13- Retina/Choroid1 Flashcards
Retinal vascular disease
-#1 cause always think
HTN
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
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
Sudden, painless vision loss DDX (5)
Retinal occlusions: C/BRVO, C/BRAO N/AAION OIS Optic neuritis Stroke/tumor
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)
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
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”
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
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
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
Branch retinal vein occlusion (BRVO)
- usual location
- if they don’t occur at an A/V crossing
SUPERIOR-TEMPORAL (60%)
Check for vasculitis
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
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
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
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
Central retinal artery occlusion (CRAO)
-signs/symp
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
Retina dies too quickly to get VEGF released
Branch retinal artery occlusion (BRAO)
- pathophys
- signs/symp
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
Breakdown of BRB
> 126 fasting
200 oral
6.5 A1C
Diabetic retinopathy
-exams/follow-ups
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
Leading cause of new cases of blindness in USA for 20-74yo
Most important risk factor = duration of dz
Diabetic retinopathy
-pathophys
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
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
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
