The SA Journal Diabetes & Vascular Disease Vol 7 No 3 (September 2010) - page 12

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SA JOURNAL OF DIABETES & VASCULAR DISEASE
98
VOLUME 7 NUMBER 3 • SEPTEMBER 2010
is often too late.
• Patients are terrified of the actual treatments (laser, intra-vitreal
injections or surgery), having heard stories about patients losing
vision after treatment, but not realising that this was often as a
result of ‘too little too late’. Some visual loss may be inevitable,
but the goal of treatment is preventing severe and debilitating
loss of vision.
What is the answer? Education, tight control of the diabetes,
management of associated hypertension and hyperlipidaemia,
timely referral for screening, increased screening potential utilising
non-mydriatic fundus photography, prompt treatment with laser
(with or without adjunctive intra-vitreal injections) when necessary,
referral for surgery in amenable cases, and rehabilitation/support
for those who still slip through the net despite all our best efforts.
Acknowledgements
We thank the Department of Ophthalmology, University of KwaZulu-Natal,
for the retinal photographs, fluorescein angiogram images and OCT images.
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than improve vision. Before doing the laser, the ophthalmologist
should assess the presence and degree of the macular oedema (as
pan-retinal laser may cause or increase macular oedema), discuss
the side effects of treatment and risks of visual loss with the patient,
and obtain informed consent (Table 5).
Vitreous surgery is frequently indicated in patients with traction
macular detachment (particularly of recent onset), combined
traction–rhegmatogenous retinal detachment, and vitreous
haemorrhage precluding pan-retinal laser. Patients with vitreous
haemorrhage and rubeosis iridis should also be considered for
prompt vitrectomy and intra-operative pan-retinal laser.
Other drugs with anti-angiogenic activity that are currently being
investigated are different inhibitors of VEGF, VEGF trap, protein
kinase C inhibitors, and growth hormone antagonists. Routes of
delivery such as oral, direct intra-vitreal injection, or intra-ocular
implantation with slow release of the pharmacological agent are
also being assessed.
Conclusions
In this day and age, with all the available treatment options,
blindness due to diabetic retinopathy should be decreasing. Instead,
it is still on the increase. Why? There are probably a few reasons:
• Diabetes itself is on the increase.
• Patients are not compliant with treatment.
• Primary-care physicians are not warning their patients often
enough of the possible complications of diabetes should they
not comply with treatment.
• Patients are not screened or referred for screening for diabetic
retinopathy until they have visual complaints, by which time it
Table 5.
Side effects and complications of treatment of diabetic
retinopathy.
Treatment
Side effect/complication
Focal/grid laser
for DME
Initial decrease in central vision
Paracentral scotomas if burns close to fovea
Permanent central scotoma from inadvertent foveal burn
Pan-retinal laser
for severe NPDR
or PDR
Central vision loss from macular oedema
Constriction of peripheral visual fields
Poor dark adaptation
Vitreous haemorrhage if new vessels present
Loss of accommodation
Vitrectomy
Recurrent vitreous haemorrhage
Retinal detachment
Rubeosis iridis
Severe visual loss
Microbial endophthalmitis
Cataract
Intra-vitreal
injections
Cataract progression (especially steroid injections)
Elevated intra-ocular pressure (more with steroids)
Microbial endophthalmitis
Transient sterile inflammatory reactions
Possible systemic effect (NB anti-VEGFs)
DME
=
diabetic macular oedema; NPDR
=
non-proliferative diabetic
retinopathy; PDR
=
proliferative diabetic retinopathy; VEGF
=
vascular
endothelial growth factor.
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