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General
- Glycosylated hemoglobin (A1c) is best test of diabetics control over
last 3 months. (5% is normal 13% likely to go into retinopathy)
- Type I insulin dependent (IDD) not hereditary (Maybe viral)
- 5% of pop is diabetic - 50% not diagnosed
- Retinopathy caused by the hyperglycemia
- Renal disease often occurs at same time as retinopathy
- 65,000 new / yr. in USA go to PDR
- 75,000 new / yr. in USA go to macular edema
- Smoking increases retinopathy chance 5%
- 50% of diabetics develop some degree of retinopathy
- If asymmetrical consider carotid or ophthalmic stenosis
- Poor night vision
- Poor photostress
- Blue yellow defects
Classic symptoms
- Hyperglycemia (Sugar in blood)
- Glycosuria (Sugar in urine)
- Polyuria (High volume urine)
- Polydipsia (Thirst)
- Polyphagia (Hunger)
- Weakness
- Weight loss
Classic Signs
- Blurred vision
- Weight loss
- Fatigue
- Slow healing
- Monilla in females
- 10% of diabetics develop retinopathy while pregnant
- Once retinopathy begins strict control may not help
- ETDRS found that 650 mg aspirin did not help. Other study found that
900 mg aspirin may help.
- Risk of retinopathy based on number of years diabetic post adolescent.
If diagnosis is made before age 30, after 15 years 97% have some retinopathy
If diagnosis is made after age 30, after 15 years 78% have some retinopathy.
Differential
- Radiation retinopathy
- Hypertensive retinopathy
- Retinal venous obstruction
- Coats disease
- Retinal telangiectasia
- Sickle cell
- Classification by the ETDRS (Early treatment diabetic retinopathy
study group)
At risk groups
- Native Americans
- Blacks
- Hispanics
- Elderly
- Family history
- Obese
- Pregnant (Screen between 24-28 weeks)
- Mothers of babies over 9 lb. at birth
Blindness risk:
- Non-white females 3.8X
- Non-white males 1.3X
- White females 1.3X
- White males 1.0X
IDD retinopathy risk
- After 10 years of diabetes - 60% have NPDR
- After 15 years of diabetes - 25% have HRPDR
- After 20 years of diabetes - 50% have HRPDR
NIDD retinopathy risk
- At time of diagnosis - 20% have NPDR
- After 15 years of diabetes - 20% have HRPDR
Diagnosis
- Random glucose >200 mg/dl with symptoms
- Fasting glucose >140 md/dl on two occasions
Incidence of retinopathy
- Often develop retinopathy after 15 yr. of insulin
- Less than 5 yr treatment - 0%
- 5-10 yr. - 27%
- 10+ yr. - 71%
- 30+ yr. - 95% and 30% PDR
- Type II Non insulin dependent (NIDD) (Adult onset)
- Runs in families. 80% are obese. 70% taking insulin are NIDD. Often
have retinopathy at diagnosis
- Non-medical treatment
- Diet
- Weight reduction
- Fat restriction
- Moderate sugar not a problem
- Exercise (Avoid with peripheral neuropathy?)
- Quit smoking
Surgery
Focal photocoagulation
- Treat all focal leaks further than 500 µ from macula
- Grid pattern of 100-200 burns over areas of diffuse leakage
- After 3 yr.'s 15% of eyes with treated CSME doubled their visual
angle vs. 32% non- treated eyes
Pan-retinal photocoagulation
- 1600-2000 burns with argon blue or green lasers
- 20% eyes with PRP developed high risk in 7 yr.'s (normally 50%)
- Treatment with PRP only indicated with high risk
Peripheral retinal cryotherapy
- Used with high risk eyes with cloudy media
- 25-38% go to traction retinal detachment
Vitrectomy
- Non-clearing vitreous hemorrhage
- Traction retinal detachment
- Pre-retinal hemorrhage
- Florid neovascularization
- Wait 6 months for spontaneous clearing
- Monitor with ultrasound
Background signs
Microaneurysms leaking fluid creates edema. Weak vessel walls allow
red blood cells to leak creating dot-blot hemorrhage. If deep in the
inner nuclear or outer plexiform it will be round or oval. If superficial
it will be flame or splinter shaped which is exactly the same as seen
in hypertension. Long-standing edema leads to hard exudates.
Bad signs:
- Dense lipid exudates in fovea
- Diffuse edema with multiple leaking areas
- Capillary closure around the fovea
- Hypertension
- Cystoid macular edema
Pre-proliferative signs
- Cotton wool (Nerve fiber infarcts. Never in macula - Usually 3 DD
away)
- Intra retinal microvascular abnormalities (IRMA) Capillaries shunting
stasis blood away. Does not leak. Fluroscein leaks from neovascularization
not cotton wool or IRMA
- Venous tortuosity and beading (Capillary closure)
- Flame hemorrhage
- 50% of eyes with 3 signs will proliferate in 2 yr.'s
Proliferative signs
- Vessels usually arise from veins
- Often on disc or detached vitreous base
Fibrotic proliferation
Forms as a base for the new vessels to grow on. Tissue death reduces
hypoxia and neovascularization retreats and becomes fibrotic and pulls
on retina creating a traction detachment. Most vitreous hemorrhages occur
during sleep so don't restrict exercise. If red blood cells behind vitreous
face they drop out of sight. If in vitreous, they persist months or years.
Vitreous contraction can drag macula decreasing visual acuity
Non-proliferative retinopathy (NPDR)
Mild NPDR
- At least one hemorrhage or microaneurysm
- If no macular edema and hemorrhage or aneurysm not near macula no
vision threat
- 5% risk of progression to PDR in 1 yrs
- 15% risk of progression to high-risk PDR in 5 yr.'s
- Annual exam and photograph and inform physician
Moderate NPDR
- Hemorrhages and/or microneurysms in 2 fields, but no fields more
sever
- Soft exudates and venous beading and mild IRMA present
- 12-27% chance of progression to PDR in 1 year
- 33% chance of progression to high-risk PDR in 5 yr.'s
- Retinologist evaluation and Watch every 6 months
- If macular edema focal laser photocoagulation
Severe NPDR
- Soft exudates and venous beading and IRMA present in 2 peripheral
fields
- Two of the three: soft exudates, venous beading, or IRMA present
in 2 peripheral fields and hemorrhages in 2 other peripheral fields
- Marked IRMA
- 52% chance of progression to PDR in 1 year
- 60% chance of progression to high-risk PDR in 5 yr.'s
- Retinologist evaluation for scatter laser treatment. If macular edema
focal laser photocoagulation
Very severe NPDR
- Very good chance of progression to PDR in 1 year
- Very good chance of progression to high-risk PDR in 5 yrs
- Retinologist evaluation for scatter laser treatment and focal laser
photocoagulation irregardless
Proliferative retinopathy (PDR)
- Neovascularization at disc (NVD) or elsewhere (NVE)
- Pre-retinal or vitreous hemorrhage
- Fibrosis
Early PDR
- New vessels
- 75% chance of progression to high-risk PDR in 5 yr.'s
- Retinologist evaluation for scatter laser treatment and focal laser
photocoagulation regardless
High Risk PDR
- NVD (On disc or within 1 DD) greater or equal to 1/4 - 1/3 disc area
- NVD (On disc or within 1 DD) greater than 1/4 disc area and fresh
pre-retinal or vitreous hemorrhage
- NVE greater than or equal to 1/2 disc area and fresh pre-retinal
or vitreous hemorrhage
- At risk of sever visual acuity loss to less than 5/200
- dilate Retinologist evaluation. Scatter laser treatment can reduce
5 yr. risk of severe visual acuity loss 50% to 10%
Clinically significant macular edema (CSME)
- Leading cause of legal blindness in diabetics
- Thickening of retina within 500 µ from fovea
- Elevated retina less red hard exudates with thickening of retina
within 500 µ
- Dot-blot can last 6-12 weeks; Lipids last years
- A zone of retinal thickening 1 DD or larger 1 DD from the disc
- Loss of pericytes in capillary beds narrows arteries and slows blood
flow. If artery occludes vaso-proliferative chemical released. Veins
dilate and may allow serum release through its wall. Extracellular
edema raises macular valley floor and loss of foveal reflex. Collateral's
develop
- May note metamorphopsia, color changes
- Best seen with Volk lenses
- Edema scatters light so normal RPE and choroid background obscured
and blurred. If pockets of fluid large enough CSME. If edema sever
lipids accumulate around leaking microaneurysms (Circinate retinopathy)
- At risk of moderate visual acuity loss to 20/80
- May be present with either PDR or NPDRLaser treatment can reduce
5 yr. risk of moderate loss to 10%
Other changes
- Refractive changes
- Elevated glucose increases myopia. May last weeks after glucose
is controlled. Reduced accommodation. Early onset presbyopia
- Pan retinal photocoagulation scars can lead to permanent internal
ophthalmoplegia due to nerve fiber damage)
- Age related cataracts at a younger age and progress faster. (Metabolic
diabetic cataracts rare and reversible)
- Cornea changes
- Slower healing and decreased sensitivity
- Recurrent erosion (RCE)
- Iris neovascularization
- Glaucoma
- Rubeosis usually begins at pupil
- Optic neuropathy AION
- Acute disc edema with pale swelling. Sudden decrease in visual
acuity and field. Pale nerve head. Very few hemorrhages. Marcus Gunn
pupil almost always and progresses to optic atrophy which is Unlikely
to improve. ANION - Acute disc edema without pale swelling. 50% bilateral.
Visual Acuity 20/50. Field negative. No Marcus Gunn pupil. Most recover
Cranial neuropathy
- Usually self limiting to 6 weeks to 6 months)
- III nerve is most common. Eye down and out. Ptosis of upper lid.
Most have pupil sparing. 20% have pupil involvement.
- VI nerve is less common (ET with no abduction and possible head tip)
- IV nerve is least common (Vertical and lateral diplopia)
Differential
- Graves
- Herpes zoster
- Cranial aneurysms
- Mass lesion
- Localized demylenization secondary to focal ischemia
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