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Retina cases Flashcards

1
Q

Macular hole DDx

A

macular pucker, CME intraretinal cyst >Pseudohole -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

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2
Q

Macular hole history questions

A

previous trauma? previous eye surgery?

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3
Q

Macular hole exam

A

complete exam, especially of macula Perform Watzke-Allen test (slit beam and see if line broken/distorted): >distortion = pucker >broken = hole

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4
Q

Macular hole evaluation

A

OCT = preferred modality IVFA with early hyperfluorescence w/o leakage for hole

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5
Q

Macular hole stage 1 definition and Rx

A

Stage 1 = impending hole Rx: Observe, as 50% will resolve spontaneously

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6
Q

Macular hole stage 2 vs 3 definition and Rx

A

Stage 2: full thickness hole 400 um, + elevated rim Rx: vitrectomy +/- ILM peel if operated w/in 1st 6 mo can regain 1/2 visual loss. others operate up to a year. small portion of patients may benefit even if long-standing history of hole Education: low risk for RD, but must explain Si/Sx to patient

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7
Q

Macular hole stage 4 definition and Rx

A

Stage 4: hole with cuff and complete PVD Rx: vitrectomy +/- ILM peel if operated w/in 1st 6 mo can regain 1/2 visual loss. others operate up to a year. small portion of patients may benefit even if long-standing history of hole Education: low risk for RD, but must explain Si/Sx to patient

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8
Q

Bulls eye maculopathy DDx

A

chloroquine/hydroxychlorquine toxicity cone dystrophy macular degeneration (AMD) Stargardt or fundus flavimaculatus battens = (AR) lysozyme storage dz. H/o seizures and progressive dementia with retinal findings of pigmentary retinopathy

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9
Q

Bulls eye maculopathy history questions

A

Medications: chloroquine/hydroxychlorquine (dosages)? History: FH of retinal dz, Sx of photophobia, seizures, ataxia, dementia

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10
Q

New macular hole grading system?

A

Small 400um

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11
Q

Bulls eye maculopathy exam

A

BCVA, IOP, DFE with special attention to macular pigment changes, drusen, macular, or peripheral pisciform (fish-like) flecks, CNV Perform a neurologic exam

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12
Q

Bulls eye maculopathy evaluation

A

If: patient younger, no RA, not taking chloroquine/hydroxychlorquine then order ERG and IVFA If ERG shows a non-recordable photopic response I would suspect a Dx of cone dystrophy If IVFA shows silent choroid I would suspect stargardt

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13
Q

Bulls eye maculopathy A/P

A

need to evaluation medication dosages. Maximum daily dose of chloroquine

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14
Q

chloroquine/hydroxychlorquine toxicity education

A

once toxicity starts, it may continue despite stopping the medication: Baseline exam vision, fundus photos, HVF (red test) OCT MAC

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15
Q

NV fronds with exudates and hemorrhage in child ddx

A

sickle cell retinopathy (sea-fan shaped) sarcoid sea fan neovascularization diabetic retinopathy eales peripheral retinopathy of unknown etiology

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16
Q

NV fronds with exudates and hemorrhage in child: history and eye exam

A

medical history of: sickle cell, DM, sarcoid, IVDA look for in eye exam: uveitis, iris nodules, NVI, DFE

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17
Q

NV fronds with exudates and hemorrhage in child:

A

tests: sickledex, ACE, lysozyme, fasting blood glucose, CT of chest if sarcoid suspected. IV FA to assist evaluation and development of Rx plan

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18
Q

Sickle cell A/P:

A

NV –> needs PRP to ischemic area located anterior to sea fan RD: PPV precautions (avoid encircling SB or taking down EOMs, avoid epi in local anesthetic, ensure O2 & hydration) For pts with sickle cell history and no evidence of retinopathy - plan f/u exams q6-12 mo for patients who develop retinopathy, plan closer f/u q3-4 mo, performing PRP as needed

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19
Q

sickle cell education

A

SC worst ocular Sx (SC>Sthal>SS>SA) SS worst systemic Sx Avoid CAI variable Px. with good patient education and comprehensive interval f/u, patients can expect to maintain good visual potential. Also need to have PCP involved to discuss si/sx of systemic sickle crisis

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20
Q

Sickle cell signs and stages

A

–Stage 1: peripheral arteriolar occlusion –Stage 2: peripheral AV anastomoses –Stage 3: preretinal sea fan NV (posterior border of nonperfusion; may autoinfarct and turn white) –Stage 4: Vitreous hemorrhage –Stage 5: Tractional RD Black sunburst (mid-peripheral pigmented lesion with spiculated borders) Salmon patch (IRH) Iridescent spots (intraretinal spots s/p resorption of salmon patch) angoid streaks (conjunctival comma-shaped capillaries in inferior fornix)

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21
Q

4 quadrants flame shaped hemorrhages following NFL, swollen ON DDx

A

CRVO DM Radiation retinopathy hypertensive retinopathy papilledema

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22
Q

4 quadrants flame shaped hemorrhages following NFL, swollen ON History

A

History Questions: HAs, transient visual obscurations glaucoma, thyroid eye disease, DM, HTN, radiation, hypercoagulable dz, vasculitis (lupus, syphilis, sarcoid) medications (OCP, diuretics, tetracycline, trenitoin), orbital tumors

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23
Q

4 quadrants flame shaped hemorrhages following NFL, swollen ON eye exam

A

VA pupils Hertel ocular motility gonioscopy (looking for NVI/NVA) IOP DFE looking for NVD and macular edema

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24
Q

4 quadrants flame shaped hemorrhages following NFL, swollen ON tests

A

IVFA to determine and define macular edema - whether condition is ischemic or non-ischemic IVFA will show non-perfused areas and the OCT macular swelling Check: BP, evaluate for DM (FBS, HgA1c) order screening labs (CBC, PT/PTT, ESR, lipid profile, homcysteine), sarcoid suspects (ACE, lysozyme, chest CT), atypical cases (FT-ABS, Lyme titer, ANA) Refer for cardiovascular and hypercoagulable work-up as needed

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25
Q

CRVO A/P

A

suspect ischemic CRVO if: 20/400 VA, APD, no pain Non-ischemic CRVO: usually has better VA and no APD Ischemic cases can develop NVI/NVA. Therefore I would follow monthly for 6 months performing eye exams and gonioscopy looking for NV. Should this develop I would initiate PRP to regress NVA/NVI. FOr macular edema I would discuss using IV triamcinolone or anti-VEGF

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26
Q

CRVO education

A

would discuss with patient that there is a 10% chance of contralateral eye developing a CRVO or branched retinal vein occlusion (BRVO)

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27
Q

retinal whitening with cherry red spot DDx

A

CRAO, Tay-Sachs, Niemann-Pick (presents in younger children)

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28
Q

retinal whitening with cherry red spot history questions

A

History of HTN, carotid dz, CV dz, sickle cell, hypercoagulable states syphilis, migraines, collagen vascular dz

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29
Q

retinal whitening with cherry red spot exam and evaluation

A

full eye exam: VA, pupils for APD, DFE to search for emboli Seek etiology of emboli as this can be helpful: (1) cholesterol emboli (hollenhorst plaque) = refractile bodies seen @ bifurcations arising from carotid artery atheromatous plaques (2) calcium emboli = white seen distally in retina and arise from cardiac valves (3) platelet -fibrin emboli = dull, white long arising from carotid atheroma CRAO can occur with GCA, evaluate for HA, scalp tenderness, jaw claudication, obtain immediate ESR/CRP.

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30
Q

Retinal vasculitis (CG pt as example)

A

Ddx for etiologies include embolus, in situ thrombosis, GCA, connective tissue disease, hypercoagulable state and less likely syphilis, Behcet’s disease, Susac’s, migraine, trauma. Plan: Control comorbidities, including BP Secondary risk stratification by PCP to include fasting BS, lipid profile, hypercoagulability workup Will obtain ESR/CRP, CBC with diff, Coag panel, FTA-ABS, ANCA, C3/C4, CXR, UA Provided h/o stroke and diffuse vascular disease, will obtain Carotid Doppler, cardiac echo RTC 5-6 weeks to review results, DFE and OCT Mac

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31
Q

CRAO plan

A

If

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32
Q

RPE pigmentary changes, macular yellow pisciform lesion, macular “beaten-metal” appearance DDx

A

Stargardt’s dz Cone’s dystrophy hydroxychloroquine or chloroquine toxicity Batten’s dz Fundus albipunctatus = white dot pattern in mid-periphery Si/Sx: night blindness, prolonged dark adaptation, normal fields, vision. Retinitis punctate albescens: declining vision, fields, night blindness, abnormal ERG

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33
Q

RPE pigmentary changes, macular yellow pisciform lesion, macular “beaten-metal” appearance history

A

Timing of vision loss, medicine, medical and family history For Batten’s: ask about h/o dementia, seizures aka: Spielmeyer-Vogt-Batten-Mayou RP + neuronal ceroid lipofuscinosis Lipofuscin accumulates in lysosomes Also: seizure, dementia, ataxia, vacuolization of peripheral lymphocytes Inheritance: AR, usu. Jewish girls ?fingerprint inclusions on EM of peripheral blood smears?

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34
Q

RPE pigmentary changes, macular yellow pisciform lesion, macular “beaten-metal” appearance exam/evaluation

A

Complete eye exam Additional testing: IVFA, ERG, EOG On IVFA = “silent choroid” pattern with abnormal ERG and EOG based on fundus appearance if Stargardt’s Cone dystrophy: if decreased color vision, attenuated ERG photopic responses, bull’s eye on fundus photo

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35
Q

Retinal hemorrhages and CWS at arcade distal to an AV crossing history A/P

A

A: evaluating for cause (HTN, atherosclerosis, DM) and managing sequelae is key to this condition P: Check BP and consider bloodwork: fasting blood glucose, HGA1c, ANA, RPR, PT/PTT, ESR, homocysteine Refer patient to internist for CV dz, HTN, CVD, hypercoagulable work-up as dictaed by my exam and history Rx: chronic macular edema that persisted for 3-6 mo with vision

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36
Q

Retinal hemorrhages and CWS at arcade distal to an AV crossing education

A

Follow qmonthly for 6 months. Council that this condition can progress and can develop NVG. Ensure they are following with PCP for HTN and DM. 10% risk for contra/L involvement.

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37
Q

Macular pigmented scar, retinitis and overlying vitritis DDx

A

Toxoplasmosis, ARN, Toxocariasis, TB or syphilis

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38
Q

Macular pigmented scar (slightly smaller than ON), retinitis and overlying vitritis history

A

History of: eating raw meat, exposure to cats, immunocompromised risk

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39
Q

Macular pigmented scar, retinitis and overlying vitritis exam and evaluation

A

Full eye exam looking for additional ipsi/L and contra/L CR scars >Look for AC rxn, spillover from vitritis >high IOP in active toxoplasmosis helps support Dx Blood work: toxoplasmosis IgG/IgM Ab titers, VDRL/RPR PPD, CXR, Toxocara ELISA, HIV test in high-risk individuals.

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40
Q

Toxoplasmosis A/P

A

A: elevated IOP, Rx with IOP lowering gtts other than prostaglandins. If immunocompromised and lesions are near the macula or disc, recommend starting primethamine, and sulfadiazine with folinic acid to prevent pyrimethamine apalastic anemia pyrimethamine: need weekly CBC Patient allergic to sulfa: consider clindamycin or azithromycin Use: topical/oral steroids, except in immunocompetent patients. Rx: typically 6 weeks, Rx immunocompromised cases longer === Other Rx protocols: Bactrim DS bid or atovaquone (expensive but acts against both tachyzoites and dormant bradyzoites) can observe pts who are immunocompetent but have peripheral retinal lesions and non-threatened vision. Consider working up: TB, syphilis, sarcoid

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41
Q

Toxoplasmosis Education

A

Immunocompetent patients: good Px with observation for peripheral lesions and medical Rx for lesions threatening vision. Immunocompromised pts have poor Px and would highly recommend HAART

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42
Q

Multiple large CWS and areas of retinal hemorrhage surrounding a normal disc DDx

A

purtscher retinopathy HTN retinopathy purtscher-like retinopathy CRVO CRAO (much less likely)

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43
Q

Multiple large CWS and areas of retinal hemorrhage surrounding a normal disc history

A

Info: trauma? h/o: pancreatitis, EtOHism, renal failure, HTN, recent retrobulbar anesthesia, intraocular injections (i.e. steroid), collagen vascular dz (lupus, scleroderma, dermatomyositis)

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44
Q

Multiple large CWS and areas of retinal hemorrhage surrounding a normal disc exam and evaluation

A

VA, APD, SLE, DFE, BP Imaging (chest, head, orbit). Consider long bone fractures and amnio embolus (femals) IVFA Work-up for pancreatitis, renal failure, HTN, CVD = BP, amylase, lipase, PT/PTT, internist consult

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45
Q

Purscher’s retinopathy A/P:

A

no ocular Rx, but must Rx underlying causes Education: f/u exams with DFE q1-2weeks in 1st month. Vision may not improve but 50% can return to baseline.

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46
Q

RPE pigmentary changes, macular yellow pisciform lesion, macular “beaten-metal” appearance DDx

A

Stargardt’s dz Cone’s dystrophy hydroxychloroquine or chloroquine toxicity Batten’s dz

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47
Q

RPE pigmentary changes, macular yellow pisciform lesion, macular “beaten-metal” appearance history

A

Timing of vision loss, medicine, medical and family history For Batten’s: ask about h/o dementia, seizures aka: Spielmeyer-Vogt-Batten-Mayou RP + neuronal ceroid lipofuscinosis Lipofuscin accumulates in lysosomes Also: seizure, dementia, ataxia, vacuolization of peripheral lymphocytes Inheritance: AR, usu. Jewish girls

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48
Q

RPE pigmentary changes, macular yellow pisciform lesion, macular “beaten-metal” appearance exam/evaluation

A

Complete eye exam Additional testing: IVFA, ERG, EOG On IVFA = “silent choroid” pattern with abnormal ERG and EOG based on fundus appearance if Stargardt’s

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49
Q

subretinal hemorhage, greenish lesion deep to the retina DDx

A

NVAMD POHS trauma (old choroidal rupture) polypoidal choroidal vasculopathy (PCV)

50
Q

Well defined area of retinal necrosis = sectoral retinal hemorrhage, retinal whitening in brush-fire configuration, CWS DDx

A

V: (less likely BRAO) I: CMV, ARN (immunocompetent)/PORN (immunocompromised), syphilis, toxoplasmosis, Pneumocystis carinii N: lymphoma D: amnioglycoside toxicity I: sarcoidosis C:n/a A: n/a T: scolpeteria E: n/a

51
Q

well-definited retinitis, hemorrhage, retinal whitening in brush-fire configuration History and Exam

A

Ask: immune status, esp HIV Full eye exam: document DFE with fundus photos. Look for retinal holes and RD Evidence of granulomatous anterior uveitis, vitritis, retinal vascuitis *PORN pts = immunocompromised, minimal inflammation and vasculitis

52
Q

Inferior arcade retinitis, hemorrhage, retinal whitening in brush-fire configuration tests

A

AC/vitreous tap PCR: HZV, HSV, or rarely CMV alternatively… blood testing: HZV, HSV (type 1 and 2) IgG and IgM Perform HIV test, CD4 count (CD4

53
Q

CMV A/P

A

Admit and initiate treatment with IV ganciclovir, foscarnet, cidofovir For patients that progress despite therapy or those that have macular encroachment can use IV injections of antiviral medications RD patients: consider PPV with SO and laser barricade to mitigate progression. Retinal holes: consider performing laser barricade for peripheral and perimacular holes. Rx: controversial with regard to benefit. Internist: help with HAART to improve CD4 count which will augment the patient’s ocular stability

54
Q

Small white flecks in FAZ, appear to be crystalline DDx

A

exogenous (tamoxifen, canthaxanthine, halothane anesthetic, oxalate crystals from methoxyflurane, and talc) Endogenous (Bietti crystalline dystrophy, hyperoxaluria, cystinosis) Calcific drusen hard exudates

55
Q

On DFE: large elevated pigment lesion DDx

A

choroidal melanoma nevus mtz melanocytoma (less likely 2/2 location and appearance)

56
Q

On DFE: large elevated pigment lesion history

A

history: prior knowledge of intraocular lesion to help with onset and timing ask about visual Sx and history of other cancers Evaluation: U/S (lesion height and extrascleral extension) A-scan: see low internal reflectivity Lesion in this case: nevus unlikely and melanocytomas typically are more darkly pigmented and near the ON Mtz: usually orange and multifocal

57
Q

Choroidal melanoma A/P

A

Ultrasound IVFA - look for double circulation pattern (not required for dx) chest/abdomen CT - look for mtz LFTs and CBC refer to an oncologist COMS (Collaborative Ocular Melanoma Study): (1) observation for small choroidal melanomas (2) plaque brachytherapy (rather than enucleation for medium-sized melanomas (3) enucleation without preceding radiation for large melanomas

58
Q

Choroidal melanoma education

A

mtz work-up with oncologist Education, in a compassionate way, need for continued monitoring afterwards over years as 10 year risk of mtz related death is as high as ~50%.

59
Q

Retinal horseshoe tear (with associated blood) DDx

A

vitreoretinal traction from syneresis trauma

60
Q

Retinal horseshoe tear history

A

timing of Sx, flashes, floaters h/o trauma h/o high myopia, family history of RD

61
Q

Retinal horseshoe tear exam and evaluation

A

exam: careful scleral depression of the periphery of both eyes to assess for other related retinal pathology (other tears or lattice degeneration) measure VA if h/o trauma –> assess for commotio, evidence of open globe injury or IOFB

62
Q

Retinal horseshoe tear plan and education

A

laser retinopexy cryotherapy RD precautions Education: causes of retinal tears (vitreous syneresis and VR traction assuming no h/o trauma). Education patient regarding Sx of further retinal tears or detachments such as flashes (new) or increased floaters or curtains. Educate regarding increased life-long risk of retinal problems in either this or the other eye.

63
Q

subretinal hemorhage, greenish lesion deep to the retina DDx

A

NVAMD POHS trauma (old choroidal rupture) polypoidal choroidal vasculopathy (PCV) myopic degeneration central serous chorioretinopathy

64
Q

subretinal hemorhage, greenish lesion deep to the retina history

A

History: FH of AMD smoking trauma, laser therapy, living in Ohio River Valley, and HTN.

65
Q

subretinal hemorhage, greenish lesion deep to the retina exam and evaluation

A

DFE: macula and periphery. Look for punched out CR lesions (histo spots). Look for drusen or CNV. Macula: look for elevation, thickening, hemorrhages near suspicious area, examine OU IVFA: look for focal leakage to ID classic vs occult OCT: baseline retinal thickness and define retinal pathology If substantial hemorrhage, obtain ICG to look for “hairpin” turns of retinal angiomatous proliferation (RAP lesion) or the polyp patterns seen in PCV

66
Q

NVAMD A/PT study.

A

Use IVFA and OCT to determine extent of CNV (occult vs classic) Consider: qmonthly anti-VEGF injections (follow macular thickness/fluid) anti-VEGF (such as ranibizumab): visual improvement in all types of anti-VEGF agents (ANCHOR, MARINA) bevacizumab equally effective (CATT study) but not FDA approved AREDS2 vitamin If lesion is temporal to fovea: (1) PDT as in TAP trial or laser photocoagulation (MPS study). neither study improved acuity or had rates of stability like MARINA and ANCHOR

67
Q

NVAMD education

A

natural history of AMD and options for treatment Counsel smoking cessation, prescribe AREDS vitamins to reduce rate of progression to end stage AMD (wet or GA) in other eye Follow q4weeks

68
Q

Small white

A

a

69
Q

Endophthalmitis education

A

Educate patient regarding natural history of disease = guarded, with ~50% chance of a return to 20/40 or better vision over the course of the next year

70
Q

Small white flecks in FAZ, appear to be crystalline exam exam/evaluation

A

Examine contra/L eye for drusen examine OU for K crystals (Bietti or cystinosis) Evidence of SRF, MA, NV that can cause hard exudates (usually circinate) If evidence of DM or NV –> IVFA, OCT, FBS

71
Q

Crystalline retinopathy (tamoxifen) A/P and education

A

Plan: d/c tamoxifen if pt sx d/w patient’s oncology Rx If aSx pt, then stopping the medication is not necessary, but would monitor closely q2-3 mo or sooner should patient have visual concerns. Education: natural history of condition = progressive visual decline if medication is continued. Vision can improve once discontinued. Crystals typically remain

72
Q

IVFA = petalloid hyperfluorescence pattern DDx

A

CME (post-cataract = Irvine-Gass syndrome) Other causes of CME: “DEPRIVEN” DM Epinephrine Pars planitis RP Irvine-Gass Venous occlusion E2 (prostagalndin Niacin/Nicotinic Acid

73
Q

IVFA = petalloid hyperfluorescence pattern history

A

MCC: complicated CE/IOL w/vitreous loss (examine for vitreous strands to the wound). Look for inflammation and signs of complicated cataract surgery such as broken capsule, chronic inflammation. Will keep in mind chronic endophthalmitis and will look for evidence of P. Acnes. prostaglandin gtts peripheral bone spicule pigmentation with RP other stigmata of DR OCT: establish baseline macular thickness IVFA to look for leakage Pemberton claims that there are false negative results with OCT detecting CME 10% of the time. This seems hard to believe.

74
Q

Irvine-Gass A/P

A

P: NSAID and pred qid and follow for resolution on OCT lysis of vitreous strands if vitreous to wound causing vitreous traction Systemic diamox SR 500 mg PO qd may have good results if patient can tolerate it. Periocular or intraocular steroids can also be used but have high risk for glaucoma. Anti-VEGF has limited success with CME Education: natural history = resolution of edema and improvement in VA with use of topical meds F/u: q4-6weeks until CME resolution

75
Q

MAs and DBHs DDx

A

DR Retinal vein occlusion HTN retinopathy radiation retinopathy HIV retinopathy CAR(?) hypercoagulable states

76
Q

MAs and DBHs history and exam

A

History of: DM, HTN, radition? Check: BP and gluocose Complete eye exam: checking vision and IOP Fundus exam for diabetic hemorrhages. look for vessel engorgement, macular edema, NV

77
Q

MAs and DBHs evaluation

A

For macular edema: baseline OCT IVFA looking for: (1) areas of leakage or nonperfusion (2) NV of disc or elsewhere (3) areas of capillary non-perfusion

78
Q

DR A/P

A

Per ETDRS, Rx with focal laser if macular edema: thickening w/in 500 um of fovea center hard exudates w/in 500 um of fovea w/assoc thickening retinal thickening > 1 disc area in size w/in 1 disc diameter of fovea center DRS: Rx w/PRP if PDR, defined as: 1/3 of the DA any NVD with VH NVE > 1/2 DA with VH NVI?NVA

79
Q

DR education

A

natural history of DR: glucose, HTN, lipid control slows progression and decreases mortality (per Diabetes Control and Complications Trial [DCCT]) >pts w/ HgA1c > 7 were 50% more likely to experience severe vision loss in 2 yrs than those w/HgA1c

80
Q

pseudophakic eye with conjunctival injection, hazy view through anterior segment, layered hypopyon, clear cornea DDx

A

endophthalmitis non-infectious/autoimmune uveitis

81
Q

pseudophakic eye with conjunctival injection, hazy view through anterior segment, layered hypopyon, clear cornea history

A

DFE looking for vitritis or subretinal abscess Exam contra/L eye for signs of inflammation

82
Q

Endophthathalmitis A/P

A

EVS - pts HM or better = do vitreous tap and inject PPV for LP or worse Inject: vancomycin 1 mg/0.1 mL and ceftazidine 2 mg/0.1 mL and culture vitreous and/or AC fluid to direct future therapy topical Abx, steroids, cycloplegics. Follow pt daily.

83
Q

Endophthathalmitis education

A

Educate patient regarding natural history of disease = guarded, with ~50% chance of a return to 20/40 or better vision over the course of the next year

84
Q

Dark lesion under vessels w/o elevation in the choroid DDx:

A

nevus CHRPE melanoma (but no signs of lipofuscin, elevation, disruption of bruchs membrane)

85
Q

Dark lesion under vessels w/o elevation in the choroid history and work-up

A

DFE with gonioscopy and dilation binocular biomicroscopy: to determine elevation (gold standard) On U/S: look for low to medium internal reflectivity or scleral excavation >2.5 mm elevation (suspicious for melanoma) If

86
Q

Choroidal nevus Rx and education

A

Rx: observation for nevus Rx if mlenaoma - COMS (small tumors = observation; medium tumors = brachytherapy [as good as enucleation]) Nevus Advice: reassure that this is benign common Nevus condition, Excellent Px, conversion to melanoma is rare. Also advise that even benign lesions may grow. If visual Sx occur such as wavy lines or flashes to contact office immediately Nevus F/u: q6mo to q12 mo with fundus photos Melanoma education: up to 50% 10 year mortality with these tumors. F/u with oncologist for yearly scans and monitoring.

87
Q

Red extra-macular retinal lesion (solitary) - associated with feeder artery and draining vein. lipoidal exudates suggest retinal edema approaching the fovea

A

retinal capillary hemangioma retinal cavernous hemangioma racemos angiomatosis choroidal hemangioma Single afferent and single efferent vessel small vessel composition of the mass iself presence of exudate

88
Q

retinal capillary hemangioma work-up, Rx/f/u

A

work-up: A and B scan U/S to confirm the inta-retinal location and also confirm high internal reflectivity consistent with a vascular tumor Perform FA and SD-OCT fo confirm and delineate the exudate. Rx: NO established FDA- approved Rx. Consider laser or cryotherapy of this benign tumor since the secondary exudation is nearing the fovea. Work-up: appropriate systemic dz Follow pt closely for progression of tumor and exudation

89
Q

retinal capillary hemangioma history

A

FH since RCH = AD also RCH can be phakomatosis assoc/w/RCC

90
Q

retinal capillary hemangioma exam

A

pay special attention to proximity of secondary exudation to the fovea

91
Q

Sectoral retinal hemorrrhages DDx

A

MCC = BRVO 2/2 DM, HTN (primary or secondary), vasculopathies DDX of causes includes: >glaucoma >tumor (hypercoagulable state) >infection (CMV 2/2 HIV) >vascular (atherosclerosis) >inflammation >iatrogenic (radiation) >trauma >autoimmune (lupus) >medications (OCP)

92
Q

Sectoral retinal hemorrrhages history and Sx

A

Ask about HTN, DM, HL, HIV, glaucoma and examine OU Painless decreased vision

93
Q

BRVO exam

A

VA, IOP –> both can e affected by the BRVO from retinal edema and NVI VA can be Px DFE: look for venous engorgement, tortuosity, and NVD, NVI, NVE, NVA Look for signs of DR in contra/L eye Look for signs of chronic HTN (AV nicking and arteriolar attenuation)

94
Q

BRVO work-up

A

OCT (quantify retinal thickness and detailed evaluation of cystic fluid) and IVFA (subtle NVE and retinal vascular nonperfusion) gonioscopy - evaluate for PAS, NVA, NVI

95
Q

BRVO Rx

A

Per BRAVO and CRUISE trials for BRVO and CRVO, will consider anti-VEGF Rx for macular edema. Laser photocoagulation can be also employed per the BVOS trial. PRP indicated for any NV dz (anteriorly or posteriorly) Surgery for cases of anterior segment neovascular glaucoma or rarely TRD involving central macular 2/2 posterior segment neovascularization

96
Q

BRVO Advice

A

vascular disease and HTN is the main etiology. Px is guarded if VA is severely decreased Goal is to Rx NV to prevent VA loss from NVG

97
Q

BRVO follow-up

A

Short-term f/u: Follow pt qmonthly to monitor for NV and macular edema. Long-term: q6mo and I will inform the patient’s PCP that the patient is at higher risk of stroke given recent studies correlating strokes and vessel occlusions Encourage optical CV risk factor control: BG, BP, cholesterol, diet and exercise manangement.

98
Q

DR Rx

A

PDR = PRP CSME = grid or focal Rx Recently, FDA approved ranibizumab for Rx of macula edema based on RISE and RIDE clinical trial These trails provided evidence that ranibizumab can Rx diabetic macular edema and improved vision.

99
Q

SRF (dome-shaped)/serous RD DDx

A

Vascular/endocrine (CSCR) Neoplasm (choroidal tumor) Inflam/Idiopathic/Autoimmune (VKH; uveal effusion syndrome*; macular detachment 2/2 RRD, pigment epithelial detachment from other causes like CNV; vitelliform macular detachment) Congenital (optic pit w/macular edema) Age: retinoschisis Trauma left out: Infection, Drugs *Uveal effusion syndrome = rare syndrome of idiopathic exudative detachments of choroid, ciliary body and retina thought to arise from impaired posterior segment drainage usually associated with sclera thickening.

100
Q

serous RD history and exam

A

History: stress, steroids, type A personality Exam: examine ON for ON pit

101
Q

serous RD/SRF Work-up

A

OCT: SRF, look for macular schisis >ON pit: ON excavations >thickened choroid: VKH, CSCR, uveal effusion syndrome >vitelliform lesions IVFA: Look for CNV PED: early hyperF with LATE pooling CSCR: leakage advancing through the stages of angiography in smoke-stack pattern (10% of time), more likely to see expansile dot ICG: CSCR: hyperF with late staining R/o CNV late staining with tumor

102
Q

CSCR Rx

A

Observation - Most cases resolve spontaneously in 6 weeks and return to baseline VA. Laser treatment or ocular PDT in pts with: >requirement for rapid visual recovery (airline pilots) >poor vision in fellow eye 2/2 CSCR >no resolution of fluid s/p several months >recurrent episodes with poor vision >severe forms of CSCR Rx reduces the DURATION of Sx but does not affect final VA. Experimental use: PO rifampin and mifepristone (RU486) in chronic or bilateral cases

103
Q

CSCR advice and follow-up

A

advice (discuss w/patient the natural history of CSCR). Commonly found in men with type A personalities in high stress jobs. Metamorphopsia is common Sx of CSR F/u: q4-6 wks until resolution of edema.

104
Q

Dome-shaped exudative RD (without corrugation or surface membranes, no obvious traction) or mass causes DDx

A

VINDICATE (left out infection and drugs) Vascular (HTN) Neoplasm (retinal capillary hemangioma/VHL, choroidal hemangioma, choroidal malignant melanoma) Inflammatory/Idiopathic/Autoimmune (uveitis: VKH, SO, pars planitis, posterior scleritis); CSCR, (glomerulonephritis) Congenital (Coats’ dz) Trauma Endocrine/Metabolic (hypoTH, pre-eclampsia/eclampsia)

105
Q

Dome-shaped exudative RD (without corrugation or surface membranes, no obvious traction or mass) EXAM

A

Exudative RD located inferiorly, display shifting fluid, and have a smooth appearance Appearance of a smooth RD behind lens is almost pathognomonic for exudative RD. Chronic exudative RD can lead to NVG DFE: evaluate for peripheral tears/breaks, R/O RRD, and R/o TRD (usually taut, immobile, concave surface that does NOT extend to ora serrata)

106
Q

Dome-shaped exudative RD (without corrugation or surface membranes, no obvious traction or mass) causes EVALUATION

A

B-scan - confirm shifting fluid, choroidal thickness, evlaute for masses A-scan: evaluate internal reflectivity if mass is found OCT - verify thickened choroid using EDI (enhanced depth imaging) in uveitis, image SRF +/- CME === IVFA - useful to evaluate: tumors (vasculature, feeder vessels) vascular abnormalities ICG - superior to FA to show intrinsic vaculature, hot spots, washout phenomenon for tumors

107
Q

High internal reflectivity on U/S

A

choroidal hemangioma

108
Q

Choroidal hemangioma Rx

A

Individualized Rx based on: >potential for visual recovery >Sx extent >loss of vision Rx goal: induce tumor atrophy with resolution of SRF and tumor-induced foveal distortion w/o destryoing fxn of overlying retina Goal: not to obliterate tumor Rx options: laser photocoagulation (moderately intense, white rxn on tumor surface to eliminate serous exudation), cryotherapy, ocular photodynamic therpay (PDT) with verteporfin (visudyne) using standard treatment parameters I-125 plaque brachytherapy, low dose XRT

109
Q

Choroidal hemangioma Px and education

A

VA loss can be progressive and irrversible when the fovea is involved in chronic cases poor VA results: can be expected despite resolution of fluid exudates from chronic macular edema and photoreceptor loss

110
Q

ARN Rx

A

Systemic IV acyclovir until resolution of retinitis then oral for 1-2 mo Alternatively: lesions more peripheral, then use oral therapy with valacyclovir instead of IV therapy Alternative: ganciclovir Follow BUN and Creatinine for nephrotoxicity Both PO and topical steroids after pt begins to respond to prevent inflammatory complications

111
Q

ARN education

A

high risk of developing RRD with numerous hole snad giant tears 2/2 retinal necrosis Careful observation of fellow eye

112
Q

Chronic vitritis history

A

ROS: >unexplained fevers, chills, night sweats, fatigue, HA, weight loss PMH: cancer history >LA (cervical, supraclavicular), CNS Sx?

113
Q

Chronic vitritis DDx

A

I: toxoplasmosis, syphilis, TB, ARN N: lymphoma (MCC = primary intraocular lymphoma) I: birdshot, pars planitis, sarcoidosis, multifocal choroiditis, APMPPE, Behcet’s Not used: vascular, drugs, congenital, age, trauma, endocrine

114
Q

Chronic vitritis work-up

A

CBC, ESR ACE HLA-B27, HLA-B51 ANA VDRL/RPR/FTA-ABS/MHA-TP If negative –> MRI of brain and LP for CNS cytology If negative –> PPV with UNdilute vitreous Bx (~1cc), flow cytometry for B and T cell markers, kappa/lambda light chains Ancillary tests: IL6, IL10 (high IL10 to IL6 ratio = suggestive of intraocular lymphoma)

115
Q

Intra-ocular lymphoma (diffuse large B-cell NHL) A/P

A

Rx: intravitreal MTX and rituximab Orbit XRT if no CNS involvement Most pts have CNS involvement, so Rx with chemoRx with blood-brain disruption or high-dose systemic MTX Perform: complete mtz survey and bone marrow Bx

116
Q

Intra-ocular lymphoma (diffuse large B-cell NHL) education/Px

A

60-80% develop CNS lymphoma w/mean 29 mo. Poor Px if CNS involvement.

117
Q

Granulomatous uveitis mnemonic for DDx

A

SVS by SW-PTT (mnemonic): Sarcoidosis, VKH, Sympathetic Ophthalmia, Syphilis, Wegener’s Phacoantigenic Uveitis/Glaucoma, Toxocariasis (posterior pole peripheral granulomas), toxoplasmosis, (anterior & posterior granulomatous), TB. Other rare conditions: leprosy, brucellosis, P. acnes, fungal infection (cryptococus, aspergillus), HIV

118
Q

Granulomatous uveitis exam

A

ciliary injection AC cell/flare; hypopyon iris nodules, rubeosis, synechiae increased/decreased IOP cataract pars planitis optic nerve hyperemia chorioretinitis periphlebitis CME

119
Q

Granulomatous uveitis work-up

A

CBC with differential, ESR VDRL/RPR, FTA-ABS, MHA-TP ELISA or indirect immunofluorescence assay (IFA) for toxoplasma IgM and IgG titers ACE, lysosyme Other lab tests: ANA, RF, anti-CCP ELISA for Lyme IgM and IgG HIV Ab CXR or CT scan (sarcoidosis, TB) sacroiliac radiograph (anklyosing spondylitis) UA If unclear Dx: HLA-A29 (birdshot) vasculitis (ANCA = Wegener’s, polyarteritis nodosa) Raji cell and C1q binding assays for circulating immune complexes (SLE, systemic vasculitis) complement C3, C4, total complement (SLE, cryoglobulinemia, glomerulonephritis), soluble IL-2 receptor

120
Q

Toxoplasmosis chorioretinitis Rx

A

Anterior inflammation: topical steroids and cycloplegia Systemic steroids for posterior pole lesions or those with intense Immunocompetent individuals: small peripheral lesions may be observed since they often heal spotaneously Rx with antibiotics 4-6 wks to kill tachyzoites (no effect on cysts) in the following conditions: >decreased VA >moderate-severe vitreous inflammation >lesions that threaten macula, papillomacular bundle, ON most pts respond well to: TMP-SUF aggressive lesions or posterior pole lesions: triple therapy (pyrimethamine, folinic acid and one of the following… sulfadiaizine, clindamycin, clarithromycin, azithromycin, atovaquone) If immunocompromised and high-risk, then may need to do prophylactic Rx.

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