1 / 24

Clinicopathologic Case

This case study discusses a 69-year-old African American female with a history of idiopathic intraocular inflammation. The patient developed advanced glaucoma and underwent enucleation. The case highlights ciliary body depigmentation, dislocated IOL, cobblestone degeneration, macular edema, thickened ciliary body epithelial basement membrane, neovascularization, chronic uveitis, chronic keratoconjunctivitis, keratic precipitates, chronic iritis, chronic choroiditis, retinal vasculitis, peripheral anterior synechiae, optic nerve cupping, and glaucoma.

leday
Download Presentation

Clinicopathologic Case

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. Clinicopathologic Case Ravi Patel MD MBA Julia Kofler MD Charleen Chu MD PhD

  2. 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)

  3. Ciliary Body Depigmentation - Likely due to previous cyclophotocoagulation DISLOCATED IOL

  4. Found in 27% of population, not believed to be clinically significant Cobblestone Degeneration

  5. Extensive Optic Nerve Cupping Vascular Sheathing

  6. Vascular Sheathing/Frosting Macular Edema

  7. 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)

  8. 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

  9. 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.

  10. Neovascularization of Iris Thin fibrovascular membrane on anterior iris surface

  11. 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

  12. 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

  13. Chronic Keratoconjunctivitis Chronic lymphocytic infiltrate into conjunctival epithelium, usually nonkeratinized stratified squamous epithelium

  14. Keratic Precipitates Inflammatory aggregates on corneal endothelium

  15. Chronic Iritis Chronic lymphocytic infiltrate into iris stroma

  16. Chronic Choroiditis Mononuclear cells “small blue cells”

  17. Retinal Vasculitis Lymphoplasmacytic Perivascular Inflammation

  18. 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

  19. 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

  20. Peripheral Anterior Synechiae Segment represented by peripheral adhesion of iris tissue to cornea

  21. Optic Nerve Cupping Paucity of Ganglion Cells Large Cup Posterior Bowing of Lamina Cribosa

  22. 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

  23. 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.

  24. Diagnosis: SECONDARY GLAUCOMA WITH INFLAMMATORY AND NEOVASCULAR CONTRIBUTIONSContributing factors: Idiopathic chronic panophthalmitis Hypertension

More Related