vessels is that they do not have
the same integrity of the blood retinal bar-
rier as normal vessels and tend to leak pro-
Clinical and Experimental Optometry 82.2–3 March–June 1999
lifically. This leakage is readily detected
by fluorescein angiography as hyperfluor-
escence, beginning in the early stage of
the angiogram and progressing through-
out the entire study.
The new vessels in NVE initially develop
chiefly from a retinal vessel close to re-
gions of capillary closure and spread over
the surface of the retina. Later, the new
vessels become attached to and spread
between the retina and the vitreous face,
where they frequently break down to form
pre-retinal haemorrhages (Figure 7). De-
tachment of the vitreous provides a space
into which the vessels can migrate and into
which leaking of whole blood may form
pre-retinal haemorrhages. These haemor-
rhages tend to have horizontal superior
borders and accurate inferior edges. Typi-
cally, these haemorrhages cause sudden
and possibly extensive visual loss, particu-
larly when they cover the fovea. Later, the
retina may be further compromised by
contraction of the fibrinous scaffold asso-
ciated with the new vessels which, when
they constrict, can cause traction retinal
detachment, producing further haemor-
rhages and initiating a ‘vicious cycle’.
NVD may derive from either the retinal
circulation adjacent to the disc or from
68
the choroidal circulation. The new vessels
may be extremely subtle and easily
missed during ophthalmoscopy. They are
best seen on fluorescein angiography,
where they become obvious because of
leakage of dye. A very careful and specific
search for these fine vessels is required
and a dilated pupil is essential. Some
clinicians find that red-free illumination
also helps.
The natural history of proliferative DR
is variable. A small proportion of patients
undergo regression of the new vessels
without serious visual loss. Figure 10 shows
the fundus of a type 1 diabetic who devel-
oped extensive proliferative retinopathy
which regressed spontaneously leaving
only the supporting glial tissue remnants.
Although the patient died shortly after
from kidney involvement, there was no
evidence of retinal detachment and cor-
rected vision was 6/9. Re-perfusion of the
capillary beds has been found to occur in
the majority of type 2 diabetic patients
who remained untreated, but despite this,
most continued to have progression of the
retinopathy.31 Eyes having untreated pro-
liferative DR, tend to have recurrent vit-
reous haemorrhages and retinal detach-
ment in addition to the retinal lesions.
Figure 11 illustrates an eye of a type 1 dia-
betic who developed proliferative DR
which progressed despite laser treatment
and was complicated by multiple vitreous
haemorrhage.
Practice reference 11
The signs and classification of
proliferative diabetic retinopathy
Proliferative retinopathy
• New vessels on or within one disc
diameter of the optic disc (NVD)
• New vessels on the retina elsewhere
(NVE)
High risk and advanced proliferative
retinopathy
• NVE and/or NVD with pre-retinal or
vitreous haemorrhage
• Retinal detachment
• Anterior chamber new vessels (NVI)
Maculopthy may be present at any stage
of retinopathy

Figure 9. Bright new vessels on the iris; these
may extend into the anterior chamber angle
and cause secondary glaucoma
High risk proliferative DR differs from
the less severe classification by the pres-
ence of pre-retinal and vitreous haemor-
rhages, retinal detachment and anterior
chamber involvement. Macular oedema is
probably present and vision is likely to be
severely affected by these processes.
Perhaps the most dramatic complica-
tion of proliferative DR is neovascular
glaucoma. This follows neovascularisation
of the anterior chamber angle, which is
accompanied by a fibrinous scaffold.
These tissues block aqueous flow into the
trabecular spaces and Schlemm’s canal. It
has been suggested that new vessels in the
iris always precede new vessels in the
angle, but cases have been reported of the
initial vascularisation being in the angle,
rather than on the iris.32 This occurred in
a significant number of eyes having cen-
tral retinal vein thrombosis and may or
may not be extended to new vessels in the
anterior chamber due to diabetes. How-
ever, the finding suggests that it would be
good practice to perform gonioscopy
whenever NVE or NVD is seen, until the
question is resolved.
Clinical and Experimental Optometry 82.2–3 March–June 1999
Diabetic retinopathy: classification and optometric management Cockburn
Figure 10. Vitreous strands remaining after
spontaneous resolution of proliferative
diabetic retinopathy in a type 1 diabetic. Note
traction of the retinal vessels.
PREVALENCE
Proliferative DR is rare in type 1 diabetics
of juvenile onset who have less than 10
years duration of diabetes, but increases
in prevalence in these patients to approxi-
mately 55 per cent after 20 years duration.
In type 2 diabetics who later require
insulin for glycaemic control, the preva-
lence of proliferative DR is approximately
20 per cent after 20 years duration. In
contrast, type 2 diabetics who are managed
successfully with oral hypoglycaemic
agents rarely develop proliferative DR.33
However, as noted above, these patients
are more likely to develop macular
oedema.
EXAMINATION TECHNIQUES
The examination techniques used to de-
tect PDR are similar to those described for
other levels of DR. Because macular oedema
is usually treated prior to pan-retinal laser
treatment, it is important to detect its pres-
ence and to ensure that it is treated prior to
the need for pan-retinal photocoagulation.
Iris and anterior chamber angle neovas-
cularisation is also more likely to be present
69
Figure 11. Pre-retinal haemorrhages are
located between the inter nal limiting
membrane and the vitreous face. Note the
flat superior border. This eye has
proliferative DR with NVD and NVE and
requires pan-retinal photocoagulation. If
there is macular oedema, this should be
treated before the pan-retinal laser treatment
is commenced.
at this stage of DR and should be actively
sought by gonioscopy. Its presence increases
the urgency of referral and its treatment
with pan-retinal laser photocoagulation.
Intra-venous fluorescein angiography is
necessary to identify sectors of the retina
which are ischaemic. The larger the total
area involved, the greater the risk of de-
velopment of high risk PDR. Fluorescein
angiography also allows planning of laser
photocoagulation placement.
MANAGEMENT OF PROLIFERATIVE
DIABETIC RETINOPATHY
The management of proliferative DR is
the responsibility of ophthalmology and
the ideal situation would be where the
patient is already under the care of an
ophthalmologist at the stage of moderate
to severe non-proliferative DR. However,
this ideal does not yet apply and people
with existing proliferative DR occasionally
present in the first instance to an optom-
etrist or general practitioner. In this event,
an appointment should be made for oph-
thalmological review within a day or two
and preferably on the same day. The
Diabetic retinopathy: classification and optometric management Cockburn
appointment should be with a retinal spe-
cialist or diabetic eye clinic with photoco-
agulation facilities. The patient’s GP should
be involved in this stage of management.
The referring optometrist should con-
tribute to the team approach by ensuring
that management from that point onward
is appropriate and that the patient is coun-
selled to comply with treatment. At the
conclusion of treatment, there may be a
need to provide low vision aids to maxim-
ise remaining vision.
CONCLUSIONS/SUMMARY
The fold-out chart (Figure 12 [page 72–73])
illustrates a schema for the guidance of
optometrists when monitoring patients
having diabetes.
The guidelines assume that optom-
etrists have well-developed skills in direct
and binocular indirect ophthalmoscopy,
slitlamp indirect ophthalmoscopy and
gonioscopy. Except in unusual circum-
stances, it is necessary to dilate the
patient’s pupils for all ocular fundus
assessments. Slitlamp inspection of the iris
for new vessels should precede the use of
mydriatic drugs.
Variations from these guidelines may be
made on the basis of the individual op-
tometrist’s interest, willingness to assume
responsibility, training and clinical skills
in this area, together with the special
needs and restrictions imposed by the
patient’s own circumstances and wishes.
Another factor that might be taken into
account when planning future monitor-
ing is the availability of, or the patient’s
existing use of, other eye care services.
Because the management of diabetic
eye disease is continually undergoing
change, it is essential that optometrists
maintain currency by continued study.
Useful resources are the Internet sites:
http://www.pslgroup.com/diabetes.htm
http://www.diabetes.org/DiabetesCare/
http://journal.diabetes.org/journals.asp
http://www.webmedlit.com/topics/
EndoLit.html
This paper does not address the many
non-retinal ocular or systemic complica-
tions of diabetes mellitus. These have
been dealt with elsewhere in this issue of
Clinical and Experimental Optometry 82.2–3 March–June 1999
the journal. There may be ocular compli-
cations secondary to the macrovascular
damage of diabetes taking the form of
stroke, anterior ischaemic optic neuropa-
thy, kidney disease and neurological com-
plications involving the optic nerve or
brain stem vascular supply. When assess-
ing diabetic patients, the possibility of sec-
ondary eye complications from these con-
ditions should be taken into account.
Patients should be encouraged to com-
ply with the treatment and the manage-
ment provided by other involved health
professionals. This is particularly impor-
tant now that evidence has shown that
strict control of blood pressure and blood
glucose levels are critical factors in delay-
ing retinopathy and other complications.
General medical practitioners should be
recognised as the co-ordinators of the
team approach to diabetic care. Optom-
etrists should report to the diabetic pa-
tient’s GP following each eye examination.
Written reports should clearly detail not
only the present status but also the pro-
posed future management so that the GP
is aware that referral to an ophthalmolo-
gist will be made if and when it is appro-
priate. Special nurse practitioner diabetic
educators are important members of the
team approach to the management of dia-
betes. Their work can improve compliance
with all forms of treatment and therefore,
improve the outcome in terms of quality
of life and delay of serious complications.
Optometrists should make contact with
these practitioners and arrange for con-
tinued case reviews.
Optometrists are often privileged to be
taken into the patient’s confidence about
alternative medical treatments. When pa-
tients use alternative therapies to the
exclusion of their conventional diabetic
medical treatment they are exposed to
serious complications of diabetes. There
is no evidence that alternative treatments
are effective in controlling diabetes and
patients should be informed of this. If the
alternative treatment is used in addition
to the conventional, then patients should
be counselled to inform their general
practitioner or pharmacist, so that the
combination of treatments is not damag-
ing to their health.
70
Finally, care should be taken to avoid
making a stereotype of a patient having
diabetes by focusing only on that disease
and its complications, with the risk of
neglecting to consider the possibility of
co-existing but unrelated morbidity. Your
diabetic patients are people, but people
with diabetes, and otherwise have the
same needs as non-diabetics.
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