keywords:
Bookmark and Share



Front Back
Grade 1 arteriosclerotic retinopathy
broadened arteriosclerotic light reflex and simple vein concealment
Grade 2 arteriosclerotic retinopathy
grade I plus deflection of veins at the AV crossings (Salus sign)
Grade 3 arteriosclerotic retinopathy
Grade II plus copper wire appearance of the arterioles and marked AV changes
Grade 4 arteriosclerotic retinopathy
grade III plus silver wire arterioles and severe AV crossing changs associated with BRVO.
Hollenhorst plaques

-most common
-transient
-made of cholesterol
-rest at bifurcations
-shiny/refractile, look larger than vessel
-not common source of CRAO/BRAO due to flatness

-refer to vascular surgeon within 7 days for vascular workup
-aspirin if safe
Fibrinoplatelet Plaque

-collection of cholesterol and platelets
-long elongated plug
-may dissolve over time
-greater risk of CRAO/BRAO
-succession of whitish bodies in vessels

-refer to vascular surgeon within 7 days for vascular workup
-aspirin if safe
Calcific Plaque

-usually from rheumatic fever or bacterial endocarditis
-from brittle heart valves or carotid arteries
-greatest risk for CRAO/BRAO
-chalky white, not shiny, not long

-refer to vascular surgeon within 7 days for vascular workup
-aspirin if safe
CRVO

Etiology and Tx
-peak incidence around 60s
-males > females
-from HTN, DM, CHF, hyperviscosity syndrome (leukemia, thrombocytopenia), sickle cell, BC, GLC, Hyperlipidemia, head injuries

-order CBC, evaluate for DM and HTN.  Refer to internist immediately.
-retinal consult for PRP if suspect neo
-follow up every 3-4wk x 6mo
-intravitreal triamcinolone
-intravitreal anti-VEGF
-fta-abs/ANA
-serum electrophoresis in younger pts (to R/O hyperviscosity syndrome)
CRVO signs
-blood and thunder
-swollen ONH resulting in (-) SVP
-flame hemorrhages
-NFLI infarcts, CWS
-Venous engorgement/tortuosity
-Macular Edema
-Vitreous hemorrhage
Venous Stasis Retinopathy

-an incomplete CRVO
-sludging of the blood
-young to middle aged pts
-rubeosis iridis rare
-dot/blot hemorrhage.
-from sickle cell, leukemia, birth control
Hemorrhagic Retinopathy (Ischemic)

-lots of bleeding, CWS, hypoxia
-more often with elderly due to uncontrolled DM/HTN
-rubeosis iridis common
-prognosis for vision is poor
-significant ONH edema
Hemi-CRVO

Tx


-FANG
-scatter PRP
-CBC
-Serum protein electrophoresis in younger pts to rule out hyperviscosity syndrome
-FTA-ABS
-ANA
-carotid assessment
BRVO

-only involves a quadrant (typically superior temporal)
-HTN is etiology in 3/4 cases
-diffuse flame and dot/blot hemes
-retinal edema
-may see resolution in 6 mo if systemic dz is controlled

-retinal consult of macula is threatened or if macular edema is persistent (>20/40)
-intravitreal triamcinolone
-no laser intervention until 3 months later, to wait for spontaneous recovery
-follow up in 1-2 months.
CRAO

-most often caused by calcific plaques, sometimes fibrinoplatelet, rarely hollenhorst
-sometimes from giant cell arteritis, migraines, BC, drug users

-(+) APD

TX

-therapy must begin within first 15-90 mins
-paracentesis
-digital massage
-CAI
-rebreathing into a paper bag
BRAO

-usually from calcific or fibrinoplatelet plaques
-tempora/superior arterioles mainly affected
-if a large area of retina involved, or macula is involved, same tx as crao.
-if macula spared and little retina involved, possibly no tx.
Sickle Cell Retinopathy

-predominantly in african americans
-sickle-shaped cells clump, inducing hypoxia via increased viscosity

Common Signs

-black sunbursts - melanin and hemosiderin (an Fe deposit)
-salmon-patched hemorrhages - round-oval hemorrhage from periph. arteriolar occlusions.
-refractile deposits - glistening deposits in periph retina from collection of hemosiderin.
-angioid streaks - breaks in bruch's membrane.

Tx

-PRP or vitrectomy to areas of ischemia which are at risk for neo.
-referral to internist to RO systemic/vascular dz
Retinopathy of Prematurity
(aka Retrolental Fibroplasia)

-affects premature infants less than 1500g or less than 36wk gestation who have exposed to high concentrations of o2.

stage 1 - distinct demarcation line between vascular and avascular retina

stage 2 - demarcation line becomes more distinct and forms elevated ridge

stage 3 - partial RD

stage 4 - total RD

-periodic DFE due to holes/tears/RD
Mild non-proliferative diabetic retinopathy
-presence of a microaneurysm
-occasional dot/blot hemes between inner nuclear and outer plexiform layers
-CWS might be present
-hard exudates away from the macula

F/U in 6mo
Moderate non-proliferative diabetic retinopathy
-increase in dot/blot hemes (moderate in 4 quadrants of severe in one quadrant)
-moderate CWS
-venous beading (sausage appearance, in less than 2 quadrants).
-IRMA -vessel shunts over non-perfused areas, doesn't leak on FANG, at level of sensory retina
-vascular loop

F/U 3-6 months
Severe non-proliferative diabetic retinopathy
4:2:1 rule

-4 quadrants of hemes
-2 or more quadrants of venous beading
-1 big IRMA

-need 2 or more of these to be severe

-F/U in 1 month
Biggest indicator of diabetic retinopathy proliferation
venous beading
Low risk proliferative diabetic retinopathy
-NVD < 1/4DD
-NVE
-neo is weak/permeable

consult in 2 weeks
High risk proliferative diabetic retinopathy
-NVD > 1/4DD
-any amount of NVD with a vitreal hemorrhage or pre-retinal heme
-NVE with pre-retinal heme or vit. hem.

consult in 24-48 hours
Clinically significant macular edema
-retinal thickening at or within 500 microns (1/3DD) of center macula
-exudates at or within 500 microns of the enter of macula with retinal thickening
-leakage occurs in outer plexiform layer and inner nuclear layers
-circinate ring - circular ring of exudates with leakage in the middle

-retinal consult within 2 weeks
-focal laser/grid laser, avastin, steroid injection, vitrectomy
x of y cards