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Clinicopathologic Case
Ravi Patel MD MBAJulia Kofler MD
Charleen Chu MD PhD
Brief History
• 69 year old African American Female• Patient had extensive history of idiopathic
intraocular inflammation. • She progressed to where her vision was NLP from
advanced glaucoma• Initially 180 degrees of cyclophotocoagulation
was attempted without reduction of pressure• Eye then became painful and patient elected to
proceed with enucleation (PHS09-28620)
DISLOCATED IOL
Ciliary Body Depigmentation- Likely due to previous cyclophotocoagulation
Cobblestone Degeneration
Found in 27% of population, not believed to be clinically significant
Vascular Sheathing
Extensive Optic Nerve Cupping
Macular Edema
Vascular Sheathing/Frosting
Discussion- Macular Edema• Most commonly caused by retinal vascular
disease from diabetes, hypertension and venous occlusive disease.
• In this patient it is most likely from chronic intraocular inflammation as macular edema is a well known complication of uveitis
• Other less common etiologies of macular edema include papilledema, choroidal neovascular membrane, macular degeneration, retinitis pigmentosa, toxic maculopathy, post-operative (Irwin-Gass Syndrome)
Treatment – Macular Edema
• Widely accepted is focal/grid photocoagulation
• Also accepted therapy is topical, periocular, intraocular or even systemic corticosteroids
• There is emerging evidence to suggest efficacy of intravitreal anti-VEGF therapy (bevacizumab)
• As a final resort, vitrectomy surgery is considered
Thickened Ciliary Body Epithelial Basement Membrane
Highlighted by PAS stainUsually this membrane is barely visible.
Becomes more prominent in inflammatory conditions, and more commonly diabetes mellitus.
Neovascularization of Iris
Thin fibrovascular membrane on anterior iris surface
Discussion - Neovascularization• Usually a sequellae of retinal ischemia, now
thought to be VEGF mediated• Commonly associated with diabetes mellitus,
venous occlusive disease, carotid occlusive disease
• Less commonly due to chronic intraocular inflammation, sickle cell disease, intraocular neoplasm, ROP, uveitis-glaucoma-hyphema syndrome
• There is evidence to suggest treatment with anti-VEGF therapy and panretinal photocoagulation
Treatment-Neovascularization• Optimal therapy is to control the underlying
disease• Ocular therapy revolves around improving
oxygenation and reducing oxygen demand• Customarily panretinal photocoagulation is
employed• Extrapolating from studies of macular
degeneration patients with choroidal neovascularization, intravitreal anti-VEGF therapy has been helpful in promoting regression of neovascularization
Chronic Keratoconjunctivitis
Chronic lymphocytic infiltrate into conjunctival epithelium, usually nonkeratinized stratified squamous epithelium
Keratic Precipitates
Inflammatory aggregates on corneal endothelium
Chronic Iritis
Chronic lymphocytic infiltrate into iris stroma
Chronic Choroiditis
Mononuclear cells “small blue cells”
Retinal Vasculitis
Lymphoplasmacytic Perivascular Inflammation
Discussion - Uveitis
• Any intraocular inflammation involving uveal tissue (iris, ciliary body, choroid) is termed uveitis. Disease is classified by which layers are affected, and chronicity.
• This is a multi-factorial disease which can be:– Secondary to systemic infection– Noninfectious from systemic inflammatory
disease– Idiopathic
Treatment - Uveitis
• Infectious Uveitis involves treating the underlying infection along with supportive periocular therapy
• Noninfectious Uveitis is usually managed using topical steroids and cycloplegics.– Recurrent episodes or posterior uveitis typically
involves the use of periocular or systemic immunosuppression
Peripheral Anterior Synechiae
Segment represented by peripheral adhesion of iris tissue to cornea
Optic Nerve Cupping
Posterior Bowing of Lamina Cribosa
Large Cup
Paucity of Ganglion Cells
Discussion - Glaucoma
• Secondary Angle Closure Glaucoma– Due to neovascularization– Due to intraocular inflammation
• Accepted theory is a fibrovascular membrane that “zips up” the angle thereby producing a resistance to aqueous outflow
Treatment - Glaucoma
• Topical antiglaucoma therapy is often employed (caution is used to avoid miotics and prostaglandin analogues as they can exacerbate inflammation)
• Second line therapy usually involve insertion of setons as trabeculectomies are subject to a high rate of failure.
SECONDARY GLAUCOMA WITH INFLAMMATORY AND NEOVASCULAR CONTRIBUTIONS
Contributing factors:Idiopathic chronic panophthalmitis
Hypertension
Diagnosis: