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Intraocular Inflammation and Uveitis (BCSC Book 9)
Terms in this set (59)
What is the SUN Grading for anterior chamber cell (when visualized with a 1mmx1mm high power beam at 46-60 degrees with full intensity light in a dim room)?
Grade 0 = <1 cell
Grade 1/2+ = 1-5
Grade 1+ = 6-15
Grade 2+ = 16-25
Grade 3+ = 26-50
Grade 4+ = >50
What is the SUN grading for anterior chamber flare?
Grade 0 = none
Grade 1+ = faint
Grade 2+ = moderate (iris and lens details still clear)
Grade 3+ = Marked (iris and lens details hazy)
Grade 4+ = Intense (fibrin or plasmoid aqueous)
1. True or false? There is a similar diagnostic value of anterior chamber and vitreous samples in diagnosing infectious causes of uveitis (like HSV, VZV, CMV)?
2. What is the role of systemic NSAIDs in the treatment of ocular inflammation?
3. How do you preform a sub-Tenon injection?
4. Periocular injection of steroid is contraindicated in patients with _____ and _____.
2. systemic NSAIDs can be used alone for treatment of mild to moderate non-necrotizing anterior scleritis
3. 25-gauge, 5/8 inch needle is injected into the superotemporal quadrant bevel down against the sclera with a side to side movement (to make sure you haven't pierced the sclera)
4. infectious uveitis and necrotizing scleritis
1. If systemic steroid therapy of _____mg or more for more than _____ months is required, you should start immunosuppressant therapy.
2. Which IMT drug is the only one currently FDA approved in the USA for treatment of uveitis?
3. Patients receiving which class of drugs need to be on TMP-SMX for PCP prophylaxis?
1. 10mg or more for 3 months or more
2. adalimumab (for noninfectious posterior/pan uveitis)
3. alkylating agents (cyclophosphamide or chlorambucil)
1. Which drugs are antimetabolites?
2. Which one tends to work the fastest?
3. Which one tends to be the least well tolerated?
4. Which one is 1st line for IMT in children?
1. azathioprine, methotrexate and mycophenolate mofetil
2. mycophenolate mofetil is fastest
3. azathioprine is least well tolerated
1. Cyclosporine, tacrolimus and sirolimus work by what mechanism?
2. What are the 2 most important side effects of cyclosporine?
3. All of them are unique drugs for what reason?
1. inhibition of T-cell signaling
2. HTN and nephrotoxicity
3. they are naturally made as products of various bacteria
1. How do cyclophosphamide and chlorambucil work?
2. What disease are they first line for?
3. Otherwise they are usually only used if other drugs have failed, why?
4. What are the most common side effects of cyclophosphamide?
5. Patients taking these also need to take what?
1. DNA alkylating agents
2. necrotizing scleritis associated with systemic vasculitis such as granulomatosis with polyangitis
3. increased risk of malignancy... up for 33-fold increased risk of bladder cancer among others
4. myelosuppression and hemorrhagic cystitis
5. TMP-SMX for PCP prophylaxis
1. Etanercept is a TNF-alpha blocker that can cause _____.
2. Infliximab is a TNF-alpha blocker that can cause _____, but the risk is limited if the patient is also treated with ____.
3. Rituximab is an antibody against ____.
4. Anakinra is an antagonist of _____.
5. Tocilizumab is an antibody against _____.
2. Infliximab can cause drug-induced uveitis, but risk is less if patient is also on methotrexate
3. rituximab is anti-CD20
4. anakinra is against IL-1
5. tocilizumab is anti-IL6
1. About 40% of scleritis cases are associated with _____.
2. What category of uveitis is most common?
3. What is a unique feature of anterior uveitis related to HLA-B27?
1. rheumatoid arthritis
2. anterior uveitis
3. HLA-B27 associated uveitis tends to be unilateral but then recur and switch between the eyes
1. Up to _____% of patients with ankylosing spondylitis are HLA-B27 positive.
2. What is the typical description of the back pain?
3. What is the 1st line treatment?
4. Why is early diagnosis important?
2. morning lower back stiffness that gets better with exertion
3. NSAIDs are fist line treatment, but anti-TNF drugs also useful
4. early diagnosis is important b/c exercise, physical therapy and smoking cessation can help slow disease progression
1. What is the diagnostic triad of reactive arthritis?
2. _____% of patients are HLA-B27 positive.
3. Reactive arthritis is often triggered by what?
4. Name 2 other conditions that are associated with reactive arthritis.
1. - nonspecific urethritis
- conjunctival inflammation (+/- uveitis)
3. infectious diarrhea
4. - keratoderma blennorrhagicum: scaly, erythematous rash of palms and soles
- circinate balanitis: persistent circumferential rash of the distal penis
1. Patients with inflammatory bowel disease and anterior uveitis are more likely to have these 2 things.
2. What differentiates uveitis associated with psoriatic arthritis from uveitis associated with other sponyloarthropathies?
1. HLA-B27 positivity and sacroilitis
2. uveitis in psoriatic arthritis is often chronic
1. What are the diagnostic criteria for tubulointerstitial nephritis and uveitis?
2. What is the typical patient population?
3. What is the treatment?
1. - anterior uveitis (often bilateral)
- elevated Cr or decrease CrCl
- abnormal UA with elevated B2-microglobulin, proteinuria, white cell casts, hematuria or eosinophils
- systemic illness... fever, fatigue, arthralgia....
2. women in teens to early 30s
3. high dose steroids
1. What is UGH syndrome?
2. What causes it?
3. What lens placement is the most common cause?
1. uveitis - glaucoma - hyphema
2. irritation of the iris root by any intraocular implant
3. a single piece acrylic IOL that was accidentally placed in the sulcus
1. Name 5 drugs that can cause uveitis.=
2. Name 2 vaccines that can cause uveitis.
3. Which topical glaucoma medication is most associated with causing uveitis?
1. - rifabutin
- systemic fluoroquinolones
- sulfa drugs
- diethylcarbamazine (anti-filarial)
2. - BCG vaccine
- flu vaccine
1. What is the most common systemic disorder associated with uveitis in kids?
2. What is the average age of onset of uveitis in these patients?
3. Are the amount of joint inflammation and eye inflammation correlated?
4. What is the prognosis of uveitis?
1. juvenile idiopathic arthritis
2. age 6
3. no, eye and joint inflammation do not correlate
4. prognosis can be poor because they eye is often white and kids tend to not complain of pain... so they need regular periodic exams
1. What is the Still disease type of JIA?
2. Describe polyarticular JIA.
3. If preforming cataract surgery in a JIA patient, what are 2 things you must do?
1. Still disease = young onset (<5 y/o) JIA with fever, rash, lymphadenopathy and hepatosplenomegaly without eye involvement
2. polyarticular JIA = more than 4 joints involved; can cause uveitis, especially if negative for rheumatoid factor
3. - only an acrylic lens should be used
- pt must be on IMT pre and post operatively
1. Describe oligoarticular JIA.
2. What are the 2 subtypes?
1. four or fewer joints involved; most likely to have uveitis
2. - type 1 = girl, under 5, ANA positive, chronic uveitis
- type 2 = boy, over 5, HLA-B27 positive, acute uveitis
1. Name 4 important signs in Fuchs heterochromic uveitis other than change in iris color (lighter eye indicating involved eye usually).
2. Patients characteristically lack these 2 things despite longstanding inflammation.
3. What infections has it been associated with?
4. What is a major complication that happens during surgery?
1. - diffuse iris stromal atrophy
- small, white, diffuse KPs
2. posterior synechiae and symptoms are often absent
3. associated with toxoplasmosis, HSV, rubella and CMV
4. can get hyphema during surgery b/c there are often abnormal blood vessels in the angle
1. In intermediate uveitis, the predominant site of inflammation is the _____.
2. What are "snowballs"?
3. What are "snowbanks"?
4. What is the most common form of intermediate uveitis?
2. snowballs = inflammatory cells aggregating in the vitreous
3. snowbanks = inflammatory exudates accumulate on the pars plana
4. pars planitis = intermediate uveitis with snowballs and snowbanks without associated infection or systemic disease
1. When does pars planitis typically present?
2. Most cases are _____lateral.
3. What is the major cause of vision loss in pars planitis?
4. What is the prognosis of pars planitis?
5. What are some longer term complications of pars planitis?
1. bimodal age distribution ... 5-15 years or 20-40 years
2. most cases bilateral
4. - 10% have self-limiting course
- 30% have smoldering course with exacerbations
- 60% have prolonged course without exacerbations
5. - cataract
- recurrent PCO despite YAG
- retrolental membranes
- chronic CME
1. Uveitis is _____ times more common in MS patients than in the general population.
2. What is the most common type of uveitis in MS?
3. What HLA type is associated with the combo of MS and uveitis?
4. What class of IMT should not be used in MS uveitis b/c it can cause MS flares?
1. 10 times more common
2. intermediate uveitis
4. anti-TNF drugs
1. What ocular manifestation of Lupus is consider an important marker for disease activity?
2. What characterizes this?
1. lupus retinopathy
2. - cotton wool spots
- retinal vascular occlusion of both arteries and veins (associated with CNS disease and antiphospholipid antibodies)
- lupus choroidopathy.... serous elevations of the retina/RPE and CNV
1. What is the most common symptom of polyarteritis nodosa?
2. How is the eye affected?
3. Why is it important to consider in any patient with retinal vasculitis and systemic disease?
1. mononeuritis multiplex
2. ocular involvement in 20% of patients related to vasculitis.... HTN retinopathy, BRAO, choroidal infarcts
3. b/c the 5 year mortality rate of untreated disease is 90%
4. p-ANCA (anti-MPO)
1. What is the most characteristic sign of granulomatosis with polyangitis?
2. Ocular/orbital involvement will occur in up to _____% of patients.
3. Why does orbital involvement occur?
5. Mainstay of treatment?
1. involvement of paranasal sinuses
3. orbits often involved from secondary extension from sinuses
4. c-ANCA (anti-proteinase 3)
5. steroids + cyclophosphamide
1. What is the triad of Susac syndrome?
2. Who is the typical patient?
3. What change do you see in the retinal vessels?
4 What do you see on MRI?
1. encephalopathy, hearing loss and BRAOs
2. young female (teens or older)
3. narrowing of arteries with "boxcar" segmentation (very apparent on FA)
4. multifocal supratentorial white matter lesions
1. What is the most common ocular manifestation of sarcoidosis?
2. What is Lofgren syndrome?
3. What is Heerfordt syndrome?
4. What can you see in the vitreous?
5. What are "candle wax" drippings?
1. anterior uveitis with mutton fat KPs and iris nodules
2. Lofgren: erythema nodosum, febrile arthropathy, bilateral hilar adenopathy, acute iritis.... responds well to steroids
3. Heerfordt: uveitis, parotitis, fever, facial nerve palsy
4. "string of pearls" of linear inflammatory strands in the vitreous
5. irregular nodular granulomas along venules
1. In sympathetic ophthalmia, which eye has the more severe inflammation?
2. What are dalen-fuchs nodules?
3. HLA association?
4. Treatment of SO?
1. initially, it is often the exciting eye
2. yellow-white mid equatorial choroidal nodules
4. topical/systemic steroids... once it has started, there is no role for enucleation of the exciting eye
1. What characterizes the prodromal phase of VKH?
2. Acute uveitic phase?
3. Convalescent stage?
4. Chronic recurrent stage?
1. prodrome: flu like symptoms that eventually lead to auditory problems that often herald the start of eye problems
2. acute uveitic: blurry vision 1-2 days after onset of CNS signs... bilateral granulomatous uveitis with optic nerve edema, multiple serous retinal detachments
3. convalescent: several weeks lateraled, resolution of exudative RDs and gradual depigmentation of the choroid
- skin changes also tend to occur during this time
4. chronic: recurrent bouts of granulomatous anterior uveitis
1. What is the most common finding in Bechet disease?
2. What is the most deadly type of Bechet disease?
3. What anterior segment finding is commonly seen with Bechet disease?
4. What is the most common retinal finding?
5. HLA association?
1. oral ulcers
2. neurologic disease
3. hypopyon that shifts with head position
4. obliterative, necrotizing vasculitis that affects the arteries and veins
6. start steroids but need early IMT (azathioprine then cyclosporine)
1. What type of KPs do you see in herpetic uveitis?
2. What does IOP do in herpetic uveitis?
3. What characteristic iris change happens in herpetic uveitis?
4. How do you treat herpetic uveitis?
1. stellate KPs
2. IOP is high!
3. iris atrophy
4. topical steroids and oral antivirals (no topical antivirals)
1. Describe the presentation of acute retinal necrosis.
2. Describe how the exam evolves over time.
3. What is a very common complication?
4. What part of the retina is generally spared?
5. What is the most common cause?
6. How do you treat it?
1. acute, unilateral vision loss with photophobia, floaters and pain
2. panuveitis with prominent vitrifies with retinal arteriolar occlusions and multifocal white-yellow peripheral lesions that coalesce rapidly if not treated
3. combined tractional-rhegmatogenous retinal detachments
4. posterior pole
5. VZV (then HSV)
6. systemic and intravitreal antivirals in combo with steroids to reduce inflammation (antivirals always first)
1. What population does progressive outer retinal necrosis occur in?
2. What is the most common cause?
3. How does the exam differ from ARN?
4. Bilateral or unilateral?
1. immunocompromised (AIDS pts)
3. unlike ARN, posterior pole involvement is common and there is minimal vitreous inflammation
4. bilateral is more common
1. What are the three variants of CMV retinitis?
2. What can CMV retinitis look like very early on?
3. What distinguishes CMV histologically?
4. How do you treat it?
1. - classic/fulminant: large areas of retinal hemorrhage over whitened/edematous retina in the posterior pole
- granular/indolent: peripheral retinitis with little or no retinal edema
- perivascular: "frosted-branch" angitis
2. a cotton wool spot
3. eosinophilic intranuclear inclusions and small basophilic cytoplasmic inclusions
4. systemic and intravitreal ganciclovir or foscarnet
1. What is the most common finding in congenital rubella?
2. What is the most common ocular finding?
3. What are 2 other common eye findings?
4. What ocular disease might be related to acquired rubella infection?
1. hearing loss
2. pigmentary retinopathy (but it is often asymptomatic)... "salt and pepper" fundus
3. cataracts and glaucoma
4. Fuchs heterochromic uveitis
1. What eye findings can you see in congenital measles?
2. What is the most common eye finding in acquired measles?
3. What is measles retinopathy?
4. What eye finding can be seen in patients with subacute sclerosis pan encephalitis?
1. congenital: cataract, optic nerve drusen, bilateral pigmentary retinopathy (but vision is typically normal)
2. acquired: keratitis and conjunctivitis
3. profound loss of vision within 1-2 weeks of the rash, diffuse retinal edema with macular star, scattered hemes and blurred disc margins... vision often improves, but they often are left with field defects
4. maculopathy with focal retinitis and RPE changes
1. Describe the typical eye findings in West Nile virus.
2. How do the lesions appear on FANG?
3. What is the prognosis?
1. photophobia, redness and a multifocal chorioretinitis with anterior uveitis and vitritis
2. FANG: lesions are target like with central hypofluroescence and peripheral hyperfloruescence
3. eye findings are usually self-limiting and pts regain normal vision
1. What causes Rift Valley fever?
2. What eye findings can it cause?
3. What is the prognosis?
1. bunyaviridae... you get it from contact with animal blood/organs (often during slaughter or domestic farm animals)
2. bilateral macular retinitis with hemorrhages and often leads to macular scars
1. What is HTLV-1?
2. What is the most common eye finding?
3. How do you treat it?
1. human t-lymphotrophic virus type 1
2. intermediate uveitis (so prominent vitritis)
3. typically responds very well to steroids and resolves in 1-2 months (but many patients have a recurrence)
1. What is the most common eye finding in dengue fever?
2. What is the most common eye finding in Chikungunya fever?
1. petechial subconjunctival hemorrhages
2. anterior uveitis and retinitis
1. How do you diagnosis ocular histoplasmosis syndrome?
2. What is the average age of symptomatic patients with OHS?
3. HLA associations?
4. Why is it sometimes called "presumed OHS"?
1. classic triad of multiple white and atrophic scars, peripapillar pigment changes and a maculopathy with CNV and no vitreous cells
2. 41 years old
3. HLA-B7 and HLA-DRw2
4. because it has never been definitely linked to histoplasmosis, but it is seen exclusively in patients who test positive for histoplasmosis and is super common in endemic areas
1. What is the most common cause of infectious posterior uveitis in adults and children?
2. What is the classic triad of congenital toxoplasmosis?
3. What is the most common finding in congenital toxoplasmosis?
2. retinochoroiditis, hydrocephalus and intracranial calcifications
3. retinal lesions, which are usually bilateral and in the posterior pole
1. Describe the classic appearance of retinal lesions in toxoplasmosis.
2. How does it differ in an immunocompromised patient?
3. When do you need to treat ocular toxoplasmosis?
4. What is triple therapy?
5. What do you add for quadruple therapy?
6. What is an alternative to triple therapy?
7. What can you give to pregnant patients to reduce risk of transmission?
1. focal, white lesions with overlying vitreous inflammation creating a "headlights in the fog" appearance that is often adjacent to a chorioretinal scar
2. immunocompromised patients are more likely to have multiple and or bilateral lesions without an associated scar
3. - lesions near the optic nerve or fovea
- decreased vision
- lesions associated with severe vitreous inflammation
- lesions >1DD in size
- persistence of activity for >1 month
- multiple active lesions
- immunocompromised pts, pregnant patients or congenital disease
4. pyrimethamine, sulfadiazine, prednisone (+folinic acid to prevent myelosuppression)
5. add clindamycin for quadruple therapy
6. Bactrim and prednisone (cheaper and easier to get)
1. What is the average age of a patient with ocular toxocariasis?
2. What is the typical presentation?
3. How do you diagnose it?
4. How do you treat?
1. 11 years old
2. unilateral decrease in vision with with photophobia, floaters or leukocoria; little to no anterior inflammation; pts typically have a granuloma somewhere
3. diagnosed clinically... can get ELISA testing but up to 1/3 of patients may have false negative ELISA
4. steroids to control inflammation, antihelminithic treatment hasn't been proven
1. What is the most common organ affected by cysticercosis?
2. What is the general age at presentation?
3. How does it commonly present?
4. What is pathognomonic?
5. What do you see on B-scan?
6. How do you treat it?
1. the eye!
2. 10-30 years old
3. unilateral vision loss with a globular, translucent cyst in the sub retinal space that moves in response to the exam light
4. motile worm in the anterior chamber
5. sonolucent zone with a well defined posterior and anterior margin
6. surgical removal of the worm and any larvae from the vitreous and sub retinal space... if left untreated, very poor prognosis
1. What is DUSN?
2. What are the two causative organisms?
3. How does it present?
4. How do you treat it?
1. diffuse unilateral subacute neuroretinitis
2. dog hook worm (ancylostoma caninum) and raccoon roundworm (baylisascaris procyonis)
3. insidious onset of unilateral loss of vision from recurrent episodes of focal, multifocal and diffuse inflammation of the retina, RPE and optic nerve and then you visualize a worm in the sub retinal space
4. zap the worm with a laser
1. Where is onchocerciasis most prevalent?
2. What is its impact in hyper endemic areas?
3. What are the common ocular findings?
4. How do you treat it and how well does treatment work?
5. Why might you also treat with doxycycline?
1. sub-Saharan africa and isolated area in central/South America
2. in hyper endemic areas, everyone over the age of 15 is infected and half of people will go blind before they die
3. microfilariae swimming in the A/c; punctate corneal stroll opacities; chorioretinal lesions and can get ocular inflammation from dead microfilariae
4. ivermectin.... will slow progression of vision loss, but does not stop new retinal lesions from forming or resolve old lesions
5. the worm can be infected with a bacteria (Wolbachia) that is necessary for sexual development, so if you treat with doxycycline you can kill the bacteria and prevent the worm from reproducing
1. What eye problems can congenital syphilis cause?
2. What is a common sign of untreated congenital syphilis?
3. What is the Hutchinson triad?
1. uveitis, optic neuritis, glaucoma, congenital cataracts and a chorioretinitis that leads to a "salt and pepper" fundus
2. non ulcerative stromal interstitial keratitis often develops if left untreated... you see ghost vessels and stromal opacities
3. Hutchinson triad: interstitial keratitis, CN8 deafness and hutchinson teeth
1. A patient with acquired ocular syphilis must be treated as if they have _____.
2. What are the most common anterior segment findings of ocular syphilis?
3. What are the most common posterior segment findings of ocular syphilis?
4. How do you diagnose syphilis?
5. How do you treat ocular syphilis?
1. ocular syphilis = neurosyphilis
2. anterior segment: iris nodules, uveitis, interstitial keratitis
3. posterior segment: chorioretinitis (including macular star neuroretinitis) with some amount of vitritis... can also get posterior placoid chorioretinits
4. diagnosis requires positive syphilitic antibody testing (FTA-ABS or T palladium antibodies) and then RPR titers can be used to monitor disease activity
5. IV penicillin G
1. What is the most common initial ocular finding of Lyme disease?
2. When does uveitis tend to occur during the course of Lyme disease?
3. What retinal findings can you see in Lyme disease?
4. A patient with Lyme disease and ocular findings needs what?
5. How do you treat Lyme disease?
1. stage 1 = follicular conjunctivitis
2. uveitis tends to occur during stage 2 and is generally intermediate uveitis
3. Lyme disease can cause a peripheral multifocal choroiditis with punched out lesions associated with vitiritis
4. LP to look for neurologic involvement
5. most common drugs are amoxicillin, doxycycline and cefuroxime
1. Who is at risk for leptospirosis?
2. Where do most of the cases in the US occur?
3. What is the most common ocular sign?
4. When does it present?
5. How do you treat it?
1. swimmers, veterinarians, fish workers, agricultural workers, slaughterhouse workers
3.. circumcorneal conjunctival hyperemia (which is pathognomonic)
4. there can be a prolonged interval between systemic and ocular disease
5. IV penicillin or PO doxycycline
1. What is the most common site in the eye to find TB and why?
2. What is primary ocular TB?
3. What is secondary ocular TB?
4. How does uveitis 2/2 TB present?
5. What does TB cause in the retina?
6. What is Eales disease?
1. the choroid b/c TB loves oxygen rich environments
2. primary: TB in which the eye is the primary portal of entry
3. secondary: caused by hematogenous spread.... most commonly presents as uveitis
4. waxing and waning course with granulmonatous mutton fat KPs, iris nodules and posterior synechiae
5. disseminated choroiditis with multiple deep, discrete, yellow lesions measuring b/t 0.5 and 3mm
6. Eales disease is a peripheral retinal perivasculitis in men 20-40 with recurrent, unilateral retinal and vitreous hemorrhage that then spreads to the other eye
1. What is the most common cause of neuroretinitis with macular star?
2. Is it unilateral or bilateral?
3. How do you treat it?
1. bartonella (cat scratch)
2. usually unilateral
3. generally treat with antibiotics (doxycycline or something similar), but there is no evidence for this
1. On average when does chronic post-operative endophthalmitis present?
2. What is the most common organism?
3. What might you see on exam? Histology?
4. What clinical cues might help you make the diagnosis?
5. How does chronic post-operative fungal endophthalmitis differ?
1. 3-4 months post op
3. whitish plaques between the lens implant and posterior capsule... histologically you see colonies of bacteria there
4. inflammation that initially responds to steroids, but then quickly worsens after they are stopped or inflammation triggered after yag capsulotomy
5. - inflammation will not improve with steroids
- may have corneal involvement or iris mass
- organism is Candida parapsilosis or aspergillum flavus
6. vitrectomy is diagnostic and therapeutic
1. What are the main risk factors for endogenous endophthalmitis?
2. What is the most common cause of endogenous endophthalmitis in Asia?
3. What do you see on exam?
4. How do you diagnose?
1. immunocompromised pts; recent GI surgery, dental procedures or endoscopy
2. Klebsiella from liver abscesses
3. periorbital edema, fibrin or hypopyon in the A/c, vitreous cell, lesions or Roth spots in the retina
4. Can do AC tap or vitreous tap
1. What is the most common cause of fungal endogenous endophthalmitis?
2. How common is it?
3. What are common risk factors?
4. What do you see on exam?
5. How do you treat?
2. Occurs in ~1/3 pts with candidemia not on treatment (about 3% of patients on treatment)
3. Gi surgery, systemic antibiotics, indwelling catheters, TPN, immunosuppression
4. multiple, bilateral, white well circumscribed lesions, <1mm across with overlying vitreous inflammation
5. - if no vitreous involvement, systemic antifungals
- if vitreous involvement, likely need intravitreal antifungals
1. What is the most common scenario you see endogenous aspergillus endophthalmitis?
2. What do you see clinically?
3. How do you treat?
1. pts who have had liver transplant
2. rapid onset of pain and vision loss with yellow infiltrates in the macula that begins in the choroid and sub retinal space
3. vitrectomy with intravitreal amphotericin or voriconazole
1. What is the most common cause of fungal eye infection in HIV/AIDS patients?
2. What is the most common ocular presentation of this infection?
1. crypto coccus
2. multifocal chorioretinitis with multiple yellow-white lesions in the posterior fundus that vary markedly in size
3. intravenous amphotericine or oral flucytosine
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