peripheral corneal ulcers and corneal degenerations

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CORNEAL DEGENERATIONS and peripheral corneal ulcers

Dr.Puneeth Isloor

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


-Epithelial basement membrane degeneration

-Corneal guttae-Retrocorneal fibrous mebraneLIPID-Corneal Arcus

-Primary Lipid degenerations

-Lipid degeneration from vascularisation CALCIUM-Calcific band keratopathy

-Focal degenerative calcification

-Toxic medications

-Calcareous degeneration


SecondaryPolymorphic Amyloid stromal Degenerations

Secondary amyloiddegenerationLimbal girdle of Vogt

Mosaic keratopathy

White ring of coatsTerrien s Marginal degeneration

Age related marginalfurrow

Epithelium and basement membrane Bowmans LayerEpithelial 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



AVASCULAR SCARRING - Density graded asTrace Barely visibleMild A cloud like nebular opacityModerate Macular opacitySevere White leukomatous opacity

Scarring can occur at 3 levelsSubepithelial Post Excimer laserStromal Post microbial keratitisDescemets membrane interstitial keratitis

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 keratoplastyFull thickness scarring Penetrating keratoplasty


Map dot fingerprint changes in the epithelium and basement membraneOccurs in aged

Due to abnormal synthesis of Basement membrane by the aging corneal epithelium

Faint gray Map like subepithelial patches most common superiorly

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

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).

HISTOPATH -Thickening of the basement membrane gray mapB.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

Management Symptomatic patients LubricantsPeeling- 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.

SALZMANN NODULAR DEGENERATION Non specific corneal response to chronic insult such as Phlyctenulosis,Trachoma and VKC3 groupsAsymptomaticSymptomatic with foreign body sensation Nodules overlying pupil with reduced visual acuity

Focal , discrete ,avascular ,circular ,gray white,elevated opacities located subepithelial unilateralOverlie areas of stromal scarring and vascularisation Persist after the inflammation has subsidedRefractile on retroillumination PAS positive material

SALZMANN S NODULAR SPHEROIDAL DEGENERATION Gray white peripheral opacities Golden yellow Focal and discrete Multiple and confluent Unilateral in 80% cases Bilateral

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

epithelial denudation as shown above (arrow 1), destruction of Bowmans layer(arrow2)

MANAGEMENTAsymptomatic 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

LIPID DEGENERATIONSPATHOGENESISCan 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 Neovascularisation

CORNEAL VESSELS AND LIPID DEPOSITSThe 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

CORNEAL ARCUSMost 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

- 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

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

BAND KERATOPATHY-There are 2 major types 1)Calcific 2)Climatic droplet

CALCIFIC BAND SHAPED KERATOPATHYA 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

3) Ocular Diseases a) Chronic Iridocyclitis of any type -JIA pauciarticular variant -Sarcoidosis Uveitis +Hypercalcemia -Phthisis Bulbi -Absolute glaucomab)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

4 types of Calcific KeratopathyCalicific Band keratopathyFocal calcific plaques- Areas of acute tissue injury /chronic epithelial defectsConcentric Limbal calcific deposits systemic disorders of Ca and PFocal calcific deposits use of topical medication



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