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Signs & Symptoms of Posterior Uveitis
 Blurred vision
 Floaters
 Pain and photophobia seen in anterior uveitis is not likely to occur
 Minimal anterior segment inflammation (if any at all)
 External eye typically white and quiet, depending upon etiology
 Anterior uveitis
 Typically asymptomatic spill-over from posterior chamber
 Occasionally granulomatous
 Vitritis
 Infiltrates
 Vascular sheathing
 Candlewax drippings
 Retinal scarring and RPE hyperplasia
 Fuzzy fundus lesions
 Inflammatory cell aggregation
 Snow balls and snow banks
 Periphlebitis
 Peripheral retinal neovascularization with attendant complications
 CME
 Retinitis
 Chorioretinitis
 Choroiditis
Types of Posterior Uveitis
 Traumatic/ surgical
 Infectious (syphilis, toxoplasmosis, etc)
 Infiltrative (sarcoidosis)
 Idiopathic (pars planitis)
Pars Planitis
 True intermediate/ posterior uveitis
 Chronic
 Bilateral
 Younger patients
 Vitreal cells
 May be asymptomatic
 Blurred vision
 Cataracts
 Vitreous debris
 CME
 Retinal inflammatory exudates (snowballs) and periphlebitis
 Inferior snowbanking of exudates
 Exacerbations and remissions
 Generally benign
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May last for years
Pars Planitis: Complications
 Posterior subcapsular cataracts (both from the disease itself and the treatment)
 Posterior vitreous detachment
 Frequent cause of rare PVD in young patients
 Neovascularization (mostly posterior segment)
 Attendant complications of vitreous hemorrhage and tractional RD
 Glaucoma (steroid induced, POAG, secondary inflammatory)
Pars Planitis: Treatment
 Observation
 Cyclocryotherapy
 To destroy the inflamed areas and infiltrates
 Removes antigenic material?
 Vitrectomy
 Oral steroids
 Must make commitment to treat for months
 Sub-tenon and intravitreal steroids
 Topical steroids only if there is concomitant anterior inflammation
 Anterior uveitis in pars planitis is not true anterior uveitis, but a spill over from the
posterior segment. These patients are typically asymptomatic.
 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
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)
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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
 Encystic organisms latent near old scar
Toxoplasmosis: Ocular Findings
 PVD
 CME
 Retinochoroiditis
 Scarring
 Arteritis
 Vasculitis
 Papillitis (totally destroys vision)
 Vitritis
 RD
Toxoplasmosis: Other Thoughts
 Activity for 4-6 months
 Diagnosed by ELISA Toxoplasmosis titre
 Self limiting, but often treated
 Lesions which must be treated include large lesions (> 3DD), severe vitritis with vision
loss, and juxtafoveal or peripapillary lesions
 Results in chorioretinal scarring which may be visually disabling
Toxoplasmosis: Treatment
 Often simply monitored if vision not threatened and patient has healthy immune system (i.e.,
Not HIV/AIDS)
 Triple sulfonamide drugs
 Sulfadiazine 1 gm PO QID or Bactrim (trimethoprim 160 mg/sulfamethoxazole- 1 double
Strength or 2 tabs BID) x 6 weeks (most common treatment)
 Bactrim DS every third day has shown to significantly reduce ocular toxoplasmosis
recurrences.
 Pyrimethamine (Daraprim- anti-parasitic)
 Causes bone marrow suppression which can be averted with folic acid supplementation
 25 mg PO QD x 6 weeks with Folic acid 5 mg Q2 days
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Clindamycin 250 mg QID
 Toxic and can cause colitis
 Spiramycin
Steroids
 Prednisone 40 mg QD (only use prednisone in conjunction with the above meds- never
alone). Begin antimicrobial therapy for a few days first. Generally not used unless vision
significantly threatened.
Clinical Pearl: Though we have long known how to treat toxoplasmosis, it is not clear that
we should treat toxoplasmosis. There is a lack of evidence based medicine that identifies
treatment benefits. Controlled studies are clearly needed.
Clinical Pearl: Not every black spot on the retina is a toxoplasmosis scar, despite what
other optometrists tell you.
Clinical Pearl: The key diagnostic sign of toxoplasmosis is an active vitritis with a
"headlights in a fog appearance" adjacent to an area of old scarring.
Clinical Pearl: When encountering active toxoplasmosis, especially in a young patient,
strongly consider HIV testing.
Toxocariasis
 Nematode - parasitic
 Puppies, eating dirt (geophagia), eating fecal matter (coprophagia) are the vectors
 Occurs in children and is usually unilateral
 Larvae travel in blood and lymph fluid
 Two forms: Never seen together
1. Ocular
 Ages 7-8
 Neuroretinitis
 Vitritis
 Papillitis
 RPE changes
 Elevated granuloma
 Decreased vision
 Leukocoria
 Chronic endophthalmitis
2. Systemic
 Ages 2-5
 ELISA
 Photocoagulation; cryo
 Corticosteroids (oral) for inflammation
 Closely related is the disease caused by the blackfly- onchocerciasis
Ocular Histoplasmosis Syndrome
 Fungal disease: Histoplasma capsulatum
 Associated with bird (pigeon, chicken) feces
 Actually in soil fertilized by bird feces
 Actually found in bat feces
 Ohio - Mississippi River Valley (or any river valley region)
 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
Ocular Histoplasmosis Syndrome: Maculopathy
 Macular granuloma
 Bruch's disruption
 Choroidal neovascularization
 4th most common cause of CNVM
 Sub-RPE hemorrhage with subsequent disciform scarring
 Lipid exudate
 Differential diagnosis
 Multifocal choroidopathy
 Acute posterior multifocal placoid pigment
 Multiple evanescent white dot syndrome
 Retinal pigment epithelialitis
 Serpiginous choroiditis
 Diffuse unilateral subacute neuroretinitis
Clinical Pearl: Ocular Histoplasmosis Syndrome can look exactly like multifocal
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 isn’t directed at the cause of Histoplasmosis, but rather at the
neovascular maculopathy using standard methods.
Clinical Pearl: There are posterior uveitic syndromes such as toxoplasmosis and some
white dot syndromes that are visually recognizable. However, the majority of posterior
uveitis syndromes present with signs and symptoms of posterior inflammation which do not
necessarily identify the causative condition.