Opth Diabetic Retinopathy Flashcards
changes with aging
Accomodation: can’t see as well with close up material, reading, muscles can’t contract as well
Glare: increased sensitivity, glossy materials
Attentional visual field: gets smaller, cognitive process
Dark adaptation: takes longer to adapt, can take more than 1 min (hazard such as when driving)
Colour discrimination: pastels look similar
Diabetic Retinopathy (DR)
Retinopathy is any damage to the retina, the part inside the eye that senses light.
• Microvascular Complications of diabetes
• Characterized by slow and progressive damage to the retinal microvasculature, retinal
neurons and glial cells
Epidemiology
- Most common cause of new-onset blindness in the working-age population
- 34.6% worldwide prevalence of DR in adults with diabetes
- Affecting ~ 500,000 Canadians
- T1DM: Rarely develops if < 10yo, sharp increase after 5y in post-pubertal patients
- T2DM: Retinopathy present in 21-39% of patients soon after diabetes diagnosis
- Sight-threatening in ~3%
- Early detection and treatment= 95% reduced risk of blindness!
Anatomy
• The retina is a thin layer of lightsensitive nerve tissue that lines the back of the eye (or vitreous) cavity, • Two vasculatures provide the retina with a constant supply of O2 and nutrients to meet the high metabolic demands
Pathogenesis
• Complex interplay of multiple mechanisms
• Chronic hyperglycemia and associated altered
metabolic pathways can lead to:
• Neurodegeneration - thinning retinal
ganglion cell and nerve fiber layers
• Vascular damage -↑VEGF, inflammatory
mediators production, RAAS activation
• e.g. Retinal hemorrhages, vascular
leakage, retinal capillary nonperfusion,
edema
• Impaired neurovascular unit function
• As DR progresses, retinal vessels close
resulting in reduced perfusion and retinal
ischemia
Classification
• Clinically defined as 2 stages:
1. Non-proliferative (NPDR) -Early stage
• Progressive, patients may be asymptomatic
• Microaneurysms, hemorrhages, hard exudates, macular edema
2. Proliferative (PDR) –Advanced stage
• Characterized by neovascularization of the disk, retina, or iris
• Patients may experience severe vision impairment
• Vitreous hemorrhage, fibrosis, traction retinal detachment, macular edema
Forms of Retinopathy
• 3 forms based on the extent of retinal vascular disease detected by ophthalmoscopy:
1) Macular Edema
▪ Diffuse or focal vascular leakage at the macula
▪ Most common cause of vision loss, can occur at any stage
2) Progressive accumulation of microvascular change
▪ Non-proliferative/Proliferative Retinopathy
3) Retinal capillary nonperfusion
▪ Form of vascular closure detected on retinal angiography, can cause blindness
Risk factors
• Longer duration of diabetes • DR develops in 50-90% of patients with DM for ≥20 years • Hyperglycemia (Elevated A1C) • Hypertension • Proteinuria • Dyslipidemia • Pregnancy (T1DM) • Severe retinopathy itself • Other: obesity, anemia, inflammatory markers, Hispanic and South Asian ethnicity, and some genetic markers, cataract surgery
Screening
• Why?
• Asymptomatic presentation is possible, rate of progression may be rapid, therapy
beneficial for both symptom amelioration and reduction in the rate of disease
progression ↓ risk of blindness
• When to initiate screening:
• Type 1 diabetes: 5 years after diagnosis in all individuals ≥15 years
• Type 2 diabetes: children, adolescents and adults at diagnosis
• If retinopathy present: yearly or more often depending on DR severity
• If retinopathy not present
• T1DM: rescreen annually
• T2DM: rescreen every 1 to 2 years
Screening Methods
- Gold standard: 7-standard field, stereoscopic-colour
fundus photography with interpretation by a trained
reader - Direct ophthalmoscopy or indirect slit-lamp
fundoscopy through dilated pupil - Digital fundus photography
• Evaluation should be performed by an experienced
vision care professional (optometrist or
ophthalmologist)
Symptoms
Most patients are asymptomatic until advanced stages of disease • Symptoms may occur in one or both eyes, includes: • blurred vision • narrowed field of vision • seeing dark spots • feeling of pressure or pain in eyes • difficulty seeing in dim light
Impact
• Significant morbidity: including increased falls, hip
fracture, depression
• 4-fold increase in premature death
• Early death (in type 1 diabetes)
Goals:
• Prevent onset of retinopathy by optimizing metabolic and blood pressure control (primary prevention) • Delay progression of retinopathy • Preserve and improve vision • Promote independence and QOL
Diabetes
Management
ABCDESSS
Delay of
Onset and
Progression
- Glycemic control
- BP control
- Lipid-lowering therapy
- Glycemic Control
• 1% reduction in HbA1C level is associated with:
• 35% ↓ risk of DR
• 15%-25 ↓ risk of DR progression
• 25% ↓ risk of vision-threatening DR, and 1% ↓ risk of blindness
• Recommendation: target A1C ≤7%
• Multiple studies (e.g. UKPDS, DCCT, ACCORD, ADVANCE) have demonstrated that
lowering A1C reduces the development and progression of DR
• T1DM: rapid improvement of glycemia may be associated with transient early worsening
of retinopathy, but this effect is offset by long-term benefits
- BP control
10 mmHg reduction in SBP is associated with a 40%-50% ↓ risk in DR progression
• Recommendation: target BP < 130/80 mmHg
• Large RCTs (e.g. UKPDS, ADVANCE, DCCT) have studied DR as an outcome
• Some variation between studies
• Overall BP control resulted in less DR and fewer complications
• Effect of RAAS blockade (ACEi/ARBs)?
• Conflicting or inconclusive evidence on retinopathy progression or development among
normotensive people with diabetes
• Recommendation: insufficient evidence for primary prevention of DR in all normotensive
patients with diabetes
- Lipid-lowering therapy
• The role of statins in preventing the development or progression of retinopathy has not
been established
• The role of fenofibrate has been assessed in 2 large RCTs (FIELD, ACCORD Eye study)
• The mechanism for any beneficial effect of fenofibrate in DR has not been established
• Recommendation: fenofibrate, in addition to statin therapy, may be used in people with
T2DM to slow the progression of established retinopathy
Nonpharm
• Moderate visual loss:
• Spectacle correction
• Enhanced magnification
• Vision aids and other measures
• Retinal photocoagulation (laser therapy) and
vitreoretinal surgery
• Laser photocoagulation: ↓severe visual loss and
legal blindness by 90% in people with severe
NPDR or proliferative retinopathy
• Focal macular laser only preserves existing vision
• Vitreoretinal surgery: necessary when DR
complicated with non-clearing vitreous bleeding,
persistent neovascularization, and vitreoretinal
traction
Treatment - Local
(intraocular)
pharmacological
intervention
- anti VEGFs agents
2. steroids
Treatment –anti-VEGFs agents
• Increased expression of the vascular endothelial factor (VEGF), a potent vascular
permeability and angiogenic factor
• MOA: inhibits binding and activating of endothelial cell receptors, suppressing
neovascularization
• First line in the management of center-involving diabetic macular edema, intravitreal
injection q4wk (Repeated doses may be needed)
• Ranibizumab (Lucentis) 0.3 mg
• Aflibercept (Eylea) 2 mg
• Bevacizumab (Avastin) 1.25 mg off-label
• Efficacy –Improves vision and ↓macular edema
• Studied in multiple trials (e.g. RISE, RIDE, RESTORE, VISTA/VIVID DME, BOLT)
• All 3 agents demonstrated improvement of visual acuity and reduction in central
macular thickness both at year 1 & 2.
• Common side effects – mild eye pain, cataract (~ 2%- 28%), conjunctival hemorrhage
(~12% - 74%)
• Precautions –↑IOP (~ 2%-12%), thromboembolic events, endophthalmitis (medical
emergency
Treatment –
Intraocular Steroids
• Triamcinolone, dexamethasone, fluocinolone
• Intravitreal injection, intravitreal implant
• Studied in multiple trials (e.g. MEAD, FAME)
• Used in the management of diabetic macular
edema (DME)
• Second-line treatment option
• Common side effects: ↑rates of glaucoma &
cataracts
