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ETIOLOGY
- unknown
RF
- old pt & dis vessel(DM. HTN)
- young & N vessel (DM, HTN, arteriosclerosis, Phlebitis dt viral or after fever in thyphoid, inc bl coagulability dt dehydration or polycythemia)
- local cause (inc intraorbital P, glaucoma open angle)
PATHOLOGY
- ab of bl itself (hyperviscosity S/ ab coagulability)
- ab of BVs wall
- P on venous wall
SYMPTOMS
- RAPID diminution of vision in morning - stasis during night (thrombosis)
- mild loss of vision in non ischemic
- severe loss of vision in ischemic
- VA: 6/9 to HM
IF MACULA IS AFFECTED -> AFFECT MORE VISION
- sudden drop & cloudiness of vision usually discovered after awakening f sleep
SIGNS
£ ISCHEMIC: occ ant to lamina cribosa (no collateral) worse vision or 20/200
- vein: marked congested
- retina: extensive hge , cotton wool exudate = severe
- macula & disc: ++ edema
- poor px
CX
- neovascular (NVE, NVD, NVI=> neovascular glaucoma, usually occur btw 2-4 mo (90 days glaucoma), in 50% of cases w ischemic CRVO, M/C cause for neovascular glaucoma is CRVO (rubeosis iridis) 1st, marcus gunn pupil))
- ch macular edema, cystoid macular edema (CME) or macular scarring following hges in the acute st.
£ NONISCHEMIC: occ post to lamina cribosa (have collateral) N vision/ slightly dec
- vein (changes), retina (hge/exudate), macula & disc (oedema) are mildly affected
- guarded Px
- may convert to ischemia
- VA: > 6/60 ch macular aodema
if CRVO occur in young adults, it's usually type of thrombophlebitis which has excellent px w complete visual recovery
Mx
- dx & tx of underlying cause
- intravitreal injection - corticosteroid or anti vasoformative drugs
- panretinal laser photocoagulation (PRP) to destroy ischemic area to guard agaist neovascular glaucoma, hge, TRD
- PRP + cyclocryotherapy (to destroy ciliary body to dec aqueous production) in neovascular glaucoma
- intravitreal triamcinolone (IVT) to reduce CME (ch. macular edema) cx M/C cause of blindness (25-65 y/o)
dt microangiopathy affecting the ret pre-capillary arterioles, the capillaries & venules => affect large vessels
incidence(dx)
-50% > 10 y duration
- 90% > 30yr duration
RISK F
- long duration of DM (>10 years) **
- poor metabolic control**
- pregnancy
- HTN
- brain dis
- others
. obese
. hyperlipidemia
. smoking
. anemia
PATHOGENESIS & signs
1) MICROVAS OCC
- thick wall (BM thickened or prolifer endothe) of capillary
- lumen occ ( dt inc RBC aggregation, inc plt agg., stickiness -> retinal ischemia + hypoxia-> vasoformative substance-> induce neovascularization of retina/ optic nerve/ iris) 3rd time jumpa
2) MICROVAS LEAKAGE
- pericytes/mural cell for structural integrity of vessel wall-> dec pericytes in diabetes -> leakage of plasma & microaneurysm-> retinal hge, retinal edema, exudates
CLASS
1)NON PROLIFERATIVE
A) MILD-MODERATE at a background??
i) microaneurysm
- small round red dots (12-100 um in diam)
- FA: fill -> leak
ii) intra ret hge
- dt rupture (microaneurysm, capillaries, venules)
- dot and blot hge (in compact middle layer of retina)
- flamed-shaped hge ( along nerve fibers)
iii) hard exudates
- yellow wax w distict border
- affinity for macula
- composed of lipoptns
iv) venous dilation
v) macular or retinal oedema
B) SEVERE (preproliferative) signs more severe
lesion dt retinal ischemia (5 changes)
- cotton wool spots: cap. occ at nerve fibers layer => micro infarct
- large ret hge
- intraretinal microvas ab (IRMA) resemble flat vessels but lie intra retinal
- venous changes: dil., beading, looping, sausage-like segment
( retinal ischemia: detect by fluorescein angiography as nonperfusion area)
2) PROLIFERATIVE (2ND M/C CAUSE OF RuBEOSIS IRIDIS 1st m/c is CRVD) 4th time jupo
i) new vs
- NVD
- NVE
- NVI-> NVG
ii) hge: preretinal hge
iii) tractional RD dt fibrous priliferation & fibrovascular complex contracts (NVD & NVE) => traction
DIABETIC MACULOPATHY... 