Académique Documents
Professionnel Documents
Culture Documents
Blurred vision
Visual acuity ranges from 20/20 to no perception of light, with a mean range of 20/4020/50
Cataracts
Vitreous debris
CME
Pars planitis is typically bilateral, with both eyes affected in 85% of the cases
Seems to have an association with Crohns disease and, especially, multiple sclerosis
45% positive association with between pars planitis and multiple sclerosis. You must give
strong consideration to ordering MRI of the brain in patients with pars planitis, especially
if the patient is in a high risk group
Vitreal cells
Retinal inflammatory exudates (snowballs) and periphlebitis
Inferior snowbanking of exudates
While vitreous snowballs and snow banks are frequently encountered, they are by no
means present in every eye with pars planitis and need not be present to make this
diagnosis
Exacerbations and remissions
May last for years
Generally benign
Treatment should be conservative and often involves only periodic monitoring, especially
if vision is only minimally disturbed by vitritis and CME
This disease has a good prognosis with a final mean visual acuity for patients of 20/3020/40 in 90% of cases
There are exacerbations and remissions and typically this disorder runs a very long
course. Inflammatory mediators will increase vasopermeability of retinal capillaries
resulting in posterior segment inflammatory cells as well as CME.
Clinical Pearl: When encountering a true PVD in a young patient, look for vitreal cells and
other signs of pars planitis.
Toxoplasmosis
Number one cause of posterior uveitis
Number one cause of focal chorioretinitis
Caused by toxoplasma gondii
Obligate intracellular protozoan parasite
Retinal
Hematogenous spread to eye
Neural
Congenital- passed from mother to child transplacentally after acquiring it during pregnancy
Most common mode of transmission
40% likelihood of fetal involvement
Acquired (must consider AIDS)
HIV testing needed
Often without associated scarring
Cat feces and undercooked meat are vectors
Sporozoite (cat)
Tachyzoit (proliferative form in humans)
Bradyzoit (encysted and dormant)
Bradyzoit sits in the NFL
Bradyzoit usually sit near old scars and may remain viable for 25 yrs
Immunosuppression can reactivate a bradyzoit
May spontaneously reactivate without immunosuppression
When active, toxoplasmosis produces a retinitis that appears as
" Headlights in a fog " due to overlying focal vitritis
Arteritis
Periphlebitis
Lesions heal within 3 weeks to 6 months
Affects the posterior pole
Vitritis usually located near an old scar- diagnostic
3
Inhaled fungus
Inhaled mycelial spores of Histoplasma capsulatum
These spores undergo transformation to the yeast phase in the lung, and from here it is
disseminated via the bloodstream to the rest of the body (including the eye where it causes
choroidal infection)
Flu-like illness
Retinal lesions reactivate 10-30 yrs later
Affects ages 20-50
Rare in patients of African descent
Circumpapillary choroidal scarring
Peripheral atrophic Histo spots & peripheral scars
Punched-out lesions
Large (1 DD) or small
Hypo- or-hyperpigmented
Foci of previously present inflammatory reaction
Site of infection with Histoplasma organism
Macular compromise
Granulomatous inflammatory mass
Diagnosis is made by presence of peripapillary scarring and at least one peripheral Histo spot
Invisible choroiditis
Not a fundus finding because it is not visible. May possibly be seen on FA
Due to an accumulation of inflammatory cells at an inflammatory focus
Will eventually result in an atrophic Histo spot
choroidopathy with one exception: OHS never causes cells to appear in the vitreous
because it is purely a choroiditis.
Clinical Pearl: Many peripheral spots look like Histo spots. To confirm the suspected
diagnosis in these cases, look for associated peripapillary scarring.
Ocular Histoplasmosis Syndrome: Treatment
Routine f/u when inactive
Home amsler to monitor for neovascularization
Oral, depot steroids when active
Some advocate that steroids are ineffective
Photocoagulation for juxtafoveal neo
Laser tx is mainstay for Histo
30% recurrence rate for neo regrowth
Risk factors are younger age and females
Neo can spontaneously involute without treatment
PDT commonly used
Anti-angiogenic drugs are used as well
60% of untreated patients develop 20/200 or worse vision
30% chance of fellow eye involvement within 7 yrs
Clinical Pearl: Treatment isnt directed at the cause of Histoplasmosis, but rather at the
neovascular maculopathy using standard methods.
Sarcoidosis
Idiopathic disseminated granulomatous disease
Non-caseating granulomas
May have lid and conjunctival granuloma
Multisystemic
Females > males
Blacks >>> Whites
Ages 20-60 yrs
Sarcoidosis: Ocular Manifestations
Keratoconjunctivitis sicca with lacrimal gland involvement by granuloma
Granulomatous anterior uveitis
Mutton fat KPs and posterior synechiae
Periphlebitis
Candlewax drippings
More common than retinal granulomas
Adjacent puff balls
7
Vitritis/retinitis
Peripheral vascular occlusion and neovascularization
CME
From inflammation
Optic neuropathy
Inflammatory, infiltrative, or compressive optic neuropathy
Disc edema
Sarcoidosis: Diagnosis
Hilar adenopathy (enlarged pulmonary lymph nodes) on chest x-ray (CXR)
Angiotensin converting enzyme (ACE)
Gallium scan
Uptake of gallium only in sarcoidosis after gallium is injected into venous system (uptake
in salivary and lacrimal glands and hilar lymph nodes)
Conjunctival biopsy or biopsy of skin granulomas
Sarcoidosis: Treatment
Recognition of sarcoid in differential diagnosis
Oral steroids and Periocular steroids
Clinical Pearl: Sarcoidosis should be high on your list of differential diagnoses when
encountering retinal periphlebitis.
Eales' Disease
Difficult to classify
Vascular occlusion secondary to posterior segment inflammation
Retinal periphlebitis
Idiopathic bilateral periphlebitis affecting retinal veins
Healthy young men in 20's-30's
25% have hearing/balance difficulties
Patient may complain of floaters, but is typically asymptomatic early in the disease
Possibly with associated anterior uveitis
Obscure inflammatory reaction to antigens
High association to tuberculoprotein sensitivity
Retinal findings include perivascular sheathing and capillary non-perfusion
Sufficient capillary non-perfusion can lead to retinal neovascularization with attendant
complications
Vitritis occurs overlying periphlebitis
Retinal telangiectasias may occur with resultant retinal/macular edema
Vision reduction can come from retinal/macular edema, vitreous hemorrhage, tractional retinal
detachment
8
Clinical Pearl: Whenever you see retinal periphlebitis, vasculitis, or candlewax drippings,
immediately think of sarcoidosis and syphilis.
Behcets Syndrome:
Painful aphthous oral/genital ulcers
Arthritis
Conjunctivitis, anterior uveitis
Endophthalmiitis
Arteritis
Periphlebitis
Necrotizing retinitis
Retinal edema, exudation
Endophthalmitis
Post-surgical
Post-penetrating foreign body
Indwelling catheter as portal of entry for microbes
Rarely endogenous
Fungi
Extremely inflamed eye
Hypopyon
Staphylococcus; streptococcus; pseudomonas
Poor prognosis
Intravitreal injections of antibiotics
Eye may be totally lost
Birdshot Retinochoroidopathy
Vitiliginous
Chronic disease in healthy middle-aged patients (females)
Bilateral decreased vision (20/50).
Floaters, blurred vision, nyctalopia, field defects
Multiple depigmented, creamy spots in posterior pole following vessels
When fresh, there is substance, but becomes more atrophic later
RPE hyperpigmentation
Chronic lesions can become confluent and spread to the macula
Vitritis
Disc edema
Retinal vasculitis
Epiretinal membrane formation
CME
Autoimmune disease
(+) HLA A29 highly correlated
Oral steroids
NVD; NVE
FA: filling delay and vessel leakage.
Prognosis is poor due to chronicity
11
12