Clinicopathologic Case - University of Pittsburgh

Report
Clinicopathologic Case
Ravi Patel MD MBA
Julia 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)
Ciliary Body
Depigmentation
- Likely due to previous
cyclophotocoagulation
DISLOCATED IOL
Found in
27% of
population,
not believed
to be
clinically
significant
Cobblestone
Degeneration
Extensive
Optic Nerve
Cupping
Vascular Sheathing
Vascular
Sheathing/Frosting
Macular
Edema
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 stain
Usually 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 antiVEGF 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
Paucity of
Ganglion Cells
Large Cup
Posterior Bowing of
Lamina Cribosa
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.
Diagnosis:
SECONDARY GLAUCOMA WITH
INFLAMMATORY AND NEOVASCULAR
CONTRIBUTIONS
Contributing factors:
Idiopathic chronic panophthalmitis
Hypertension

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