13- Retina/Choroid1 Flashcards by Elyse Kohl

Retinal vascular disease

-#1 cause always think

HTN

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Central retinal vein occlusion (CRVO)

epidemiology
risk factors/etiologies

3rd most common vascular cause of vision loss (#1 DM)
~7% will have CRVO in fellow eye

Risks: HTN (61%), DM, CV dz, open-angle glaucoma
-up to 40-60% of pts with CRVO have POAG (kinks/compresses veins)

Young pts: oral contraceptives (DVTs), collagen vascular dz, AIDS

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Retinal vein occlusions (C/BRVO)

-pathophys

HTN/DM -> artery compresses vein -> turbulent blood flow -> THROMBUS* -> VEGF
*thrombus stays where it’s formed

Central = @/near lamina cribrosa
Branch = @ A/V crossing

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Sudden, painless vision loss DDX (5)

Retinal occlusions: C/BRVO, C/BRAO
N/AAION
OIS
Optic neuritis
Stroke/tumor

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Central retinal vein occlusion (CRVO)

-signs/symp

Signs: thrombus -> ischemia -> VEGF

retinal hemorrhages in all 4 quads
collateral veins
dilated, tortuous veins
CWS
disc edema

Symp: SUDDEN, UNILATERAL, PAINLESS VISION LOSS (esp in elderly)

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Central retinal vein occlusion (CRVO)

-collateral vessels

Congenital - just not used normally
Become visible over several wks-mos
Often on disc, permit flow b/w retinal + choroidal circulation

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CRVO + BRVO

-vision-threatening complications (2 major concerns)

Macular dz: ischemia, edema (#1 vision loss), intra-mac hemes

Neovascularization* -> NVG, preret/vit hemorrhage, tractional RD

DRVOS concerns!
NVG with CRVO = “90-day glaucoma”

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Central retinal vein occlusion (CRVO)

-neovascular glaucoma

“90-day glaucoma”
-most likely in first 3 mo of dx

60% of ischemic cases develop iris neo, up to 33% NVG
6% of non-ischemic cases develop rubeosis or angle neo

Importance of gonio with suspected CRVOs
Treated with PRP

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Central retinal vein occlusion (CRVO)

-ischemic vs non-ischemic

I: defined as 10DD+ NON-PERFUSION ON FA

90% present with 20/200 or worse
poor prognosis: final VA at CF or worse, high risk for NVG

NI: majority (67%), up to 16% progress to ischemic

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Branch retinal vein occlusion (BRVO)

epidemiology
risk factors

By far the MOST COMMON RVO dz

Risks: HTN (60%), CV dz, incr BMI at 20yo, open-angle glaucoma

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Branch retinal vein occlusion (BRVO)

usual location
if they don’t occur at an A/V crossing

SUPERIOR-TEMPORAL (60%)

Check for vasculitis

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Central retinal artery occlusion (CRAO)

epidemiology
risk factors
eiotiolgy

Elderly, 10% risk in fellow eye

Risks: HTN (67%), DM (33%), CAD (25%), cardiac valve dz (25%)

Young: IV drug use, contraceptives

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Central retinal artery occlusion (CRAO)

-recall layers of retina CRA, choroid supplies for

CRA = inner 2/3: OPL -> ILM

Choroid (S/LPCA’s) = outer 1/3: RPE -> OPL
-cilioretinal can save macula

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Retinal artery occlusions (C/BRAO)

-pathophys

#1 EMBOLUS:
-Calcific = large, from calcified heart valves, esp in CRA near optic nerve
—more likely CRAO - gets stuck at lamina
-Carotid = smaller cholesterol plaques (Hollenhorst)
—more likely BRAO - gets past lamina, into branch artery

Other: GCA, acute elev in IOP
-IV drug use, oral contraceptives, sickle-cell, syphilis

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Retinal artery occlusions (C/BRAO)

-pts with retinal emboli should be eval for

Underlying carotid artery and cardiac dz: carotid doppler and EKG/echo, respectively

25% with retinal emboli also have acute cerebral infarct

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Central retinal artery occlusion (CRAO)

-signs/symp

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Signs: superficial WHITENING* of inner retinal layers, narrowed vasculature, cherry red spot (VISIBILITY OF UNDERLYING CHOROID), APD (secondary to optic disc pallor)
*once perfusion is restored, color returns, function does does

Symp: ACUTE, PROFOUND VISION LOSS (20/400 or worse) unless cilioretinal artery is present (15-30%)

Why NVG is rare in arterial occlusions

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Retina dies too quickly to get VEGF released

Branch retinal artery occlusion (BRAO)

pathophys
signs/symp

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90% due to emboli (Hollenhorst #1, calcium, fibrin, platelet)

Signs: superficial WHITENING in distribution area (90% TEMPORAL), visible emboli in 62%
-like central, color returns, function does not (VFD is permanent)

Symp: often asymptomatic

VFD*, sudden unil painless vision loss
defect respects midline, mimics glaucoma - est VF for “new normal” once “healed”

Diabetic retinopathy

think equals __
blood sugar levels of DM

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Breakdown of BRB

> 126 fasting
200 oral
6.5 A1C

Diabetic retinopathy

-exams/follow-ups

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Initial:

DM1 = within 3-5 years after dx
DM2 = at the time of dx

Follow-ups:

no retinopathy = annual
mild-mod ret = 6-12mo
severe N/PDR = 2-4mo

Diabetic retinopathy

-epidemiology

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Leading cause of new cases of blindness in USA for 20-74yo

Most important risk factor = duration of dz

Diabetic retinopathy

-pathophys

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Loss of pericytes + damage to retinal capillary basement membrane -> breakdown of BRB

recall: pericytes = autoregulation (ret vessels, optic nerve)
recall: BRB = TJ b/w RPE cells and on ret vessels

Non-proliferative diabetic retinopathy (NPDR)

-mild vs mod vs severe vs very severe

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Mild: 5% risk of progression to PDR in 1 year
Mod: 15%
Severe: 52%
Very severe*: 75% 
*meets 2+ criteria from 4:2:1

Diabetic retinopathy

-4:2:1 rule

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Diagnosis for SEVERE NPDR: pt meets 1 of 3 criteria

4: severe retinal hemorrhage in 4 quads
2: venous beading in 2 quads
1: IRMA in 1 quad

*very severe = 2+ criteria

Diabetic retinopathy | -high risk characteristics (HRCs)

For pts with PDR who are at most risk for VISION LOSS 1) size + location: NVD >1/4 disc diameter within 1DD of optic nerve 2) hemorrhage: NVD/E with an associated vit/preret hemorrhage

Diabetic retinopathy | -signs/symp

Signs: many, most important are macular dz + neo Symp: often asymptomatic; blur, metamorphopsia

Diabetic retinopathy | -macular disease

Ischemia: hypoxic = initially thickens -> thins + dies -FA shows enlarged foveal avascular zone (hypofluorescent) Edema: thickens (stays thickened), #1 loss of vision with DR, can occur at any stage

Diabetic retinopathy | -CSME criteria

One need 1/3 for dx: key retinal THICKENING 1) retinal thickening within 500um (1/3DD) of foveal center 2) hard exudates within 500um of foveal center with adjacent retinal thickening 3) retinal thickening of at least 1DD within 1DD of foveal center Recall: new/worsening caused by pioglitazone

Diabetic retinopathy | -neovascularization threats to vision

DRVOS! Preret/vit hemorrhage NVG Tractional RD

Hypertensive retinopathy - pathophys - symp

Recall retinal vessels are autoregulated - this is altered at extremely high/chronically elev systolic pressures -> retinopathy BP of at least 140/110 for latter stages to occur Commonly asymptomatic; macular edema (star), papilledema, serous RD, vein occlusion Recall: 130-139/80-89 is grade 1 HTN, >180/>120 is malignant HTN

Hypertensive retinopathy | -signs/stages

``` Bilateral, asymmetric 1: skinnery artery narrowing 2: stage 1 + A/V nicking 3*: stage 2 + 3 things: HEME, CWS, HARD EXUDATES (star config) 4: stage 3 + PAPILLEDEMA ``` * stage 3 is when we start to see color (blood, CWS) * *elschnig spots: choroidal infarcts, occur in severe hypertensive ret

Retinal artery macroaneurysm - epidemiology - signs/symp

Elderly women (70’s) with HTN, atherosclerosis Signs: unilateral focal area of dilation in retinal artery (100-250um) with MULTI-LEVEL HEMORRHAGES from ruptured aneurysm Symp: asymptomatic; gradual vision loss from edema or sudden from vit hemorrhage

Ocular ischemic syndrome - epidemiology - pathophys

aka venous stasis retinopathy, part of DRVOS Men, 50-80, HIGH CHOLESTEROL -assoc with HTN, DM, cardiac dz Occlusion of ICA and/or Ophthalmic artery (less common) Usually secondary to atherosclerosis, may occur with GCA

Ocular ischemic syndrome | -signs/symp

Signs: UNILATERAL (80%), dot-blot hemes of MID-PERIPHERAL fundus, dilated non-tortuous veins, narrow arteries, 67% PRESENT WITH NVI/NVA at time of dx Symp: GRADUAL VISION LOSS (90%), dull periorbital pain/headache (40%), amaurosis fugax

Ocular ischemic syndrome vs Venous stasis retinopathy

VSR: retinal findings (-)ant seg signs OIS: retinal findings (+)ant seg signs

Amaurosis fugax vs TIA vs stroke

AF: type of TIA, transient monocular vision loss, RETURNS TO NORMAL after event TIA: TEMPORARY neurologic deficits due to loss of blood flow, perfusion restored in <24hrs (usually <15min), no permanent damage Stroke: PERMANENT neurological deficits due to prolonged blood loss

13- Retina/Choroid1 Flashcards

(36 cards)