4JUNE 2014

Detection and treatment of diabetic
The vital role of OCT

Gurdeep Bidhesha
BScOptom(Hons) GradCertOcTher
UNSW

CASE REPORTTHE PRESENT Optometry Clinic at
UNSW Australia, Kensington openedin 2000 with the purpose of teaching
Year 4 and 5 students the clinicalskills necessary to become competent
practitioners. The clinic is open tomembers of the public, university staffand students. About 4,000 patients
present annually, many of whom havevision-threatening pathology.
According to the International DiabetesFederation, diabetes mellitus (DM)affects 366 million people worldwide.
That number is predicted to rise to552 million by 2030.1 Prevalence andincidence of type 1 and 2 DM varies
greatly among different populations
and affects male and females equally.2
Diabetic eye disease is rare on initialdiagnosis of type 1 DM and about 20
per cent of type 2 DM, rising to 90
per cent and 60 per cent, respectively,
after 20 years disease duration.3 It
is common for undiagnosed type 2DM, retinopathy discovered during aroutine eye examination to be the firstsign of systemic disease.

A 59-year-old Bangladeshi malepresented to the UNSW optometryclinic in June 2013. He had been
experiencing reduced vision in hisright eye for three months and wanted
a second opinion. He reported himself
to have been a well-controlled type 2
diabetic sufferer for eight years, withaverage blood sugar levels (BSL) of6-7 mmol, blood pressure (BP) levelsof 110/70 and three-to-four monthly
checks with his general practitioner.
Ocular history was unremarkable apartfrom bilateral cataract extraction.
Presenting vision was R 6/12 andL 6/7.5. Best-corrected vision witha low hyperopic script were R 6/7.5(niph) and L 6/6. Intraocular pressures
were 17 mmHg both eyes with Perkins
applanation tonometry.
Dilated fundus examination revealed
scattered dot-blot haemorrhages at bothposterior poles. Scattered exudates
and micro-aneurysms were foundwithin the right macula region whilst
the left eye had an unusual innerlimiting membrane (ILM) reflex at themacula with dot haemorrhages andmicroaneurysms. (Figures 1A, 1B, 2A
and 2B)
After an urgent assessment at the eye
hospital two weeks later, the registrarrecommended better BSL control,in conjunction with the generalpractitioner, as first line treatment. On
review in October 2013, the registrar
decided to continue to monitor theretinopathy, while maintaining strictglycaemic and blood pressure control.
The patient returned to UNSW
optometry clinic February 2014 witha review booked at the eye hospitalin April 2014. He reported no visualcomplaints with well controlled BSL
and BP levels. Best-corrected vision
was R 6/6-2 and L 6/6-2. Slitlamp
examination was unremarkable.
Fundus examination (Figures 3A and3B) revealed an increase in retinal
haemorrhages and exudates within theright macula region. In the left eye,there was a cotton wool spot near thedisc and a circinate ring of exudates
within one disc diameter of the macula.
OCT also reflected these new findings(Figures 4A and 4B).
In light of these findings, the eye
hospital was contacted to organise amore urgent assessment. Despite thepatient reporting compliance withsystemic control, it was evident that
this alone was not enough to prevent
retinopathy progression.
Discussion

Hyperglycaemia induces a number ofbiochemical reactions such as vascularendothelial growth factor (VEGF),
aldose reductase and angiotensin
enzyme expression.4,5 These culminate
into vessel leakage, haemorrhaging andischaemia. Inflammatory pathways andleukostasis are also being investigatedas pathomechanisms of diabetic eyedisease.5
Diabetic retinopathy (DR) is theleading cause of preventable blindnessof the working age population indeveloped countries4 and is gradedbased on the clinical features present.
The Early Treatment of Diabetic
Retinopathy Study (ETDRS) scaleis the gold standard from which a
number of other grading scales havebeen adapted.6
In the case of this patient, on firstpresentation, he had mild NPDR botheyes and diffuse macula oedema in
the right eye. On second presentation,
he had moderate NPDR both eyes
and CSME in the left eye. This is alsoclassified as vision threatening (VTDR).
Global estimates worldwide found DR
present in 34.6 per cent, PDR in 7.0 percent, DME in 6.8 per cent and VTDR in
10.2 per cent of diabetic patients.7,8Microaneurysms are small round‘protrusions’ that occur locally at
capillary walls which have weakened
due to capillary closure. These canpresent de novo or within circinate
exudate rings.9

5JUNE 2014

macular oedema
in diagnosis and effective comanagement
AB

Figure 1A and Figure 1B. Fundus images of patient (artefact at 2 o’clock)Figure 2A and Figure 2B. OCT of OD revealed exudates and cystic spaces confirming the presence of macular oedema. This also supported
the reduced vision findings in OD.

permeable capillary walls. These canform singularly or as a circinate ringfollowing rupture of a microaneurysm.9

Intra-retinal haemorrhages occur asa result of blood vessel rupture andare classified based on their location
within the retina. Flame haemorrhages
lie within the tightly packed nerve
fibre layer (NFL). Dot haemorrhages
are round, well-defined and foundwithin the outer plexiform layer (OPL).
Blot haemorrhages are larger and lessdefined compared to dots and occur
within the less compact inner nuclear
layer (INL).9

In the presence of increasing nonperfusion, venous beading presents as
focal dilation and thinning of a venous
wall and is highly associated withrisk of PDR developing. Cotton wool
spots represent localised NFL swelling
secondary to obstructed axoplasmic
flow.9Hard exudates occur at the OPL andrepresent leakage from increasingly

Intraretinal microvascularabnormalities (IRMA) represent

abnormal communication between
arterioles and venules and look similar
to neovascularisation (NV). Unlike NV,
IRMA lie within the retina, do not leakand do not form abnormal attachments
to the vitreous.9
Proliferative changes occur whensignificant retinal ischemia stimulates
angiogenic factors such as VEGF,
resulting in new blood vessel formationon the retinal surface.10
Continued page 66JUNE 2014

Figure 3A. Increase in retinal haemorrhages andexudates within the right macula region

Figure 3B. Single cotton wool spot adjacent tooptic disc and a circinate ring of exudates within 1
disc diameter of the macula in the left eye

Figure 4A and Figure 4B. OCT confirms findings of bilateral macula oedema

Vital role of OCT
From page 5

Diabetic macula oedema (DME) isdefined as retinal thickening (build-upof fluid and proteins in the Henle Layerand INL) secondary to a breakdown ofthe blood retinal barrier.11 DME is theleading cause of vision loss in type2 diabetese.3 As this case illustrates,
urgent ophthalmological assessment isessential.

Treatment

The three major risk factors for DR are
duration of diabetes, hyperglycaemic
levels and hypertension.2 The Diabetes
Control and Complication Trial (DCCT)and UK Prospective Diabetes Study(UKPDS) both found that intensive
systemic treatment—maintaining blood
glucose levels as close to the normal
range (HBA1c 7.0 per cent) and strict
blood pressure control (< 140/80)—
delays the onset and progressionof micro-vascular complicationsof type 1 and 2 diabetes including
retinopathy.12,13
It is essential that a multi-disciplinary
team of GPs, endocrinologists,dietitians and nurse educators isinvolved in achieving this alongsideeye-care providers.

The ETDRS found that following focal
laser photocoagulation, there was
50 per cent reduction in moderatevision-loss in CSME patients14 andfor a number of years focal laser has
been mainstay treatment for suchpatients. Focal laser seals leaking
microaneurysms, while grid laser isused in diffuse cases. It is hypothesisedthat the reduced retinal blood flow,
due to increased local oxygenation via
photocoagulation, results in reductionof macula fluid.15
Anti-VEGF therapy, such as
bevacizumab is fast replacing laser as
first-line treatment for centre involved
macular oedema, due to its greater
efficacy and increased safety involving
the central macula.5,15 It is an antibodyof VEGF-A and inhibits angiogenesis.5,10
For proliferative retinopathy, ­­pan-7

JUNE 2014

retinal photocoagulation is still firstline treatment for fibrous regressionof neovascularisation, reduction invitreous haemorrhage and reduction intractional retinal detachment.5
Conclusion

Effective screening programs are
essential for early diagnosis of diabetic
retinopathy. This case report showsthat OCT is a valuable tool that canmake a rapid diagnosis of macularoedema as well as monitor forprogression. It would be worthwhile
for all optometrists to have access to an
OCT to use alongside dilated fundus
examination and stereo-photos inensuring timely diagnosis, effective
comanagement and appropriate
treatment.

1. Scanlon PH, Aldington SJ, Stratton
IM. Epidemiological issues in diabetic
retinopathy. Middle East African Journalof Ophthalmology 2013; 20: 293-300.
2. NHMRC. Guidelines for the Managementof Diabetic Retinopathy. Edited byAgeing DoHa2008.
3. Chistiakov DA. Diabetic retinopathy:
pathogenic mechanisms and current
treatments. Diabetes & Metabolic
Syndrome 2011; 5: 165-172.
4. Ciulla TA, Amador AG, Zinman B.
Diabetic retinopathy and diabetic
macular edema: pathophysiology,screening, and novel therapies. Diabetes
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5. Heng LZ et al. Diabetic retinopathy:
pathogenesis, clinical grading,management and future developments.
Diabetic Medicine 2013; 30: 640-650.
6. Grading diabetic retinopathy fromstereoscopic color fundus photographs—
an extension of the modified Airlie
House classification. ETDRS report
number 10. Early Treatment DiabeticRetinopathy Study Research Group.
Ophthalmology 1991; 98: 786-806.
7. Ding J, Wong TY. Current epidemiology
of diabetic retinopathy and diabetic
macular edema. Current Diabetes
Reports 2012; 12: 346-354.
8. Yau JW et al. Meta-Analysis for Eye
Disease Study G. Global prevalence andmajor risk factors of diabetic retinopathy.
Diabetes Care 2012; 35: 556-564.

9. Hudson C. The clinical features andclassification of diabetic retinopathy.
Ophthalmic Physiol Optics 1996; 16
Suppl 2: S43-48.
10. Gupta N, Mansoor S, Sharma A,Sapkal A, Sheth J, Falatoonzadeh P,
Kuppermann B, Kenney M. Diabetic
retinopathy and VEGF. The OpenOphthalmology Journal 2013; 7: 4-10.
11. Antcliff RJ, Marshall J. The pathogenesisof edema in diabetic maculopathy.
Seminars In Ophthalmology 1999; 14:223-232.
12. The effect of intensive treatment ofdiabetes on the development andprogression of long-term complicationsin insulin-dependent diabetes mellitus.
The Diabetes Control and Complications
Trial Research Group. New England JMed 1993; 329: 977-986.
13. Krentz AJ. UKPDS and beyond: intothe next millennium. United Kingdom
Prospective Diabetes Study. Diabetes,Obesity & Metabolism 1999; 1: 13-22.
14. Early Treatment Diabetic Retinopathy
Study research group. Photocoagulation
for diabetic macular edema. Early
Treatment Diabetic Retinopathy Study
report number 1. Archives Ophthalmol
1985; 103: 1796-1806.
15. Shamsi HN, Masaud JS, Ghazi NG.
Diabetic macular edema: New promisingtherapies. World J Diabetes 2013; 4: 324338.

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