P-PosteriorSegment Flashcards
ddx for bull’s eye maculopathy
*PAC a punch to SBCCCthe target
-plaquenil
-AMD
-chronic macular hole
-Stargardt: advanced
-benign concentric annular macular dystrophy: AD, good VA
-cone-rod dystrophy
- hx: onset (infancy to late childhood), progression (can be stationary or progressive), FHx (AR or AD)
- sxs: decreased VA, decreased color, photophobia
- exam: ocular VS, color vision, VF
- ERG: non-recordable photopic response
-ceroid lipofusinosis = batten’s disease: neurodegenerative 2/2 accumulation of lipopoigments
- sxs: rapid vision loss, nyctalopia, loss of color vision -> ataxia, seizures, psych.
- exam: bulls eye maculopathy, optic atrophy
- testing: abnormal ERG
- No treatment.
-central alveolar choroidal dystrophy: looks like AMD and in similar age group but AD PRPH2, lesion more well defined and regular with rosettes (answer pic); bilateral, symmetric, 20/20-scotoma, decreased color vision. No treatment
55f h/o RA p/w decreased vision, nyctalopia and poor color discrimination
- description
- eval
- mgmt
Bull’s eye maculopathy:
chloroquine / hydroxychloroquine toxicity:
- hx: onset, progression, sxs (blurry, red deficit, missing central vision, flashes, metamorpsia), RFs (chloroquine (<2.3 mg/kg/day) or hydroxychloroquine (<5.0 mg/kg/day), >5yrs, liver / renal disease, pre-existing retinal disease, tamoxifen)
- exam: VA, K verticillata, Amsler grid, DFE (bull’s eye, disc pallor, peripheral pigmentation), eyelash whitening (a/w plaquenil)
-testing:
– OCT: parafoveal thinning of the outer retinal layers = UFO sign
– HVF 10-2 / 24-2 for asians: central defects
– fundus autofluorescence: ring of parafoveal hyperfluorescence (picture)
-mgmt:
–stop plaquenil and seek other forms of treatment
–counsel that once toxicity is evident, visual function may continue to progress despite stopping the medication. Rarely recovers.
68F p/w poor vision and visual distortions
description
ddx and eval
subretinal hemorrhage with greenish lesion deep to the retina
neovascular AMD
-hx: onset, progression, sxs (decreased VA, metamorpsia, central scotoma), RFs (age, female, caucasian, Fhx, smoking, HTN, hyperopia, light iris color)
- exam: drusens, CNV (green discoloration, SRF), RPE atrophy
- testing: IVFA (drusen staining and window defect), OCT (drusen, CNV, SRF)
trauma (choroidal rupture - picture)
polypoidal choroidal vasculopathy (PCV)
- a/w HTN
- testing: ICG (hairpin turns of RAP lesions or polyp patterns)
angiod streaks
-linear cracks in calcified bruch’s membrane
-mintor trauma -> SR heme
-50% a/w systemic, 50% idiopathis: PEPSI (pseudoxanthoma, Ehlers, Paget’s disease, Sickle, Idiopathic)
-ddx lacquer cracks (breaks in Bruch’s)
pathologic myopia
-axial length >32, >-8D
-hx: lacquer crack -> sudden decrease in VA, metamorphopsia, often in teenagers
-exam: long oval disc, temporal crescent, posterior staphyloma, tigroid fundus, lacquer cracks, RT/RD
multifocal choroiditis
-hx: onset (20-50yo, F>M)
-exam: multiple white lesions at level of choroid -> atrophic, uveitis
-FA: acute lesions block, older lesions = window defects
-FAF: hypo
-OCT: discontinuous outer segment
-mgmt: steroids
-complications: CNV
POHS
idiopathic
Mgmt of nAMD
monthly anti-VEGF, follow macular thickness via OCT
ANCHOR (anti-VEGF vs. PDT) + MARINA (anti-VEGF vs. sham) show that anti-VEGF x24mo is effective at improving vision. PDT / local laser photocoagulation are rarely used and only for extrafoveal CNVM
Counsel:
- progressive nature of AMD
- options for treatment
- stop smoking
- AREDS for intermediate dry AMD in fellow eye
- amsler grid monitoring
68F p/w decreased vision
-Description
-DDx
-Eval
W additional info:
- dx
- plan
- fundus photo w central red spot containing yellow precipitates, surrounding gray cuff of subretinal fluid
- macular hole
- macular pucker
- CME intraretinal cyst - hx:
–onset, progression
–sxs (vision, distortions, flashes)
–RFs (trauma, surgery, sun-gazing, h/o CME, ERM) - Exam:
–ocular VS
–macula exam: Watzke-Allen (broken slit beam = hole, distorted = pucker)
–RT/RD - Test: OCT, FA (autofluorescence; if concurrent tractional ERM, then maybe leaking)
- FTMH with no subretinal fluid or tractional ERM
- Stage macular hole:
1: impending hole: observe (50% resolves spontaneously)
2: <400um, no PVD
3: >400um, no PVD or operculum
4: hole with cuff and complete PVD**
2-4:
–vitrectomy +/- ILM peel (face down positioning required for >400um but not under)
–ocriplasmin 40-60% successful but concerns about pan-retinal ERG abnormalities thus less often used now - prognosis good if operated <6mo and <400um; poor if >1yo and large
- counsel regarding low risk of RD and surgical risk (may enlarge hole)
20yo p/w painless and gradual loss of vision over years
description
ddx
RPE pigmentary changes, macular yellow pisciform lesion
Stargardt - common hereditary macular dystrophy
- hx: onset (<20yo), progression (to middle age, lesions come and go, final VA 20/200), FHx (mostly AR)
- sxs: decreased VA, nyctalopia, color vision impairment
- exam: b/l pisciform flecks @ level of RPE, beaten-metal appearance of fundus, bull’s eye maculopathy, foveal atrophy
- testing: FA silent choroid, flecks are hyperfluorescent on FAF (both due to accumulation of lipofusion in RPE)
- genetic testing: ABCA4 (AR)
Batten Disease (neuronal ceroid lipofuscinosis)
cone / cone-rod dystrophy
Rod dystrophy = Fundus albipunctatus (picture), part of CSNB (which has entities w normal fundus and those w abnormal fundus)
- hx: onset (congenital), progression (stationary), sxs (nyctalopia; normal VA, color vision and field), RFs (FHx AR)
- exam: midperipheral deep yellow spots spare macula (similar appearance to Alport syndrome: AD, kidney failure, deafness, anterior lenticonus and anterior polar cataract)
- ERG: abnormal scotopic normalizes after dark adaptation, almost normal photopic
Retinitis punctate albescens
- night blindness, abnormal vision and field
-depressed ERG does not recover after dark adaptation
Dark choroid on FA
Management of Stargardt
-no treatment -> vision services
-avoid vitamins, quit smoking, UV protection
-genetic counseling
15yo, sequential involvement of both eyes
-likely dx
-eval
-ddx
-prognosis
Best disease = vitelliform dystrophy - 2nd most common inherited macular dystrophy
hx: onset (1st decade), progression (progressive, from none to 20/100, no correlation to lesion appearance), sxs (hyperopia, decreased VA -> strab), RFs (AD)
exam: small round macular dot -> egg yolk -> scrambled egg (picture) -> atrophic scar -> CNV in 20%
testing:
-FA: blockage by egg yolk lesions -> window defect
-FAF: hyper in early -> hypo in atrophic
-OCT: look for CNV
-normal ERG (retinal response to light) *surprisingly good VA; abnormal EOG (arden <1.5) *egg is abnormal [abnormal ERG + normal EOG = stargardt]
DDx
-CACD
-adult-onset foveomacular vitelliform dystrophy
-CSCR
-AMD
-toxoplamosis
-macular hole
good prognosis unless CNV
16M p/w blurry vision
ddx and what to look for
mgmt
Seafan neovascularization
Sickle Cell
- medical hx
- exam: black sunburst (RPE hypertrophy), salmon patch (intraretinal heme), iridescent spots (intraretinal spots after resorption of salmon patch), angioid streaks (breaks in thickened bruch’s), conj comma-shaped capillaries in inferior fornix
- testing: sickledex (qualitative screening, needs followup w electrophoresis), hemoglobin electrophoresis
-mgmt:
– IOP control for any secondary glaucoma
– PRP to ischemic area anterior to sea fan -> surgery for NCVH
– hyperbaric o2 if symptom onset within 24 hrs
– f/u 6-12mo if no retinopathy, 3-4mo if yes retinopathy
– prognosis is variable
Sarcoid
- exam: uveitis, iris nodules
- testing: ACE, lysozyme, CT chest
- mgmt: steroid -> immunosuppressive agents
Eales (idiopathic peripheral obliterative vasculopathy)
- a/w TB
- lethal complication of cerebral vasculitis (same as APMPPE)
- steroids for active inflammation; PRP to non-perfused areas
Embolic retinopathy (e.g. talc from IVDU)
Stage sickle cell disease
1: peripheral arteriolar occlusion
2. peripheral AV anastomoses
3. NV
4. VH
5. RD
55M p/w painless decrease in VA to 20/400 and RAPD
description
ddx and what to look for
4 quadrant flame shaped hemorrhages + swollen optic disc
CRVO
- hx: onset, progression, sxs (painless loss of vision, TVOs), RFs (cardiovascular disease, hypercoagulable [OCP, hyperhomocysteinemia, cancer, pancreatitis], glaucoma / thyroid)
- exam: ocular VS (+RAPD), hertel, gonioscopy, macular edema, NVD/NVI/NVA/NVE, disc edema, BP
- testing: IVFA or ERG (to assess if ischemic or non-ischemic, non-ischemic typically has better vision and no RAPD; ERG normal in non-ischemic, reduced photopic b-wave in ischemic), OCT (to assess macular edema), A1c, CBC, lipid
- If age<50yo, assess rare causes (hypercoagulable PT/PTT, protein S/C, factor V, homocysteine; collagen vascular diseases RF, ANA, anti-dsDNA; syphillis)
DR
radiation retinopathy
HTN retinopathy
Management of CRVO
- for NV: PRP (this only occurs in ischemic disease)
- for macular edema: anti-VEGF or steroids
- for systemic disease: CV and hypercoagulation workup and referral if needed
- for followup: q monthly x 6mo
- for counselling: 100day glaucoma, 10% chance of contralateral eye developing CRVO/BRVO
- guarded prognosis
65M p/w painless loss of vision
- description
- ddx and what to look for
- mgmt
- retinal whitening with cherry red spot
- CRAO
–hx: onset, progression, sxs (painless loss of vision, TVOs), RFs (cardiovascular disease, GCA [temple pain, jaw claudication], sickle cell, hypercoagulable [OCP, cancer, pancreatitis, hyperhomocysteinemia, collagen vascular diseases like lupus] , IVDU/fillers/steroids)
–exam: look for emboli (hollenhorst cholesterol refractile, calcium white, platelet-fibrin dull white long), BP
–test: IVFA, ESR/CRP, A1c (consider EKG, echo, holter, carotid ultrasound), PT/PTT, electrophoresis
-Mgmt
–if <90min, try ocular massage, lower IOP, hyperventilate -> ED for stroke workup
–if GCA : stat steroids
–medicine for underlying disease, ASA 81
–Monitor monthly x3mo for OIS and NV (5% develop) -> PRP or anti-VEGF if found - Tay-Sachs
–intellectual disability, seizures
–internal medicine for metabolic disease
-Nieman-Pick’s
–ataxia, muscle disturbances
–internal medicine for metabolic disease
- Commotio Retinae
–trauma
65M p/w painless decreased vision
description
ddx and eval and mgmt
- retinal hemorrhages and cotton wool spots in inferior arcade distal to an AV crossing
- BRVO
–hx: onset, progression, sxs (painless decreased VA), RFs (cardiovascular disease, hypercoagulable [OCP, hyperhomocysteinemia, cancer, pancreatitis], glaucoma / thyroid)
–exam: ocular VS, hertel, gonioscopy, macular edema, NVD/NVI/NVA/NVE, BP
–testing: IVFA (to assess if ischemic or non-ischemic), OCT (to assess macular edema), A1c, PT/PTT, lipid, homocysteine
–mgmt:
-if macular edema: anti-VEGF or steroid if VA < 20/30
-Monitor monthly x6mo for NV -> PRP or anti-VEGF if found
-refer to medicine for underlying disease
-Counsel 10% risk of contralateral involvement - HTN retinopathy (picture)
–sxs: eye pain, headache, reduced vision
–exam: arteriole attenuation / copper wiring w AV nicking, retinal heme, hard exudates, CWS, macular edema, disc edema
–mgmt: reduce BP - radiation retinopathy
–sxs: slowly progressive microangiopathy 6mo-3yrs after radiation, threshold dose 300rads / 45Gy
–exam: microaneurysms, telangiectasia, nonperfusion, hard exudates, cotton wool spots, macular edema, disc edema-> neovascularization, vitreous hemorrhage
–mgmt: PRP for NV / focal laser for macular edema / anti-VEGF for CME; follow monthly -> extend
–prognosis: worse for thicker tumors close to the fovea, >50% of brachy patients have low vision (20/200 or worse) - goal is to preserve globe, not conserve vision - DR
45yo p/w painless decreased vision and elevated IOP
description
ddx
- temporal macular scar + IT retinitis + vitritis
- toxoplasmosis
–hx:
-sxs: painless decreased VA. Acquired [flu-like, rash, meningoencephalitis]. Congenital [MR, seizures, intracranial calcifications, microcephaly, hydrocephaly, hepatosplenomegaly, v/d]
-RFs (raw meat, cats, immunocompromise)
–exam: other chorioretinal scars, AC cell / vitritis, elevated IOP in active toxo
–testing: toxoplasma IgM (2-6 wks after initial infection) and IgG
- toxocariasis (answer pic)
–leukocoria, in 3 presentations depending on age [kids endophthalmitis, teenagers localized granuloma, adults peripheral granuloma],** vitritis, dragging of macula -> XT, TRD**
–testing: ELISA for toxocara ab; AC tap for eosinophils
–mgmt: steroid for uveitis; vitrectomy; RD repair
- ARN 2/2 viral retinitis
- TB / syphillis
mgmt of active toxoplasmosis
for IOP: gtts except prostaglandin
if inflammation is mild in immunocompetent patient and lesion is non-vision threatening: no tx
If immunocompromised (babies, pregnant, HIV) + lesions near macular or optic disc, treat w one of the following for 6+ wks:
-pyrimethamine + sulfadiazine + folinic acid + weekly CBC while on pyrimethamine -> PF 48hrs after
-bactrim DS BID (cheaper and easier)
-atovaquone (also acts against tachyzoites and dormant bradyzoites but is expensive)
-if allergic to S: clinda or azithro
workup for TB/syphilis/HIV if planning systemic steroids
prognosis:
- good in immunocompetent patients
- poor in immunocompromised
unconscious patient
-description
- ddx and eval
Large CWS + retinal heme, normal disc (though Purtcher’s can have optic disc edema),
Purtscher’s (occlusive microvasculopathy)
-hx: indirect (non-ocular) trauma, esp head trauma, long bone fracture for compressive injury to trunk
-exam: retinal whitening, heme, CWS, papillitis -> may have RAPD
-IVFA: blocked choroidal fluorescence (either due to retinal whitening or blood), leakage
Purtscher-like
-hx: pancreatitis, cancer, renal failure, collagen vascular disease (lupus, dermatomyositis), retrobulbar anesthesia, embolism (fat, air, amniotic fluid), TTP, HELLP
-tests: amylase/lipase, PT/PTT
HTN retinopathy
CRVO
management of Purtscher’s
counsel
-no ocular treatment, manage underlying cause
-f/u 2-4 wks when retinal lesions typically resolve but may take up to 3mo to resolve
-50% return to baseline VA
45yo p/w painless decreased vision and floaters
description
eval
ddx
superior arcade retinitis + retinal heme in a brushfire pattern
hx: onset, progression (progressive hemorrhagic necrotizing retinitis involving all layers), sxs (often asymptomatic), RFs (HIV - very high risk of CMV if CD4 <50)
exam:
-3 variants: 1. pizza pie posterior pole necrosis + heme, 2. brushfire = peripheral granular atrophy (picture) 3. frosted branch angiitis
- retinal hole / detachment
test:
-AC fluid or diagnostic vitrectomy for PCR (CMV, HSV, VZV, toxo)
-RPR/FTA, pneumocystis carinii; consider neuroimaging for intracranial involvement
CMV retinitis
ARN
pneumocystis: multifocal choroiditis
toxoplasmosis
TB
syphillis
mgmt of CMV retinitis
tx CMV: IV cidofovir (fx anterior uveitis can be treated w steroids to allow continuing use + renal damage) or PO ganciclovir (fx myelosuppression). If progressive despite systemic treatment or macula threatening: intravitreal injection (cidofovir, foscarnet - fx anemia, renal, seizures)
tx retinal hole / detachment: laser barricade (controversial), if large requiring vitrectomy, use SO
decrease risk: medicine management of HIV w HAART
f/u:
- active lesions daily -> weekly; look at size and activity @ border of lesions
- q3mo if CD4<100
counselling:
- risk of RD and worsening vision
- guarded prognosis
- 20% will experience involvement in fellow eye despite treatment
50yo p/w worsening vision
description
ddx and eval
elevated pigmented lesion in ST macula
choroidal melanoma
- hx: onset (first note of lesion), progression, sxs(decreased VA and VF, flashes), RFs (sunlight, smoking, caucasian race, ocular melanocytosis, uveal nevi)
- exam:
–assess melanoma vs nevus via To (thickness >2mm) Find (SRF) Small (sxs) Ocular (orange pigmentation - accumulation of lipofuscin in RPE) Melanoma (margin within 3mm of optic disc) Using Helpful (ultrasound hollow) New Hints (no halo); sentinel vessel; drusen is more likely to be benign
–secondary glaucoma
- testing: Ascan (low internal reflectivity, mushroom shape 2/2 invasion through bruch’s membrane - picture)
choroidal met
- hx: cancer
- exam: orange and multifocal
melanocytoma
- exam: darkly pigmented and near optic nerve
choroidal detachment
- hx: recent surgery or trauma
choroidal hamartoma
Management of choroidal melanoma
Workup for mets: uveal melanomas go to liver/lung, so LFT, CBC, chest and abd CT. Refer to onc.
collaborative ocular melanoma study:
-large (>16mm basal OR >10mm apical OR within 2mm to optic nerve and >8mm apical): enucleation (no pre-enuc radiation needed)
-medium (<=16mm basal and 2.5-10mm apical): brachytherapy (as good as enucleation; enucleated patients have 10% risk of mets anyway)
-small (<=16mm basal and 1-3mm apical): observation (mortality = 1% at 5yrs)
counsel:
- treatment options
- risk of mets: 10yr risk of met-related death is up to 50%
- FNA can aid prognostication but not necessary for dx or tx
- spindle A config better prognosis than spindle B (epithelioid)
p/w painless flashes
description
ddx
eval
management
horseshoe tear with minimal detachment
RRD from vitreoretinal traction
RRD from trauma
hx: onset, progression, sxs (VA, flashes, curtains), RFs (FHx, high myopia, trauma, lattice, ED/Marfan’s)
exam:
- scleral depression, ?lattice degeneration.
- If trauma: heme? commotio? open globe? IOFB? uveitis?
laser retinopexy or cryotherapy (tear <2’, superior 8’)
Counselling:
- causes of RD
- return precautions, also for the fellow eye
- increased life time risk of retinal problems
52F PMH breast ca.
description
ddx
small white flecks that appear to be crystalline
crystalline retinopathy
-exogenous (m!Chtt, asx or decreased VA / color disturbance): tamoxifen (breast cancer, foveal location), canthaxanthine (tanning), halothane (anesthetic), methoxyflurane (anesthetic), talc (IVDU, may lead to peripheral nonperfusion and NV)
-endogenous: bietti (picture, K crystals, diffuse, triad similar to RP of vision loss, progressive nyctalopia and VF loss in third decade of life), hyperoxaluria, cystinosis (K and conj crystals in first year of life -> photophobia and blepharospasm)
- hard exudates
-hx: diabetes, HTN
-exam: subretinal fluid, microaneurysms, NV
-testing: OCT, IVFA, glucose testing
calcified drusens
- exam: drusens in fellow eye
