peripheral corneal ulcers and corneal degenerations

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  1. 1. Dr.Puneeth Isloor
  2. 2. DEGENERATIONS DYSTROPHY Peripherally located most often Centrally located Asymmetric Bilateral and symmetric Older age group Young age Progression could be slow or rapid Progression is slow Not inherited Corneal vascularisation Inherited No vascularisation Corneal degenerations refer to the conditions in which the normal cells undergo degenerative changes under the influence of age or some pathologic condition
  3. 3. CLASSIFICATION - BASED ON TYPE OF MATERIAL DEPOSITED SCARRING -Pannus -Epithelial basement membrane degeneration -Corneal guttae -Retrocorneal fibrous mebrane LIPID -Corneal Arcus -Primary Lipid degenerations -Lipid degeneration from vascularisation CALCIUM -Calcific band keratopathy -Focal degenerative calcification -Toxic medications -Calcareous degeneration DROPLET KERATOPATHY CORNEAL AMYLOIDOSIS OTHER DEGENERATIONS DEGENERATIVE CORNEAL THINNING Primary Secondary Polymorphic Amyloid stromal Degenerations Secondary amyloid degeneration Limbal girdle of Vogt Mosaic keratopathy White ring of coats Terrien s Marginal degeneration Age related marginal furrow
  4. 4. Epithelium and basement membrane Bowmans Layer Epithelial basement membrane degeneration - Pannus ,Pterygium - Salzmanns Nodular degeneration - Corneal arcus - Calcific Band keratopathy - Limbal girdle of Vogt - Nodular amyloid - Climatic droplet keratopathy - White ring of coats STROMA ENDOTHELIUM AND DESCEMETS MEMBRANE -Scarring with or without vascularisation -Lipid degeneration -Polymorphic amyloid degeneration -Crocodile shagreen -Pre descemets filiform -Cornea farinata -Terrien s Marginal degeneration - Corneal arcus - Posterior collagenous layer -Cornea guttae -Hassal henle warts -Retrocorneal fibrous membrane CLASSIFICATION BASED ON LAYER MOST PROMINENTLY INVOLVED
  5. 5. CORNEAL SCARRING AND VASCULARISATION -Avascular Scar -Vascular Scar AVASCULAR SCARRING - Density graded as - Trace Barely visible - Mild A cloud like nebular opacity - Moderate Macular opacity - Severe White leukomatous opacity - Scarring can occur at 3 levels - Subepithelial Post Excimer laser - Stromal Post microbial keratitis - Descemets membrane interstitial keratitis
  6. 6. Management For vascularisation - If peripheral intervention not necessary -Laser photocoagulation To decrease lipid leak into stroma To close large stromal vessels before PKP - For Scars - If scar is anterior to Bowmans layer Mechanical scraping or peeling can be done. - Anterior 2/3 of stroma Lamellar keratoplasty - Full thickness scarring Penetrating keratoplasty
  7. 7. EPITHELIAL BASEMENT MEMBRANE DEGENERATION - Map dot fingerprint changes in the epithelium and basement membrane - Occurs in aged - Due to abnormal synthesis of Basement membrane by the aging corneal epithelium - Faint gray Map like subepithelial patches - most common superiorly
  8. 8. - Each Map has one distinct edge and fades off at the other edge Coastline appearance. - Fingerprints Fine refractile parallel short lines in the cornea tram lines or gray mare s tail - Tear film thin over the maps.Does not stain on fluorescein
  9. 9. Note the central epithelial basement membrane dystrophy (EBMD) in the visual axis of the right eye (left). In the left eye, note the trace paracentral EBMD (right).
  10. 10. HISTOPATH -Thickening of the basement membrane gray map - B.M within epithelium --- blocks desquamation-- -- traps cells intraepithelially -- Necrosis ---- Cogan s microcysts - Subtle folds of the BM with fibrillogranular material fingerprints - CLINICAL - Irregular astigmatism -Recurrent epithelial erosions -Dry eye symptoms-particularly when there is increased evaporation of tear
  11. 11. Management - Symptomatic patients - Lubricants - Peeling- In patients with astigmatism and recurrent epithelial erosions. can be done with a surgical blade A gentle sweep towards the Limbus The limbal stem cells can differentiate into normal epithelial cells that produce normal BM.
  12. 12. SALZMANN NODULAR DEGENERATION - Non specific corneal response to chronic insult such as Phlyctenulosis,Trachoma and VKC - 3 groups - Asymptomatic - Symptomatic with foreign body sensation - Nodules overlying pupil with reduced visual acuity - Focal , discrete ,avascular ,circular ,gray white,elevated opacities located subepithelial - unilateral - Overlie areas of stromal scarring and vascularisation - Persist after the inflammation has subsided - Refractile on retroillumination PAS positive material
  13. 13. SALZMANN S NODULAR SPHEROIDAL DEGENERATION Gray white peripheral opacities Golden yellow Focal and discrete Multiple and confluent Unilateral in 80% cases Bilateral
  14. 14. HISTOPATHOLOGY - PAS positive material deposited between epithelium and Bowman s membrane- originating from damaged stromal fibrocytes - Overlying epithelium is thin--- recurrent epithelial breakdown stimulates further deposition of PAS Irritation and Foreign body sensation - IHC staining demonstrates decrease in adhesion molecules - Collagen present between E and BM creates surgical cleavage plane during peeling
  15. 15. epithelial denudation as shown above (arrow 1), destruction of Bowmans layer(arrow2)
  16. 16. MANAGEMENT - Asymptomatic nodules no treatment - Symptomatic Scraping along the edge of the nodule until it lifts and peels off - Excimer laser can be used to remove the superficial scarring - Lamellar or penetrating keratoplasty if underlying corneal opacification and vascularisation is severe
  17. 17. LIPID DEGENERATIONS PATHOGENESIS - Can be Primary/Idiopathic - - Secondary to corneal vascularisation - Its a Vicious cycle Lipids leak from corneal vessels Lipid phagocytosis by keratocytes and macrophages Mild chronic inflammatory response Continued Neovascularisat ion
  18. 18. CORNEAL VESSELS AND LIPID DEPOSITS The lipid deposits leave a clear zone around the vessels ---Lucid interval in Arcus Lipid deposits In deep stromal keratitis -- deep vessels are invisible-- but the clear zones around these vessels --- appear like snail tracks HISTOPATH OF LIPID DEPOSITS - Central portion of the deposit is a dense yellow mass with spiculated edges -There is intracellular and extracellular lipid - Lipid laden macrophages and keratocytes
  19. 19. CORNEAL ARCUS - Most common peripheral corneal opacity - Annular deposit of lipid parallel to corneal limbus- cholesterol,cholesterol esters,phospholipids ,TGs - The lipid deposits leak from the limbal blood vessels - Gray white with a 0.3mm lucid interval of Vogt - The Limbal margin is sharply demarcated and the inner margin is diffuse Starts at the level of Bowman s layer superiorly and inferiorly It is more common in black and brown races. Prevalence is 75% in the seventh decade and 100% over the age of 80 years
  20. 20. - Vision is not affected - Bilateral usually - Unilateral arcus - Unilateral occlusive disease -Ocular hypotony after surgery or trauma --- Possibly due to increased vascular permeability - Early deposits are best seen on Sclerotic scatter or broad tangential illumination - In cross section on slit beam Hourglass shape -Corneal arcus is younger than 30 yr old pts arcus juvenilis -In men younger than 50 years --familial type 2 and type 3 hyperlipoproteinemia--- Amount of arcus correlates with plasma LDL levels -Association with dupuytren s contracture
  21. 21. Differential diagnosis - 1)Peripheral mosaic crocodile shagreen Mosaic pattern distinguishes it from diffuse haziness of arcus - 2)Limbal girdle of Vogt seen only at 3o clock and 9 o clock positions and subepithelial
  22. 22. BAND KERATOPATHY -There are 2 major types 1)Calcific 2)Climatic droplet CALCIFIC BAND SHAPED KERATOPATHY - A degenerative change associated with deposition of calcium salts in Bowmans Membrane ,Superficial stroma. ETIOLOGY 1) Abnormal Calcium and Phosphorus metabolism -Hyperparathyroidism primary & secondary -Chronic Renal Failure -Milk alkali syndrome 2) Keratoprosthesis and ocular prostheses
  23. 23. 3) Ocular Diseases a) Chronic Iridocyclitis of any type -JIA pauciarticular variant -Sarcoidosis Uveitis +Hypercalcemia -Phthisis Bulbi -Absolute glaucoma b)Corneal diseases -Interstitial keratitis -Keratoconjunctivitis Sicca -Exposure keratitis -Following PKP c)Exposure to toxins /drugs 1)Mercury, 2) Phenyl mercuric nitrate(preservative) affects inferonasal paracentral cornea, 3) Phosphate containing steroids, 4)Silicone oil in AC 50% Cases and Viscoelastics
  24. 24. 4 types of Calcific Keratopathy 1) Calicific Band keratopathy 2) Focal calcific plaques- Areas of acute tissue injury /chronic epithelial defects 3) Concentric Limbal calcific deposits systemic disorders of Ca and P 4) Focal calcific deposits use of topical medication 5) PICTURE FROM LEIBOWITZ
  25. 25. PICTURE OF PATHOGENESIS FROM LEIBOWITZ
  26. 26. HISTOPATHOLOGY - In chronic ocular diseases Extracellular calcium deposits in - Epithelial BM - Bowman s layer and - Superficial stroma. - In cases of Hypercalcemia Intracellular deposits may be seen. - Hydroxyapatite is deposited adhere to collagen - Earliest change on Microscopy fine stippling of epithelial Basement membrane. - STAINS USED Alizarin red Von kossa method -Black Calcium red - Von kossa Black Murexide Stains calcium- Bluish purple Hydrogen peroxide AgNO3-Stains Ca Black
  27. 27. Begins at Nasal and temporal limbus - Subepithelial plaques with sharp discrete edge that borders a clear zone next to limbus - Feathery edges that extend centrally - As the central borders meet The narrow central part appears turbid and the periphery chalky white - Bow tie shaped opacity obliterates the clear zone - Does not dissapear spontaneously.May reappear
  28. 28. 3 types of clear zones in the band -Discrete

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