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DIABETES AND THE EYE
LEARNING OBJECTIVES
Identify systemic risk factors
Differentiate clinical stages
Describe treatment strategies
Recognize importance of team approach
Introduction
Types
Type 1 (IDDM) – young, insulin deficiency
Types 2 (NIDDM) – older, related to obesity, lack
of response to endogenous insulin
U
S
:
E
P
I
D
E
M
I
O
L
O
G
Y
135 million people with diabetes worldwide
(90% type 2)
300 million people with diabetes projected by
2025
Introduction
DIABETES MELLITUS:
EPIDEMIOLOGY
NZ 200,000 diagnosed and approx 100,000
undiagnosed
http://www.moh.govt.nz/diabetes
Maori / Pacific (3x) and South Asians
www.diabetes.org.nz
www.diabetesyouth.org.nz
www.maoridiabetes.co.nz
www.letsbeatdiabetes.org.nz (Pacific)
Introduction
T
I
N
O
P
A
T
H
Y
Retinal complications of diabetes
Leading cause of blindness in working-age group
Introduction
Primary care physician
+
Ophthalmologist

Systemic control,
timely screening,
and early treatment
Introduction
DCCT: INTENSIVE GLUCOSE CONTROL, NO
BASELINE RETINOPATHY
27% reduction in developing retinopathy
76% reduction in risk of developing progressive
retinopathy
Systemic Controls
T
R
O
L
,
M
I
L
D
T
O
M
O
D
54% reduction in progression of retinopathy
47% reduction in development of severe NPDR or PDR
59% reduction in need for laser surgery
Pre-existing retinopathy may worsen in early stages of
treatment
Systemic Controls
UKPDS: TYPE 2 DIABETES
Increased glucose and BP control decreases
progression of retinopathy
Systemic Controls
UKPDS: RESULTS
Hemoglobin A1C reduced from 7.9 to 7.0 = 25%
decrease in microvascular complications
BP reduced to <150/85 mm Hg = 34% decrease
in retinopathy progression
Systemic Controls
N
S
I
O
N
C
O
N
T
R
O
L
As important as glucose control in lowering rate
of progression of diabetic retinopathy
ACE inhibitor or beta blocker decreases
microvascular complications
Systemic Controls
DIABETIC RETINOPATHY: PATHOGENESIS
Increased glucose

VEGF

Increased capillary permeability/
abnormal vasoproliferation
Pathogenesis
Pathogenesis
Normal Diabetic retinopathy
H
Y
:
C
L
I
N
I
C
A
L
S
T
A
G
Peripheral retinopathy
Nonproliferative diabetic retinopathy (NPDR) –
mild, moderate and severe
Proliferative diabetic retinopathy (PDR)
Macular oedema – CSMO
Clinical Stages of Retinopathy
E
R
A
T
E
N
P
D
R
Microaneurysms
Hard exudates
Intraretinal haemorrhages
Patients may be asymptomatic
Clinical Stages of Retinopathy
Severe NPDR
MAs and haemorrhages in 4 quadrants or
Venous beading 2 quadrants or
IRMA 1 quadrant
Clinical Stages of Retinopathy
Microaneurysms
Clinical Stages of Retinopathy
Intraretinal hemorrhages
Clinical stages of Retinopathy
Severe NPDR
DIABETIC MACULAR EDEMA
Diabetes ≤5 yrs = 5% prevalence
Diabetes ≥15 yrs = 15% prevalence
Clinical Stages of Retinopathy
CSMO
From centre of FAZ:
Oedema within 500μ
HE within 500μwith oedema
Oedema >1DD in size within 1DD
Clinical Stages of Retinopathy
Clinical Stages of Retinopathy
Healthy macula Edematous macula
Clinical Stages of Retinopathy
CSMO
Clinical Stages of Retinopathy
Cotton-wool spots
C
A
L
S
I
G
N
S
Neovascularisation – disc (NVD), elsewhere in
retina (NVE), iris (rubeosis / NVI) or angle (NVA)
Vitreous hemorrhage
Tractional retinal detachment
Neovascular glaucoma
Clinical Stages of Retinopathy
Clinical Stages of Retinopathy
New vessels at the disc New vessels elsewhere
Clinical Stages of Retinopathy
Pre retinal haemorrhage
H
A
G
E
:
S
Y
M
P
T
O
M
S
Floaters
Severe visual loss
Requires immediate ophthalmologic
consultation
Clinical Stages of Retinopathy
Clinical Stages of Retinopathy
Severely distorted retinal architecture
Clinical Stages of Retinopathy
New vessel growth - rubeosis
INSULIN USERS Dx <AGE 30
Duration (yrs) PDR
Prevalence
5 negligible
10 25%
15 55%
Clinical Stages of Retinopathy
INSULIN USERS Dx >AGE 30
Duration (yrs)
PDR Prevalence
20 20%
Clinical Stages of Retinopathy
PDR less common among noninsulin
users
REVIEW OF CLINICAL STAGES
NPDR: Patients may be asymptomatic
Severe NPDR: Laser therapy at this stage may
help prevent long-term visual loss
PDR: Major cause of severe visual loss
Clinical Stages of Retinopathy
Diagnosis
Slit-lamp biomicroscopy Indirect ophthalmoscopy
OCT
OCT – macular oedema
Diagnosis
Fundus photography Fluorescein angiography
Diagnosis
Dark, hypofluorescent patches indicative of ischemia
Late leak suggestive of new vessels
Treatment
Laser photocoagulation surgery
ETDRS
Macular laser for CSMO reduces risk of MVL
Panretinal laser for high risk PDR
Aspirin not useful for DR but also did not
increase vitreous haemorrhage
Treatment
Macular laser
Treatment
Acute panretinal laser photocoagulation burns
Treatment
C
O
A
G
U
L
A
T
I
O
N
(
P
R
P
Outpatient procedure
Approximately 1000 to 2000 burns per session
1 to 3 sessions
Treatment
PRP: SIDE EFFECTS
Decreased night vision
Decreased peripheral vision
Treatment
Intravitreal injections
Avastin or Lucentis – anti VEGF
Triamcinolone – steroid causes cataract and
glaucoma
Intravitreal triamcinolone
VITRECTOMY
Remove vitreous hemorrhage
Repair retinal detachment
Allow treatment with PRP
Treatment
Treatment
Treatment
I
O
N
S
:
S
U
M
M
A
R
Y
Laser photocoagulation surgery
Focal macular laser for CSME
Panretinal photocoagulation for PDR
Intravitreal injections
Avastin
Lucentis
Triamcinolone
Vitrectomy
May be necessary for vitreous hemorrhage or retinal
detachment
Treatment
T
I
E
N
T
S
W
I
T
H
T
Y
P
E
1
Annual ophthalmologic exams starting 5 years after
diagnosis and not before puberty
Screening Guidelines
PATIENTS WITH TYPE 2 DIABETES
Annual ophthalmologic exams starting at time
of Dx
Screening Guidelines
DIABETES AND PREGNANCY
Ophthalmologic exam before conception
Ophthalmologic exam during first trimester
Follow-up depends on baseline grade
Screening Guidelines
S
K
O
F
B
L
I
N
D
N
E
S
S
Team approach: primary care physician,
ophthalmologist, nutritionist, endocrinologist,
nephrologist
Access to eye care
Early treatment of DR
Systemic control
Conclusion

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DIABETES AND THE EYE.pptx