Post-Uveitis - PDF
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This document discusses Post-Uveitis, a condition characterized by symptoms like blurred vision, metamorphopsia, and micropsia. It details key characteristics, symptoms, and stages. The document appears to be a medical analysis or case study.
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= Pt got endopthalmitisnotusing alb and lost his eye Traumatic Injury welding on can battery that blew up Fibrin Membrane Retinal Dialysis...
= Pt got endopthalmitisnotusing alb and lost his eye Traumatic Injury welding on can battery that blew up Fibrin Membrane Retinal Dialysis retinal tear giant is never foudin the organism scause eye ex 2 to lo Presumed Ocular. lung infection Histoplasmosis Syndrome (POHS) Key Characteristics Histoplasma capsulatum –fungus, inhalation of spores Prior exposure to chickens or pigeons Histo Belt: Ohio & Mississippi River valleys Maculopathy - 6 x’s more frequent in whites than blacks Macular involvement usually between 20-50 years of age (pts are asymptomatic unless maculopathy) Classic triad- 2 of the 3 histo spots (PPM) Peripheral atrophic histo spots (may have linear streaks of C/R atrophy in periphery)- asymptomatic Peripapillary atrophy Maculopathy Craver than other 2) * Symptoms Blurred vision/painless Metamorphopsia/micropsia Asymptomatic A. Peripapillary Atrophy Characterized by a diffuse circumferential, choroidal atrophy May extend up to half a disc diameter beyond the disc margin Rarely focal peripapillary atrophy Has accompanying RPE hyperplasia Up to 5-10% of POHS patients develop CNVM ↳ anytime you has defect in RPE you have choroidal neovascular rub torea is temporal to ONH ⑳ Hepa Nasal PPA ↳ 8 Echorrido rb Vascular here , world take temporal lot a to sal & face reach na need Don't have to in allchanges eyes both bitoffen medo B. Histo Spots Atrophic spots consist of roundish, slightly irregular, yellowish-white, punched out lesions measuring between.2 and.7 DD in size Pigment clumps in and at margin May number 1 to 70, bilateral 60% Linear streaks of chorioretinal atrophy in periphery noted in less than 5% of patients with POHS Clooks like histo spots connected) Peripheral streaks ↑ punched out - Lesions blacklesions D not punched Y so out histosport out & wh epunched typical white spotistion be will * active a choroat strated. C Maculopathy Fluffy yellow-white focus of active lesion Stage I choroiditis near macula (very vare almost , never spot see white Since in pic asymptomatic) how Sa Stage II Pigment (green/black ring) nodule with overlying serous detachment morasclar b we use subretinal its more instead of choroidal since & organized Stage III- & I. Exudative detachment--SRNVM, severe V reduction in vision Q #chic is V specificwhich alle 2 Subretinal Heme (red) or subretinal pigment & hemorrhages (grey/green) S 3 from net stage ut 3 , Hard exudates. is ? ret 4 Disciform scar/fibrotic scar atuhats. ↳ disk/round shaped scar Do Choroidal Neovascularization (CNVM) Late manifestation of POHS between the ages 20-45 yrs Can be idiopathic Bilateral macula involvement more common in - men May be triggered by stress Most often associated with an old macular scar (histo spot in disc/macula area, rarely absence of scar) if one eye has a net/scar, the fellow eye has a 9- histo 22% chance of development within 6-7 yrs. if Hit & - v presence of histo spot in disc macula area. Spot May develop within the peripapillary atrophy E around On macaothe in macela 8 D 22 Ju Concerned it / a - has OD chance of hum ? CNVM Hyperpigmentation (round or oval ring within light gray area) indicates new growth of vessels WITHIN subretinal space rather than sub-RPE space (SRNUM) Some cases develop large grayish green membrane or mound indicating reactive proliferation of RPE attempting to surround CNVM? 3 CNUM choroidal ? ? val later ar SRN 8 ther Num S QADittb as bretinal C , 7 ame Skim offerent S or are they but same Q * is N D atropic scan As can have b unning indementh retina G can cause find = more scoming & but most time at tays "stage Cul = loosely grouped wb ult well tined = wb canget involution selE histo el don't but for wait That lead I'll & 3 can to concerning more were me vision if develop · Ul case un u Ams use so fast xweek n d gr O ↓ - Choradovascul Nasalto Ona nt effecting a -chance PPA visin - - histo spots - ↑ hisspot macener to a have pouse them sed. OCTA ① will se black Soon lood Do S See pt a wat FA thorescein : times angiography In to ↳ wel CNUM can do FA. ⑳ in da FA Dome appearance - L of area ! large Concern blood FA relearn phases , Black here' blood blocking u [ M fored kil Laser to fora watch it comes back mestroyed mb that don'tanymore this is funders exam , its diff than optos photo mass grey green - home , [ ↑ inforce , s car only saw motion hand , this to avoid trying ↓ scar another , still active - / Diagnosis A clinical diagnosis based on typical clinical signs Lab testing of no value except in atypical cases Skin testing may reactivate ocular condition Linked to HLA-B7 and HLA-DRw2 ① Suggests genetic predisposition ?autoimmune/allergy response to antigen vs infection ② IVFA (early hyperfluorescence and late leakage) and OCT ③ someppe do chest X-ray if they're having other problems ppA Large No CNUM a -activdipan peridpot - Large area of carm Management Patient education-at risk managing risk Routine exam and monitoring of vision, esp. if histo spots near macula IVFA & OCT if suspicious active maculopathy Antifungals are not beneficial Sinceorganism not in eye ? value of oral steroids in Stage I maybe but not really - Amster grid Signs of Recurrence of Net New areas of hypopigmentation near edge of scar New areas of subretinal fluid or blood as mb always chanceof reccerance goes away to location esp adjacent past Clinical Course May have metamorphopsia, blurring of central vision, and scotoma with subtle serous depending how much elevation & focal yellow-white or gray lesion, forea involved may progress or resolve A dark green- black ring and subretinal & intraretinal blood High risk of maculopathy in good eye if atrophic scar in good eye & maculopathy in other eye: 9 to 22% chance * Must check vision with Amsler grid Differential Diagnosis cause Just ARMD CaM Degenerative myopia doesn't - to Y his Angioid streaks mean Choroidal ruptures Idiopathetic net histo related to birds is fungus , 2. ↳ protozoa related , histo Diffthan to cats Toxoplasma gondii Toxoplasmosis One of the most common causes of posterior uveitis in the USA- 30-50% of all posterior uveitis in USA Systemic Et.- obligate intracellular protozoan parasite- toxo gondii Cat- final host, other animals as well as human are intermediate hosts: sporozoite, tachyzoite & bradyzoite The organism has a predilection for nerve tissue and can persist encysted in retinal tissue for years Systemic features- usually asymptomatic, AIDS (severe disease) Congenital or acquired toxo aquired more common Recurrent active ocular toxo Ways Humans Infected Ingestion of tissue cyst in undercooked meat Ingestion of sporocysts present in contaminated soil, food (dairy products) or water Inhalation of spores from soil Contaminated blood transfusions Cranchs) Transplacental infection of the fetus from non- immunized infected mother Diagnostic Tests Serum antitoxoplasma antibody titers Indirect immunofluorescent antibody tests (IFA) Haemagglutination tests Enzyme linked immunosorbent assay (ELISA) Sabin- Feldman dye test PCR of ocular fluids Congenital Toxoplasmosis Primary maternal infection occurs during pregnancy from exposure to cat feces or raw meat 60-70% of females at risk during child bearing yrs. Infection during early pregnancy may result in stillbirth Rate of fetal infection increases during pregancy:15% during first tri (severity of disease greater), 30% 2nd tri, & 60% during 3rd tri. Infection in pregnancy may cause convulsions, intracranial calcifications, retinochoroiditis, paralysis, hydrocephalus, visceral involvement, intellectual impairment, & epilepsy - > Notserve enough for observable SX Most cases are subclinical with bilateral healed chorioretinal scars that maybe discovered later in life either by chance or a child is found to have defective vision (85% with ocular lesions without treatment) Toxoplasma Retinitis Most common cause of retinitis in otherwise a healthy individual Recurrence usually takes place between the ages of 10- 35 when the cysts rupture from an old congenital reactive toxo scar or acquired toxoplasmosis Compromised immune status of patient Clinical features Iridocyclitis- non or granulomatous- red eye Focal (Y/W), fluffy, white, retinitis adjacent to an old scar (satellite lesion), overlying vitritis (headlights in fog), may be focal ↳ sometimes so bad all Papillitis is you see glare ↳ Hinflammation significant enough Toxo in HIV patients Multifocal deep retina Occur without vitritis High incidence of toxo encephalitis Key Symptoms Hazy vision Floaters J 1st 2 things that ppe complain about it Field loss Red eye Pain is absent Key Signs can have Anterior uveitis J (unlike histo Vitritis Detached posterior face with inflammatory vitreous precipitates Retinitis Arteritis of neighboring vessels (Inflamm of arteries) Optic nerve inflammation < papillitis) Clinical Course In uncompromised host, the retinitis heals within 1-4 months (don't wait ! Always give TX) Vitreous haze gradually clears, the inflammatory focus is replaced by a sharply demarcated atrophic scar surrounded by hyperpigmented borders fell thickness to where out scaris adja reocurance happens Eyes With Toxo Lose Vision by I scarfill thickness in paplo maculo Direct involvement of the fovea, papillomacular bundle , bundle, optic nerve head, or major blood vessels lose you can Indirect involvement may result in CME & macular vision pucker Cystoid edema macular based on Tractional retinal detachment by severe vitritis location of Visual field defects by lesions scor - Scar can Lead defect to arerate Indications for Treatment Not all lesions need to be treated esp. small peripheral lesions A lesion threatening or involving the macula, papllomacular bundle, ONH, or major blood ↳ from ONHto around macula vessel A very severe vitritis- if 2 line reduction in S All AIDS pts & Treatment · Prednisone steroids + Systemiz meds Enlist infectious disease specialists anti-toto Systemic (Prednisone) steroids; never without anti- toxo meds, never subtenon injections Clindamycin : lb a sarcoidosfro ↳ unlilefor th of toxo Sulphonamides (Sulfadiazine) Pyrimethamine plus folinic acid to minimize bone marrow toxicity Co-trimoxazole alb : Azithromycin : alb Atovaquone > - antifungal antiparasite + Management Attempt to educate the community regarding expectant mother avoidance of cat litter and undercooked meat Serological monitoring during pregnancy Educate patient regarding inactive scars and follow at routine intervals sion recovers + X = wicker · cer qu KP's in vitritis Q activelesion; - edge aematory flute, active Loss vision - NFL damaged - scarred Old quiet scar Nerve fiber defect old scan ↓ Active lesion Healing lesion detect toxo screate Note NF defect causing & Inactive defect & lesion & S Recurrent Active Toxo Fresh active lesion without scarring thickened fluffy F appearance FONH blurry very pf from Jamaica trip D * Hanammatories spot New inflammatory ↑ toxo Scor. 3 Ocular Toxocariasis Canis Diff than totoplasmosis · Ais war o Intestinal parasite (nematode) lut. camm - Toxocara canis - Intri , Young children Symptoms of unilateral floaters, ↳ vitriters larfiltrates blurred vision and photophobia tinitic Parureits pos u Icharade tira pe calitis) affectsint X Indo Lisi out tis charid choroid Caka horaid , i I of B Grea no flammatio x Aka S ~ in · Lis! Critis tre in lamm includes X eli inf V Pos -Sp Xi Inflamm alae. his Aneits Toxocariasis Caused by infection with a common intestinal ascarid (roundworm) of dogs called Toxocara canis, especially puppies Human infection by accidental ingestion of soil or food contaminated with ova shed in dogs feces Young children (2-4yrs) who eat dirt (pica/ geophagia) or are in close contact with puppies are at particular risk, ova can exist for long periods in the soil Visceral larva migrans is the systemic form of acute toxocariasis Ocular Toxocariasis Canis Ocular Signs Inflamm , of vitreous + ageous hervor : Ina was wa ↑ tis vitrites - Unilateral chronic endophthalmitis: Uveitis, vitritis, and large elevated white granulomatous retinal lesion in either posterior pole or a - - White, raised, granulomatous mass in periphery- 1DD in size- most common Retinal/fibrous tractional folds radiating from lesion, deviated blood vessels towards mass and optic nerve dragging VA will be extremely decreased (20/200 or worse) if lesion affected the macula Diagnostic Tests Enzyme – linked immunosorbent assay (ELISA)- the test of choice Ultrasonography makesure not tuor ex. Retinoblastoma Ocular Toxocariasis Chronic endophthalmitis Posterior pole granuloma Peripheral granuloma OR] uncommon to get both A. Chronic Endophthalmitis Presentation between the ages of 2 & 9 with leukocoria, strabismus, or unilateral visual loss Signs: uveitis, vitritis, posterior or peripheral ↳ vitreous inflammation granuloma Poor visual prognosis Is it retinoblastoma or ? granuloma includes -central retina between sups Infacteries IGNH , B. Posterior Pole Granuloma macula Presentation is typically with unilateral visual loss between the ages of 6 & 14 in young kids Signs: anterior uveitis & vitritis are absent: round, y-w , solid granuloma (1-2 DD in size), usually located at the macula or between the macula & ONH, retinal stress lines ever wher weit's grandma doesn't go away , vitreitis goes dis away # is there a drag Post Pole grandma Q too in. elevated white - L mass , not white im spot retro Asdroydic gandom e pulling vasclatureganome out , to towards appearance pulling C. Peripheral Granuloma Presentation is usually during adolescence or adult as a result of visual impairment from distortion of macula or retinal detachment Signs: anterior uveitis & vitritis are absent, a white hemispherical granuloma located at equator, vitreous bands, dragged disc Treatment Important to rule out retinoblastoma in young children No real treatment except steroids to suppress the & inflammation In some cases, vitreoretinal surgery ↳ this is once if corsing traction detachment - of retina Visual Loss Heterotropia of the macula > - macula displaced from original Retinal detachment position fibrou on - that e goes - the dis Y fibrous off # coming galoma 4 Congenital Rubella Syndrome. First 8 weeks of pregnancy Triad of hearing defects (100%), heart defects (70%), and ocular defects (30-60%) nothing 4 hear nothing pump see nothing , , these usually lead to glaucoma Passed from mom-baby Congenital Rubella-Systemic Features Results from transplacental transmission of virus to the fetus from infected mother usually during the first trimester of pregnancy May lead to serious fetal infections and malformations Spontaneous abortion, stillbirths, heart malformations, deafness plus others Ocular Signs affects retinal pigment in RPE - disease that > Pigmentary retinopathy- atypical RP or salt/pepper fundus ↳ RPE layerimpacted retinopathy Bilateral nuclear cataracts earlier in age Microphthalmos (smaller eye Glaucoma get sick RPE = problems assoc sick RPE Ocular Rubella No Retinal sheen , -forea yellowishdue to yellow pigments have p - saltt pepper = good - fouso vessels nor O > - Poor focus hell due fluid to Riskfactors of Retinal detachment - Pilocarpine car risk pilocarpine : multinal detachment of If someone usl Sick RPEgets RD we're relying on RPE to stick , butifrctiva already sickit'll keep detaching This was badluck and Sarcoidosis - race case 4 - forms gahlomas : masses of inflamm tissue · Class: granulomatous, inflammatory System: Multisystem, usually pulmonary Pathology: granulomatous Sex: F>M, most common in 20-50 Etiology: Possible allergy to airborne antigen, unknown Race: B>W 10x in the USA Symptom: Coughing and breathing difficulty: pt feels sick, fever, arthralgias Systemic treatment: Steroids, Antimetabolites Uveitis: granulomatous and chronic uveitis - 25-50% of all patients get U- maybe the presenting sign Ask all U pts if they have a dry cough or chest pain Associated with disc edema papilloedema specifically reservedfur , IIH it's bilateral diff from disc Chest X-ray , get , - edema Sarcoidosis Idiopathic multisystem granulomatous infection: Skin, lungs, lymph, liver, spleen, and eyes African descent, southern, eastern, and gulf states; Scandinavian countries Females > males Inflammatory disorders more common in females in general Uveitis occurs independently of the activity or severity of systemic disease Ocular Features Anterior segment (conj, episclera, sclera & lacrimal)- granulomas Inflammed lacrimal gland dacryo adenitis = Keratoconjunctivitis sicca Anterior uveitis: acute/chronic; granulomatous,- so more systemic mutton-fat KPs, severe posterior synechiae, iris nodules: problems older pts with chronic granulomatous uveitis- secondary glaucoma Vitreous- Intermediate uveitis (R/O sarcoidosis), vitritis with snowballs -white /yellow exudates along retinal veins Periphlebitis- perivenous candle-wax drippings Retinal granulomata ↳ If see this concernfor sarcoid , but if don't have that then doesn't mean Choroidal granulomata (maybe mistaken for amelanotic melanoma) they don't have Acute retinopathy Sarcoid Peripheral retinal neovascularization Optic nerve lesions also seventh nerve palsy Management Systemic steroids for 1st line therapy Other treatments- oral NSAIDs, immunosuppressive agents can use sarcoidosi atuhy r X Ocular subtero f no Topical steroids & cycloplegic- anterior uveitis Lots Unlike t Sub-Tenon & oral steroids for intermediate and ↳ Injection of steroids toxo posterior uveitis Sarcoidosis but Not toto > Can use steroids to TX ↓ body overacting WANT to suppress immere system of steroids -Sarcoidosis is Inflammatory so you Toxo its external Infection want immune system to fight it off so is so you - No occlar steroids but can give systemic steroid + anti-toxomed , front eye balkeye candle wax hipping , often a Candle wax drippings of ONH & 5. Tuberculosis like sarcoidosis G Class: chronic, granulomatous, infectious disease ↑ System: Multisystem; usually pulmonary Etiology: Mycobacterium tuberculin bacteria; contagious by inhalation of infected respiratory particles in lungs Symptoms: cough, fever, & malaise Treatment: Antibiotics (Isoniazid- INH) Any type of patient- intercity Uveitis: chronic, granulomatous for both Sarcoid more than TB common but should be fasting Send Infections DX - This is Infectious DX if , the , person to. weitis alla initis (affectivist chamber) ant ant Ocular Features of raised bumps car appear anywhere on ant eye Phlyctenular keratoconjunctivitis (PKC) " Chronic iridocyclitis (ant weitis affecting ciliary body hiris) - en -Pupil border surface- Iris · o 'Buscaca Koeppe & Buscaca nodules like ? what do they look Bilateral Choroiditis Tubercles * Diffuse multi-focal y/w nodular lesions (miliary) Retinallikevasculitis (periphlebitis): R/O Eales’ disease ↳ in sarcoidosis ↳ Dz of retina vasculature may progress to neovascularization Optic neuritis May resemble ocular sarcoidosis (so often get testing for both same TB Causes veitis when active but curable time) Treatment of TB “one of the few uveitis that can be cured by antibiotic treatment” Isoniazid (INH) Trial for 3 weeks i A/B Pyrazinamide Pyridoxine (Vit B6) Rifampin : Alb Ethambutol Streptomycin · - PKC > - phlecteurles & how O so can I from tell PK2 nochlar epischeritis Is PKC just subepithelial - so need to check the corres , and episcientis is under the conjunctiva? main cause of phiectacles most time is staph b. Syphilis > can - look like anything Bacterial infection– multisystem ↳ Etiology: sexually- transmitted spirochete Treponema pallidum - genital ulcer Symptoms: Chancre, fever, & malaise; joint pain; lymphadenopathy, rash on palms or soles i causes Primary, secondary & tertiary stages swelling Ask all U pts if they have a rash of palm, sole of feet nodes 1% of all U pts have syphilis Crave) “The Great Imitator” - test for it even though Lab testing relatively rare - FTA-ABS - MHA-TP Venereal Dz Research Lab test also tests antibodies - VDRL > , - RPR - PCR solt's Pepper fundus CongenitalRebellay Ocular Features Syphilis Congenital Salt & Pepper fundus: asymmetric VFs, may resemble RP ↳ Like congenital Rubella Pigment scarring with areas of depigmentation and pigmentation ① Bilateral Interstitial keratitis: between ages of 5 & 25 ② External features: widely spaced peg teeth (incisors) (Hutchinson’s), depressed nasal bridge, deafness,③ mental retardation & frontal bossing ⑰ Hutchison’s triad: IK, Deafness & teeth changes Iridocyclitis ↳ like Ribello Multifocal chorioretinitis Unifocal choroiditis Neuroretinitis Congenital Syphiltis similar rubella congenital to ↳ Inflamm of ON Neuro-ophthalmic Features Argyll Robertson pupils > do not - constrict on bright light Optic Nerve Atrophy congenitaluphillis > sarcoidosis has 7th Ocular motor palsies (3rd & 6th nerve) - nerve palsy Visual field defects Management DX w/ Lumbar puncture IV/ IM penicillin Alternative to Penicillin-Tetracycline & erythromycin cars C/R atrophy in congenital syphilis olds from d 8 fallo Grantmaki Case Review Patient Referred for Glaucoma Eval Decreased Mental Capacity Hx of Blepharospasm BCVA: 20/20 OD, OS Pupils = 1mm OD, OS > tiny pupils - IOP: 13, 14 mmHg Pachs: 511 and 502 > - thin packs Case Review Gonio: Moderate Depth Lens: 1-2+ NSC Difficult View Secondary to Small Pupils Post Dilation didn't dilate eveneidilation pupils well bestview of nervel dilation KB Photos ↳ cupping isn't bad OCT ① Look at quality , Signal strength is 7/10 and 6/10 ② Showing bilateral - 00 field loss G O VF > - enlarged blindspot Sup - - nasal loss field -generalidloss field VF -enlapd natde ural field loss - ring Scotorra caused by place time his Case Review Small Pupils Thin Pachs IOP max 14 Chronic Blepharospasm > he - takes botox for Pale ONH’s Generalized Loss on OCT Enlarged Blind Spot with Generalized Constriction What’s the Next Step? Does Not sound like = glaucoma Treat or Monitor? Conclusion Multiple Aspects to Consider in a Glaucoma Eval Beware of Mimicking Disorders Multiple Visits are Valuable Pieces of the Puzzle he had zongenital Syphilis g ↑ Acute Retinal Necrosis or Progressive Outer Retinal Necrosis -usually always zoster Necrotizing herpetic retinopathies represent a spectrum of diseases induced by viruses of the herpes family Patients with intact immunity tend to develop acute retinal necrosis and patients with severely impaired immunity with progressive outer retinal necrosis Tests: PCR- very high sensitivity and specificity: aqueous & vitreous biopsy 8. a. Acute Retinal Necrosis Syndrome Rare, but devastating necrotizing retinitis, in typically healthy individuals 20-50, males greater, tends to be caused by herpes simplex in younger patients and herpes zoster in older Blurred vision (floaters), ocular pain, photophobia SAVAPER The classic triad: arteritis & periphlebitis, confluent necrotizing retinitis of peripheral retina, moderate to severe vitritis, anterior uveitis, episcleritis/ scleritis, also disc edema Clinical course: resolution of retinitis in 4-12 weeks with transparent & necrotic retina, with second eye involved in 2 mos. in 30-50% of pts Cause of visual loss: retinal detachments & ischemic optic neuropathy, poor prognosis Treatment: refer ASAP to retinal specialist, IV & systemic Acyclovir, systemic steroids, aspirin, laser, surgery relatively normal abnormal ont - Indistinat margins, edemators Inflammed, - - congestil By -Respir K Review FA stages -early stage arrows = Inflammatory lesions - pale yellow wh ped blob unit -aker petehep mestand funders -follow get them On IV # immediately & Barricade laser for Th - all dead tissue 9. Idiopathic Multifocal White-Dot Syndromes Rare, inflammatory disorders affecting retina, RPE, & choroid White Dot Syndromes B AMPPE C , Serpiginous Choroiditis ↳ snake like A , MEWDS E Multifocal Choroiditis with Panuveitis F. PIC D Birdshot Retinochoridopathy As Multiple Evanescent White- Dot Syndrome (MEWDS) Rare condition with no treatment but good prognosis One eye of young, healthy female with an acute onset of unilateral vision impairment, photopsia Paracentral scotomas occurring in approximately 50% of the like colds) patients soon after a flu-like illness (recent from Active lesions consist of numerous, very small white dots at the level of the RPE at posterior pole papillitis/ Associated features include mild vitritis and optic nerve edemat swelling with enlarged blind spot Vision recovery to 20/20 to 20/30 in 6-12 weeks Sometimes LAN due to papillitis - blimed margins - NFL more - visiblejust margin Indis - w) this get Blindspot t etagenen crite BS (blindspot) enlargement Normal MELDS to tends be chilateral around - look at areas seathesh beam to spots ICG like FA , but highlights Choroid ↓ ↓ FAc)Mewds AFCautofluorescence) B Acute Multifocal Placoid Pigment. highlight Epitheliopathy (AMPPE) pin similar Rare, bilateral disorder of the RPE in young adults with flu-like prodromal syndrome, visual prognosis is good ↳ like Mends exceptits bilateral - - Presenting symptoms: subacute unilateral depends I upo wived ↳ only spot eye since it and imp impairment of VA & paracentral scotomas, on where usually worse in 1 eye A more than other st followed by other eye in a few days same SX Mends as - AMPPE more common in Mild vitritis and multiple, chorioretinal lesions of a deep placoid cream-colored appearance confined to the posterior pole; ½ to 1 DD IVFA is critical in diagnosis Mends : Less vitritis , AMPPE more common to get Vitritis Management Up to 80% recover vision to 20/40 or better untreated Fundus lesions resolve over 9- 14 days leaving RPE mottling No specific treatment splotches in AmppE - C. Serpiginous or Geographic Choroidopathy Unlike AMPE or MEUDS Ammpe Uncommon, idiopathic, chronic progressive, bilateral like disease in pts between the ages of 4-6 decades, poor prognosis (midlife) Starts Later poorer prognosis than others like Chorioretinal lesions (deep, cream-colored opacities with ↓ hazy borders), jigsaw-puzzle-shaped lesions, starting Ammpe around the optic nerve head and spreading out in all directions in propeller like fashion; bilateral but asymmetric: lesions old atrophic scars Associated features: mild anterior uveitis & vitritis [like other 2) CNVMs in 25% of cases (like POHS) Treatment: systemic & intravitreal steroids & cyclosporin like sarcoidosis ↳ Immunosuppressant that disrupts bruchs my anything risk of choroido vascular rub can have Classic pic starts offul and patch keeps growing nemes assoc w/it Do Birdshot Retinochoroidopathy & like AmmpE , serpiginous a Uncommon, bilateral, chronic condition in healthy middle-aged white women Presenting symptoms: floaters, decreased central vision Acute lesions: bilateral, flat, creamy- yellow, deep, ovoid spots with distinct margins Midperiphery to posterior pole to retire shotgen Vision Loss Can cause sig Birdshot Retinochoroidopathy Bilateral and symmetrical - Serpiginous bilateral's symmetrical Lesions Middle aged like serpiginos Vitritis, chorioretinal lesions with shotgun (birdshot) appearance < ½ DD Strong relationship to HLA-A29 Treatment: poor prognosis without > like - treatment, oral or local steroids, sepiginous immunosuppressive agents wi have Vision loss even can sig everly spaced lesions , symmetrical lesions E. Multifocal Choroiditis with Panuveitis Syndrome hard to diffe birdshots this bew flikeAmmpe ; mends Typically affects middle- aged females with recent flu like syndrome, fair prognosis ↳ birdshot Like + serpiginous Anterior uveitis- may have severe uveitis with hypopyon: typically bilateral birds hot sepiginous > - + Vitreous inflammationNitritis Yellow-gray multifocal cream colored choroidal lesions > birdshot - scattered throughout the posterior pole + Serp Optic disc edema > - Mewds Like Pseudo POHS-later punched out scars: CNVMs Treatment with periocular and oral steroids, antiVEGF Inflammation in out Panneitis - more seg -this is more than treatable birdshots serpiginous - fuzzy lesions since pic taken thm vitritis F. Punctate Inner Choroidopathy (PIC) Young, healthy patients ages 16-40 90% of patients with PIC are women Most are moderately myopic No history of preceding illness In flamma * pola - post , - so small lesions around forca PIC – Signs andSymptoms Blurred vision Central or paracentral scotoma Photopsia Bilateral > - birdshot , serp , Panreitis Clustering of yellow spots with indistinct borders 100-300 microns in size Level of the RPE and Choroid May be associated with overlying serous detachment Crave) Posterior pole and mid-periphery just like > - bird shot very small lesions at 1st but scar overtime , grows PIC May have Amsler Defect Can have enlarged blind spot (like mends' Ampe) Lesions resolve into punched out, pigmented scars (grow as become scarred) ↳ like Panureits PIC Prognosis Like Mewds , Ammpe - Typically good prognosis if do not develop CNV 75% of eyes retain 20/25 or better vision Very small spot scare growing O O PIC with CNVM Choridovascular mb Others to Know 9 Systemic Lupus Erythematosus Cutaneous disease Secondary Sjogren’s syndrome Retinal vascular lesions Most common ophthalmic manifestation Cotton-wool spots with or without intraretinal hemorrhages Neuroophthalmic lesions + antweitis Scleroderma ↳ causes post Relapsing Polychondritis Diffuse Unilateral Subacute Neuroretinitis (DUSN) Grave , more in tropical climates ↳ nemotode its leaving tracks's destroying retire