Friedman posterior segment Flashcards
DDx causes of exudative RD
V: HTN, glomerulonephritis, eclampsia/pre-eclampsia
I: uveitis (VKH, SO, pars planitis, posterior scleritis)
T:
A:
M: hypoTH
I: CSR, Coat’s
N: retinal capillary hemangioma/VHL, choroidal hemangioma, choroidal malignant melanoma
Characteristics of exudative RD
>located inferiorly >display shifting fluid >smooth appearance >chronic exudative RD can lead to NVG >important to perform depressed exam and R/O RRD
In contrast, traction RDs are usually taut and immobile with a CONCAVE surface that does not extend to the ora serrata
Work-up for Exudative RD
FA: evalute tumor (intrinsic vasculature, feeder vessels) and vascular abnormalities
ICG: superior to FA to show intrinsic vascularity, hot spots, wash-out phenomenon for tumors*
B-scan: confirm shifting fluid, evaluate choroidal thickness, evaluate for masses
A-scan: evaluate internal reflectivity if mass is found
OCT: verify thickened choroid using enhanced depth imaging techniques in uveitic conditions, image SRF and/or CME
Rarely necessary: orbital imaging
*Wash-out phenomenon: rapid increase in hyperfluorescence, which peaks around 3 to 4 min. In the late phases of the ICG angiogram, a “washout” effect with reduction of the initial hyperfluorescence is observed secondary to the outflow of dye from the hemangioma
Choroidal hemangioma Rx
Individualized, based on:
> extent of Sx
>loss of vision
>potential for visual recovery
Aim: induce tumor atrophy with SRF resolution and reduce foveal distortion without destroying retinal function (NOT to obliterate the tumor)
Rx: laser photocoagulation (moderately intense, white reaction on tumor surface to eliminate serous exudation)
cryotherapy
PDT with verteporfin (visudyne) using standard treatment parameters
transpupillary thermotherapy
I-125 plaque brachytherapy
low-dose XRT
Choroidal hemangioma Px
visual loss can be progressive/irreversible if fovea involved in chronic cases
Poor VA results 2/2 fluid resolution from chronic macular edema/photoreceptor loss
Serous RD over macula DDx
CSR (central serous chorioretinopathy)
inflammatory choroidal disorders (VKH syndrome)
uveal effusion syndrome
ON pit (no leakage)
choroidal tumor
vitelliform macular detachment
PED from other causes including CNV (+leakage)
Serous RD over macula work-up
OCT: characterize features present along with the obvious SRF
>checking for macular schisis or ON excavations seen with an ON pit
>thickened choroid seen in VKH, CSR and uveal effusion syndrome or the characteristic OCT appearance of vitelliform lesions
FA: useful to R/O CNV and to visualize the early hyperF with late pooling of a PED and the SRF
If both of these tests fail, ICG can show hyperF with late staining in CSC, vascularity with tumors, and R/O CNV
CSR Rx
observation initially since most cases resolve spontaneously over 6 weeks
laser Rx or verteporfin (Visudyne) ocular PDT can be considered for pts who require more rapid visual recovery 2/2:
> occupational reasons
>poor vision in fellow eye 2/2 CSC
>no resolution of fluid after several months
>recurrent episodes with poor vision
>severe forms of CSC
Rx reduces the duration of Sx but does not affect the final visual acuity. Experimental use of oral rifampin and mifepristone (RU486) has been suggested in chronic/bilateral cases.
ARN DDx
ARN PORN syphilis CMV toxoplasmosis sclopteria lymphoma sarcoidosis amnioglycoside toxicity
ARN exam findings
possibly:
granulomatous anterior uveitis
vitritis
retinal vasculitis
Lab tests for ARN
PCR tap for HZV, HSV, CMV
blodo testing for HZV and HSV type 1 and 2 IgG and IgM
immunocompetent (ARN)/immunocompromised (PORN)
ARN Rx
systemic IV acyclovir until resolution of retinitis then PO for 1-2 months.
Atlernatively if lesions are more peripheral then use PO therapy with valacycovir instead of IV therapy
Ganciclovir is alternative
Important to follow BUN and creatinine for nephrotoxicity
Both PO and topical steroids can be started s/p patient begins to respond to prevent inflammatory complications
ARN complications
high risk of RRD 2/2 holes/tears 2/2 retinal necrosis
important to observe fellow eye
Chronic vitritis DDx
V
I: infections/noninfectious uvetitis - birdshot chrioretinopathy, pars planitis, toxoplasmosis, syphilis, sarcoidosis, multifocal choroiditis, APMPPE, Behcets, TB, ARN
T
A
M
I
N: primary intraocular lymphoma (diffuse large B-cell non-hodgkin’s lymphoma)
chronic vitritis work-up
R/O uveitis: CBC, ESR, ACE, HLAB27 and 51, ANA, VDRL or RPR, FTA-ABS/MHA-TP
MRI to evaluate CNS involvement with LP for CNS cytology
If negative: Dx PPV: undilute vitreous biopsy (1 cc) should be sent for cytology, flow-cytometry analysis for B and T cell markers, kappa/lamda light chains
Measure: IL6 and IL10 (high IL10 to IL6 ratio is suggestive of intraocular lymphoma)
Intraocular lymphoma Rx
Intravitreal MTX and rituximab and orbital radiation if no CNS involvement (however majority of pts - [60-80% within 29 months] - develop CNS involvment) so usually Rx with blood-brain barrier disruption and high-dose systemic MTx
Poor Px if brain involvement
Need to complete metastatic survey (chest/abdomen) and bone marrow biopsy
Granulomatous uveitis DDx
V
I: Syphilis, TB, leprosy, brucellosis, toxoplasmosis, P. Acnes endophthalmitis, fungal infection (cryptococcus, aspergillus), HIV
T
A
M
I: sarcoidosis, VKH, SO, phacoanaphylactic rxn
N
Granulomatous uveitis findings
Ciliary injection AC cell and flare hypopyon iris nodules rubeosis synchiae increased/decreased IOP Cataract Pars planitis ON hyperemia chorioretinitis periphlebitis CME
Granulomatous uveitis work-up in pt with negative history/ROS/exam
CBC with differential ESR VDRL or RPR with FTA-ABS or MHA-TO ELISA or indirect immunofluorescence assay (IFA) for toxoplasma IgM and IgG ACE, lysozyme
+/- the following: ANA, RF, ELISA for LYme (IgM and IgG), HIV antibody test, CXR or CT (for TB/sarcoidosis), sarcroiliac radiographs and urinalysis
+/- HLA typing (HLA-A29 for birdshot)
if vasculitis present (ANCA)
Raji cell and C1q binding assays for ciruclating immune complexes (SLE, systemic vasculitides)
C3, C4, total complement (SLE, cryoglobulinemia, glomerulonephritis)
soluble IL-2 receptor
Toxoplasmosis chorioretinitis Rx
topical steroids and cycloplegics for anterior inflammation
Systemic steroids added for posterior pole lesions or those with intense inflammation
Small peripheral lesions: observe since they often heal spontaneously esp in immunocompetent pts
Rx with antibiotics if:
>Decreased vision
>moderate/severe vitreous inflammation or lesions that threaten the macular, papillomacular bundle, or ON
Rx with 4-6 wks with Abx to kill tachyzoites in the retina (Rx does not affect cysts) - Rx with Bactrim (TMP-SUF) For aggressive lesions or posterior pole lesions - use triple therapy: primethamine (daraprim) folinic acid (leucovorin) and one of the following: >sulfadiazine >clindamycin >clarithromycin >azithromycin >Atovoquone
IOFB classification
Inert (do not require removal) - glass, plastic, sand, stone, ceramic, gold, platinum, silver, aluminium
Reactive (cause inflammation/toxicity and must be removed) - copper (>= 85% severe endophthalmitis,
Chalcosis findings
mild intraocular inflammation
copper deposition in the anterior lens capsule (sunflower cataract) and DM (Kayser-Fleischer ring)
retinal degeneration
Iris may become green and the pupil sluggishly reactive to light
Siderosis findings
iris heterochromia (Hyperchromic on involved side) Mid-dilated minimally reactive pupil lens discoloration (brown-orange dots from iron deposition in lens epithelium, generalized yellowing from involved cortex) vitritis pigmentary RPE degenration vessel sclerosis retinal thinning atrophy
DDx for causes of cotton wool spots
MCC = DM and HTN
V: ischemic (RVO, ocular ischemic syndrome, severe anemia, pre-eclapmisa, carotid artery obstruction)
embolic (carotid embolic, cardiac emboli, deep venous emboli, WBC emboli - Purtcher’s retinopathy)
Blood disease (aplastic anemia, dysprotenimiea, perniciious anemia vitamin B12 deficiency),
Hyperviscosity syndromes (multiple myeloma, Waldenstrom macroglobulinemia), hypercoagualibity syndromes (factor V Leiden, prothrombin 20210A, hyperhomocysteinemia, protein C/S deficiency, antithrombin 3 deficiency, dysfibrinogenemia, factor 13 deficiency)
I:HIV, RMSF, Cat-scratch fever (b. henselae), toxoplasmosis, subacute bacterial endocarditis, leptospirossis, onchocerciasis
T: severe chest compression/long bone fractures, foreign bodies, amniotif fluid embolization
traumatic nerve fiber layer laceration (in which case CWS will not resolve)
Toxic (interferon, MTX), radiation induced
A: immune-mediated (SLE, sarcoidosis, dermatomysosis, scleroderma, cryogloublinemia)
M
I: ERM traction
N: neoplastic (lymphoma, leukemia, mtz carcinoma, Hodgkin’s dz)
cotton wool spot work-up
CBC with diff, platelet count
HgA1c
ANA
HIV antibody test
+/- cardiac valvular dz, carotid stenosis, Deep venous source of emboli
CWS resolve spontaneously in 1-2 months
Macular hole DDx
macular hole
psuedohole (Appearance of hole w/ steep walls
Caused by vascular tortuosity around macula)
lamellar hole Thin layer of retina lifted w/ walls “bulging out”; Maybe precursor or resolved macular hole
CME, ERM
solar retinopathy (usually bilateral)
CSR, wet AMD
Macular hole work-up
Clinical test?
Watzke-allen test (absolute scotoma in the hole)
Stages (antiquated)?
Stage 1: 1A (pseudocyst); 1B (outer layer loss)
50% spontaneously resolve (no surgery)
Stage 2: Full-thickness hole 400um + elevated rim
Stage 4: Hole with PVD
New grading system?
Small 400um
Risk factors for macular hole
CME, VMT, trauma, post-surgical, post-laser Rx and post-inflammatory disroders
Rx for macular holes:
Jetrea (if 250um) + ILMP (if >400um)
PPV Treatment success? 92% closure ; 50% if re-op short-acting gas (SF6 or 10% C3F8) ILMP (↑ closure) if >400um Face down (3 days; ↑ closure if >400um) Treatment for traumatic MH? Observation (no traction; spontaneous closure ~2 mo)
Px for macular holes
Good for recent onset & smaller diameter holes, as well as patients with good pre-operative visual acuity
Px: poor for holes > 1 year and > 400 um wide.
PVD exam
retinal tear (10-15% of PVDs) and RRD esp when pigmented anterior vitreous cells are present VH (seen in 7.5% of PVDs) from a torn vessel during vitreous separation (70% of a retinal tear)
Repeat DFE in 4-6 weeks
Risk factors for retinal tears
Age history of RD in fellow eye (15%) high myopia/axial length (7%) FH lattice degeneration trauma, cataract surgery (1% s/p ICCE, 0.1% s/p ECCE with intact posterior capsule) DM YAG for PCO
DDx for inflammatory disorders
white dot syndromes (birdshot, MEWDS, APMPPE)
pars planitis
PIC
sarcoidosis
infectious: TB, syphilis, DUSN, toxoplasmosis
masquerate process: ocular lymphoma, mtz dz, choroidal lymphoproliferative dz
Birdshot work-up
FA findings?
subtle compared with ophthalmoscopic appearance (mild hyperF early with active lesions my hypoF early) and late stianing
Late views: vascular incompetence with leakage
CME, 2ndary retinal staining
“quenching” (dye disappears quickly from vessels)
HLA-A29 (90-98%) although 7% of general population positive for HLA-A29
Other signs of birdshot
Mild vitritis; vascular attenuation & leakage Optic disc edema or atrophy; CME Painless eye Decreased scotopic ERG CNV is rare
Birdshot demographics
Usually occurs in middle-age (age 40-60) females = 70% almost exclusively in Caucasians of N. european descent
Birdshot Treatment & Prognosis?
Treatment & Prognosis?
Early aggressive IMT (cyclosporine, azathioprine, MTX, Cellcept)
Intravitreal triamcinolone
Poor prognosis chronic & recurring
Neuroretinitis/macular exudate DDx
B. henseale syphilis lyme TB tularemia toxoplasmosis viral retinitis (HSV, HZV, EBV) DUSN toxocariasis
Non-infectious; HTN, DM, AION, RVO, acute macular neuroretinopathy, sarcoidosis, papilledema
Neuroretinitis/macular exudate work-up
BP VDRL/RPR FTA-ABS/MHA-TP PPD indirect fluorescent antibody test for B. Henselae
Neuroretinitis etiology and Rx
2/2 pleomorphic gram negative bacillus called B. henseale (also assoc/w/ cat-scratch dz)
No definite Rx: controversial to use systemic antibiotics (Doxy, cipro, Bactrim)
immunocompetent: doxycycline for 2-4 weeks, IV doxycycline can also be given along with rifampin
Neuroretinitis px
good with 67% regaining >= 20/20 vision and 97% regaining > 20/40 vision
Disc edema resolves over 8-12 weeks vs. macular star takes 6-12 mo
optic atrophy and RPE changes may develop late
Presumed Ocular Histoplasmosis Syndrome (POHS) findings and ddx
Findings? Over 60% bilateral Punched-out “histo spots” in the midperiphery and posterior pole Peripapillary atrophy CNV (peripapillary) No vitritis
DDX: pathologic myopia, inflammatory disorder (multifocal choroiditis or PIC)
POHS work-up and demographics
OCT/FA to look for CNV
Lab testing is unnecessary - althoug histoplasmin antigen skin testing can be performed (60% of the adult population of the Ohio and Mississippi River Valleys have a positive reaction to histoplasmin skin testing)
Ohio-Mississippi River Valley
San Joaquin Valley
dimorphic fungus: histoplasma capsulatum
Present on feathers of chickens, pigeons, bat droppings –> humans inhale the droppings. Rare in AfrAms. Assoc/w/HLA-B7
POHS Treatment and Px?
Extra/juxtafoveal CNV Rx: laser (MPS), anti-VEGF (but not subfoveal CNV)
Subfoveal CNV: PDT, steroids, anti-VEGF
Prognosis?
44% severe VA loss (>6 lines) in 5 yrs
Risk of CNV in fellow eye (
Bull’s eye DDx
Stargardt’s disease
Cone (and rod) dystrophy
Chloroquine/Hydroxychloroquine toxicity
AMD
Chronic macular hole
Also: central areolar choroidal dystrophy, olivopontocerebellar atrophy, ceroid lipofuscinosis
Bull’s eye work-up
FA: classic “bull’s eye” = hypoF with ring of hyperF visible before the fundus lesion
Use it to R/O dark choroid seen in Stargard
OCT: thinning of retina at Bull’s eye without IS/OS junction in ring
Bull’s eye history
SLE, RA
short-term treatment for GVH disease
amebiasis
toxic medications - quinolones (hydoxychloroquine/chloroquine)
FH - stargard, cone/rod dystrophy
Risk factors for hydoxychloroquine/chloroquine
Plaquenil >6.5mg/kg/day
Chloroquine >3mg/kg/day
Total daily dose more critical than cumulative dose
Increased toxicity w/ age, obesity, liver or renal dx. Maculopathy can progress even s/p medication discontinued b/c the drug concentrates in the eye.
Findings? Decreased color (red) vision Paracentral scotomas Bull’s eye maculopathy RP-like changes late
hydoxychloroquine/chloroquine work-up and Px?
Red 10-2 HVF @ baseline and q6 mo (chloroquine) or 12 mo (hydroxychloroquine)
color fundus photos if abnml
SD-OCT (loss of IS/OS jn) and color vision (blue-yellow axis)
Multifocal ERG
visual loss rarely improves and can even progress s/p drug is discontinued
Potentially lethal forms of albinism?
Chediak-Higashi syndrome
>Recurrent pyogenic infections/anemia/thrombocytopenia
>White forelock & silvery hair
Hermansky-Pudlak syndrome
>Platelet dysfunction
>Puerto-Rican heritage
Oculocutaneous Albinism vs. ocular albinism
Oculocutaneous Albinism (sytemic)
Less MELANIN in all melanosomes - tyrosinase positive (some pimgnet which increases with age) vs. tyrosinase negative (no pigment)
Inheritance: AR
Ocular Albinism (only in eye)
Less MELANOSOMES but each melanosome has pigment
Inheritance: XR, AR
ocular albinism description and DDx
generalized fundus hypopigmentation with deep choroidal vasculature visible. Foveal hypooplasia with no luteal pigment or foveal light reflex present
DDx: blond fundus (variant of normal) or ocular albnism
True albinism vs. albinoidism
degree of ocular involvement:
1) true albinism: pts have low VA (20/100 to 20/400) and nystagmus 2/2 foveal hypoplasia
2) albinodism: pts have normal or only slightly diminished VA w/o nystagmus
albinism demographics and Px
AfrAms have higher incidence of albinism than caucasians but often have incomplete forms of ablinism
Px variable depending on form of albinism but dz is not degenerative and VA can improve over 1st two decades of life.
Severe NPDR
4:2:1 rule, any one of: 4 quads: IRH + MAs 2 quads: venous beading 1 quad: IRMA 15% chance of progression to high-risk PDR within 1 year CWS are NOT predictive
Very severe NPDR
Any 2 of the 4:2:1 rule
45% chance of progression to high-risk PDR within 1 year
CSME:
Any edema within 500μm of fovea
Hard exudates within 500μm of fovea + adjacent edema
Edema >1 disc area in size within 1 disc diameter of fovea
Macular Ischemia:
FA: microaneurysms at margins of zone of capillary nonperfusion
FAZ enlargement >1000um usu. associated with visual loss
High risk PDR
Any NVD with VH
1/4-1/3 disc area NVD (≥standard photo 10A)
1/2 disc area NVE with VH (standard photo 7)
Why do we care about high-risk PDR? What study is it from?
Diabetic Retinopathy Study: if high-risk, immediate PRP
DCCT (Diabetes Control and Complications Trial) and UKPDS (United Kingdom Prospective Diabetes Study) studies
DCCT
Intensive > conventional glycemic control in DM1 pts, reduces onset & progression of DR & macular edema
UKPDS
Intensive > conventional glycemic control in DM2 pts, reduces onset & progression of DR
Intensive BP control slowed progression of DR
No difference bet. ACEi & BB
ETDRS (Early Treatment Diabetic Retinopathy Study)
Early PRP (for severe NPDR) Small improvement in risk of severe VA loss (
Retinitis Pigmentosa (RP) 2 types?
type 1 rod-cone; type 2 cone-rod
RP Clinical Findings?
Bone spicules Waxy optic disc pallor Attenuated vessels Pigmented vitreous cell Macular edema w/o leakage on FA PSC Progressive loss of night vision Tritan color deficiency (blue) mild hearing loss (30%, excluding Usher's pts) 50% of female carriers with X-linked form have golden reflex in posterior pole
HVF: mid-peripheral scotomas, eventually becomes ring scotoma
RP DDx
V: congenital rubella syndrome, syphilis, DUSN
I: thioridazine/chloroquine drug toxicity
T
A
M: CSNB, vitamin A deficiency
I
N: CAR
Sector RP/inverse RP
Sector RP
RP in part of retina (usu. Inferotemporal) that doesn’t enlarge, good ERG response
Inverse RP
RP in macula and posterior pole (central/color vision reduced earlier than other types, pericentral/central scotoma)
Retinitis punctata albescens & RP sine pigmento
Retinitis punctata albescens
RP + white spots (50-100 um) at level of RPE scattered in mid-periphery with attenuated vessels & bone spicules. Slowly progressive (as opposed to fundus albipunctatus)
RP sine pigmento
RP without RPE changes (20% cases, assoc/w/more profound cone dysfunction)
Bassen Kornzweig (abetalipoproteinemia)
RP + hereditary abetalipoproteinemia
>minimal pigmentary changes
Poor vitamin A absorption & steatorrhea (malabs of fat-soluble vitamins - A, D, E, K and TG/chloesterol)
Also: ataxia, acanthocytosis
Inheritance: AR
Treatment?
Low fat diet, vitamin A + E
Refsum Disease
RP + phytanic acid oxidase deficiency
>minimal pigmentary changes
High phytanic acid, copper & ceruloplasmin
No bone spicules; enlarged K nerves
Also: Ataxia, deafness, anosmia, ichthyosis, cardiomyopathy, symmetric short 4th toes
Inheritance: AR (7q21-22; PEX1)
Treatment?
low phytanic acid diet (avoid fats, milk)
Spielmeyer-Vogt-Batten-Mayou (neuronal ceroid lipofuscinosis)
RP + neuronal ceroid lipofuscinosis
>infantile, juvenile, or adult onsets
Lipofuscin accumulates in lysosomes
Also: seizure, dementia, ataxia, vacuolization of peripheral lymphocytes
conj bx: granular lipopigments that also accumulate in neurons causing retinal and CNS degeneration.
Inheritance: AR, usu. Jewish girls
Usher Syndrome
RP + deafness (congenital, neurosensory)
Cilia defect (photoreceptors & hair cells)
MC syndrome assoc/w/RP (5%)
Also: ataxia, MR, low phosphate (rickets)
Inheritance: AR (Ch 1q41; USH2A)
Alstrom Syndrome
RP + deafness + obesity + endocrine dx
(DM, hypertriglceridemia, etc.)
>early profound visual loss, baldness, renal failure, cataracts
CPEO / Kearns-Sayre
RP + CPEO (EOM limitations + ptosis) Also: heart block (Kearns-Sayre) Path findings: ragged red fibers on muscle bx Inheritance: mitochondrial Treatment? Coenzyme Q10
Choroidal melanoma work-up
U/S to differentiate between tumor and other diseases. B-scan: shows shape of tumor
A-scan: low to medium internal reflectivity with reduction in amplitudes from front to bck and high-amplitude spikes consistent with break in Bruchs’ membrane.
FA: “double” circulation within tumor from filling of both the retinal and choroidal vasculature. Lesion itself would be hypoF early with pinpoint leakage late.
Although not required, neuroimaging can be performed. Melanoma is bright on T1 and dark on T2 MRI imaging
Choroidal melanoma Risk factors?
Risk factors?
Melanosis oculi, nevus of Ota
Mushroom-shaped when tumor breaks through Bruch’s membrane
Choroidal melanoma other findings
Glaucoma develops from liberation of melanin clogging TM
Sentinel vessel?
Sign of ciliary body melanoma
Choroidal melanoma Metastasis to?
Metastasis to?
Hematogenous to liver
(also lung/bone/skin, CNS). LFTs and CT of chest/abdomen
Collaborative Ocular Melanoma Study (COMS) - large
Large (>10mm height, >16mm dia)
Enucleation = pre-XRT + enucleation
Large tumors: ~ 50% pts have mtz within 5 yrs
Collaborative Ocular Melanoma Study (COMS) - medium
Medium (2.5-10mm height,
Collaborative Ocular Melanoma Study (COMS) - small
Small (1.5-2.4mm height, 5-16mm dia)
Choroidal melanoma Risk factors
To Find Small Ocular Melanomas Using Helpful Hints Daily
Thickness >2mm Fluid (SRF) Symptom Orange (pigment) Margin (near optic nerve) Hollowness (on B-scan) Halo (absence) Drusen (absence)
0 factors = risk of 4%, each risk increases relative risk ~ 3x
Choroidal melanoma Factors predicting survival?
Size of scleral contact and cell type Mean of 10 largest melanoma cell nuclei (MLN) Monosomy 3 (correlates with mets)
Callender classification?
Spindle cell nevus = Spindle A cells = slender, cigar-shaped nucleus with finely dispersed chromatin. low nuclear to cytoplasmic ratio, no miotic figures
Spindle B cells = oval with larger nucleus and prominent nucloelus
Spindle cell melanoma = Best prognosis
Mix of spindle A & B cells
25% 15-year mortality
Mixed
50% 15-year mortality
Epithelioid melanoma
Worst prognosis
Epithelioid cells = abundant ctyoplasm and large nueclues with peripheral margination of chromatin, pooly cohesive with distnct borders
75% 15-year mortality
Complications of melanoma radiation Rx
radiation retinopathy
Cataracts (PSC in 42% w/in 3 years of proton beam therapy)
dry eye
I-125 brachytherapy (high risk of substantial visual loss) - up to 49%
ERM risk factors
Can be idiopathic or secondary to vascular occlusions, inflammation, surgery, trauma, or retinal breaks (allows RPE migration onto retina)
Stable (>75% maintain >20/50)
ERM Treatment?
PPV/MP if VA
DDx of optociliary shunt vessels?
RVO, ON meningioma, low-grade ON glioma, chronic papilledema, chronic glaucoma
DDx of submacular fibrosis in a child?
Coat’s disease ROP FEVR Fascioscapulohumeral muscular dys. VHL
