corneal degenerations

CORNEAL DEGENERATIONS

MODERATOR-DR UMAPRESENTER-DR AKSHAY NAYAK

WHAT IS CORNEAL DEGENERATION

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

CLASSIFICATIONS

• A. DEPENDING UPON LOCATIONS I. AXIAL CORNEAL DEGENERATION

1. FATTY DEGENERATION2. HYALINE DEGENERATION3. AMYLOIDOSIS4. CALCIFIC DEGENERATION(BAND

KERATOPATHY)5. SALZMANN’S NODULAR DEGENERATION

II. PERIPHERAL DEGENERATION

1. ARCUS SENILIS2. VOGT’S WHITE LIMBAL GIRDLE3. HASSAL-HENLE BODIES4. TERRIEN’S MARGINAL DEGENERATION5. FURROW DEGENERATION(SENILE

MARGINAL DEGENERATION)

B. DEPENDING UPON ETIOLOGY

A] AGE RELATED DEGENERATION:- ARCUS SENILIS, VOGT’S WHITE LIMBAL

GIRDLE, HASSAL-HENLE BODIES

B] PATHOLOGICAL DEGENERATION:- FATTY DEGENERATION, AMYLOIDOSIS,

CALCIFIC DEGENERATION, SALZMANN’S DEGENERATION, FURROW DEGENERATION, SPHEROID DEGENERATION, TERRIEN’S MARGINAL DEGENERATION

Epithelium and basement membrane Bowman’s Layer

Epithelial basement membrane degeneration

- Pannus ,Pterygium - Salzmann’s Nodular degeneration - Corneal arcus - Calcific Band keratopathy - Limbal girdle of Vogt - Nodular amyloid - Climatic droplet keratopathy -

STROMA ENDOTHELIUM AND DESCEMET’S MEMBRANE

-Scarring with or without vascularisation-Lipid degeneration-Polymorphic amyloid degeneration-Crocodile shagreen-Cornea farinata-Terrien ‘s Marginal degeneration

-Corneal arcus -Cornea guttae -Hassal henle warts -Retrocorneal fibrous membrane

CLASSIFICATION BASED ON LAYER MOST PROMINENTLY INVOLVED

AGE RELATED CORNEAL DEGENERATIONS

PHYSIOLOGICAL CHANGES OCCURRING IN CORNEA DUE TO AGEING

• FLATTENING IN VERTICAL MERIDIAN • THINNING AT PERIPHERY• INCREASE IN DESCEMETS MEMBRANE THICKNESS• ENDOTHELIAL CELL LOSS• INCREASED VISIBILITY OF CORNEAL NERVES• DECREASED LUSTRE OF CORNEA• EPITHELIAL BASEMENT MEMBRANE WILL BE THICKENED

WITH NON SPECIFIC DEGENERATION OF STROMAL GROUND SUBSTANCE.

ARCUS SENILIS (GERONTOXON/ARCUS LIPOIDES)

• ARCUS SENILIS REFERS TO AN ANNULAR LIPID INFILTRATION OF CORNEAL PERIPHERY.

CLINICAL FEATURES• THE ARCUS STARTS IN THE SUPERIOR AND INFERIOR QUADRANTS AND THEN PROGRESSES CIRCUMFERENTIALLY TO FORM A RING WHICH IS ABOUT 1 MM WIDE.

• PERIPHERAL BORDER- SHARP

• CENTRAL BORDER -DIFFUSE

• SEPARATED FROM THE LIMBUS BY A CLEAR ZONE.

• LIPID IS FIRST DEPOSITED AT DESCEMET’S MEMBRANE AND SUBSEQUENTLY AT

BOWMAN’S LAYER.• HISTOPATHOLOGICALLY, THE

ARCUS HAS AN HOURGLASS APPEARANCE.

• EXPERIMENTS HAVE SHOWN THE LIPIDS –• VASCULAR ORIGIN.• LDL• PATIENTS UNDER THE AGE OF 40 WITH CORNEAL ARCUS

HAVE AN INCREASED RISK OF CORONARY ARTERY DISEASE AND SHOULD BE EVALUATED FOR HYPERLIPOPROTEINEMIA.

• HYPERLIPOPROTEINEMIATYPES IIA AND IIB ARE ASSOCIATED WITH PREMATURE CORNEAL ARCUS FORMATION, THE MOST COMMONLY OBSERVED BEING TYPE IIA HYPERLIPOPROTEINEMIA

VOGT’S WHITE LIMBAL GRIDLE• IT APPEARS AS

BILATERALLY CHALKY WHITE OPACITIES IN THE INTERPALPEBRAL AREA BOTH NASALLY AND TEMPORALLY .• HERE MAY OR MAY

NOT BE A CLEAR BETWEEN OPACITY AND THE LIMBUS.• THE OPACITY IS AT THE

LEVEL OF BOWMAN’S MEMBRANE .• 60PC IN OVER 4O

YEARS, WOMEN

• TYPE 1 – VARIANT OF BAND KERATOPATHY, SWISS CHEESE HOLE PATTERN AND A CLEAR AREA SEPARATING THE LESION FROM SCLERAL MARGIN.

• TYPE 2 – MORE PREVELANT, DISTINGUISHED BY ABSENCE OF HOLES AND TYPICALLY OF A JUXTALIMBAL CLEAR ZONE

CORNEA FARINATA

• VISUALLY INSIGNIFICANT • BILATERAL MINUTE, FLOUR LIKE DEPOSITS IN DEEP STROMA• THESE OPACITIES ARE BEST SEEN ON RETROILLUMINATION AND ARE

GRAY-BROWN TO WHITE.

CROCODILE SHAGREEN

• ASYMPTOMATIC. GREYISH WHITE POLYGONAL STROMAL OPACITIES SEPARATED BY RELATIVELY CLEAR SPACES

• MOST CASES-ANTERIOR 2/3RD OF STROMA(ANTERIOR CROC SHAGREEN), OCCASIONALLY- POSTERIOR

• HISTOPATHOLOGICALLY, THE STROMA IS THROWN INTO FOLDS.

• THE ANTERIOR FORM OF THIS DEGENERATION MAY BE SEEN AS A SENILE CHANGE.

• THE ANTERIOR MOSAIC ALSO HAS BEEN DESCRIBED IN KERATOCONUS PATIENTS WITH HARD CONTACT LENSES, TRAUMA, BAND KERATOPATHY, HYPOTONY.

• THE POSTERIOR FORM HAS BEEN DESCRIBED SOLELY AS AN AGE RELATED DEGENERATION

HASSAL-HENLE BODIES/DESCEMET’S WARTS

• HASSAL-HENLE BODIES ARE DROP LIKE EXCRESCENCES OF DESCEMETS, HYALINE MATERIAL PROJECTING INTO THE ANTERIOR CHAMBER AROUND THE CORNEAL PERIPHERY.

• THESE FORM THE COMMONEST SENILE CHANGE SEEN IN THE CORNEA.

• IN PATHOLOGICAL CONDITIONS THEY BECOME LARGER AND INVADE THE CENTRAL AREA AND THE CONDITION IS CALLED CORNEAL GUTTATA

• EXCRESCENCES ARE BEST SEEN ON SPECULAR REFLECTION AND APPEAR AS DARK, ROUND HOLES IN THE SPECULAR REFLECTION.

PATHOLOGICAL CORNEAL DEGENERATION

CALCIFIC DEGENERATION (BAND SHAPE KERATOPATHY )

BAND SHAPE KERATOPATHY

CALCIFIC DEGENERATION (BSK)• BAND SHAPE KERATOPATHY

(BSK) IS ESSENTIALLY A DEGENERATIVE CHANGE ASSOCIATED WITH DEPOSITION OF CALCIUM SALTS IN

1. BOWMAN’S MEMBRANE2. MOST SUPERFICIAL PART OF

STROMA 3. DEEPER LAYERS OF

EPITHELIUM.

ETIOLOGY

• OCULAR DISEASE COMPLICATED BY BAND KERATOPATHY INCLUDE CHRONIC UVEITIS , CHILDREN WITH STILL’S DISEASE, PHTHISIS BULBI,CHRONIC CORNEAL OEDEMA• AGE RELATED- AFFECTS HEALTHY INDIVIDUALS• METABOLIC(METASTATIC CALCIFICATION)-

INCREASED CALCIUM AND PHOSPHORUS, HYPERURICEMIA AND CHRONIC RENAL FAILURE• HEREDITARY CAUSES INCLUDE FAMILIAL CASES

AND ICHTHYOSIS

PATHOLOGY

• CALCIUM DEPOSITS ARE INTRACELLULAR WHEN ASSOCIATED WITH HYPERCALCEMIA AND CAN BE FOUND BOTH INTRANUCLEARLY AND INTRACYTOPLASMICALLY ON HISTOLOGIC EXAMINATION.

• THE DEPOSITS MAY BE FOUND EXTRACELLULARLY WHEN THEY OCCUR WITH LOCAL DISEASE OR RENAL FAILURE.

• CONJUNCTIVAL DEPOSITS OF CALCIUM MAY ALSO BE FOUND WHEN ASSOCIATED WITH HYPERCALCEMIA.

• CALCIUM IS DEPOSITED IN THE FORM OF HYDROXYAPATITE, A PHOSPHATE SALT.

THEORIES

• THE CAUSE OF CALCIUM SALT PRECIPITATION-1. ALTERATION OF CORNEAL METABOLISM THAT CAUSES

INCREASED TISSUE PH AND PRECIPITATION OF CALCIUM2. EVAPORATION OF THE TEARS BECAUSE OF EXPOSURE OF

THE INTERPALPEBRAL ZONE WHICH CAUSES CALCIUM PRECIPITATION.

CLINICAL FEATURES

• INTERPALPEBRAL ZONE• CLEAR INTERVAL BETWEEN THE ENDS OF

THE BAND AND THE LIMBUS.• EARLY, THE OPACITY IS GRAY AND LATER

BECOMES WHITE AND CHALKY.• LUCENT HOLES ARE SCATTERED

THROUGHOUT THE OPACITY. • THE LESION IS SUBEPITHELIAL BUT MAY

BREAKTHROUGH THE EPITHELIUM IN ADVANCED STAGES.

• A COMPLETE BANDFROM LIMBUS TO LIMBUS MAY FORM IN LATER STAGES.

• ADVANCED LESIONS- NODULAR AND ELEVATED

• THESE LESIONS PROGRESS SLOWLY OVER MONTHS TO YEARS.

• IN PATIENTS WITH DRY EYE,HOWEVER, THE CALCIUM DEPOSITION HAS

BEEN REPORTED TO OCCUR OVER WEEKS.• IN MOST CASES, THE ASSOCIATEDDISEASE CAUSING THE BAND KERATOPATHY IS KNOWN.

CONDITIONS TO CONSIDER IN DIFFERENTIAL DIAGNOSIS

• PRIMARY AND SECONDARY CALCAREOUS DEGENERATION OF CORNEA

• CALCIPHYLAXIS• SPHEROID DEGENERATION• SALZMANN NODULAR DEGENERATION

TREATMENT

• TREATMENT ONLY IF VISION IS THREATENED OR EYE UNCOMFORTABLE.

• TREAT UNDERLYING CAUSE

• CHEMICAL REMOVAL OF CALCIUM SALTS –-WHEN THE PATIENTBECOMES SYMPTOMATIC, THE MAINSTAY OF TREATMENT IS THEAPPLICATION OF ETHYLENE DIAMINE TETRAACETIC ACID (EDTA).

• PHOTOTHERAPEUTIC KERATECTOMY(PTK)• KERATOPLASTY.

SALZMANN’S NODULAR DEGENERATION

• SALZMANN’S NODULAR DEGENERATION IS A SLOWLY PROGRESSIVE CONDITION IN WHICH GRAY-WHITE TO BLUISH NODULES MEASURING 1-3 MM ARE SEEN ANTERIOR TO BOWMAN’S LAYER OF THE CORNEA.

• THEY ARE CLASSICALLY ROUND AND LOCATED IN THE MID-PERIPHERY.

PATHOGENESIS

• IT HAS SINCE BEEN DEFINED AS A DEGENERATIVE PROCESS THAT FOLLOWS EPISODES OF KERATITIS.

• THE MOST COMMON SETTING NOW SEEMS TO BE IDIOPATHIC OR IN ASSOCIATION WITH SIGNIFICANT CORNEAL INFLAMMATORY DISEASE, ESPECIALLY MEIBOMIAN GLAND DYSFUNCTION (INCLUDING OCULAR ROSACEA)

• CAN OCCUR IN CHRONIC CORNEAL IRRITATION OR INFLAMMATION- DRY EYE, TRACHOMA, CHRONIC BLEPHARITIS AND CHRONIC ALLERGIC BLEPHEROCONJUNCTIVITIS• ADDITIONAL ASSOCIATIONS- CROHNS DISEASE , CONTACT LENS USE

• IN SALZMANN'S NODULAR DEGENERATION RAISED HYALINE PLAQUE ARE DEPOSITED BETWEEN EPITHELIUM AND BOWMAN’S MEMBRANE

• THERE IS ASSOCIATED DESTRUCTION OF BOWMAN’S MEMBRANE AND THE ADJACENT STROMA

CLINICAL FEATURES • GENERALLY ASYMPTOMATIC• PATIENT MAY EXPERIENCE DISCOMFORT DUE TO LOSS

OF EPITHELIUM FROM THE SURFACE OF THE NODULES.• GRADUAL PAINLESS LOSS OF VISION, FOREIGN BODY

SENSATION• NODULES ARE OFTEN ANNULAR IN LOCATION AND IN

THE MIDPERIPHERY. • THE BASE OF A NODULE MAY BE ASSOCIATED

WITH PANNUS AND EPITHELIAL IRON DEPOSITION

DIFFERENTIAL DIAGNOSIS

• CORNEAL SCARRING AND ASTIGMATISM• SPHEROIDAL DEGENERATION• CORNEAL ABRASION CAN PRESENT WITH SIMILAR

DETERIORATION OF VISION

COMPLICATIONS

• SUBEPITHELIAL NODULES- SECONDARY RECURRENT EROSIONS

• NODULES- STEEPENED MID PERIPHERAL CORNEA AND FLATTER CENTRAL- HYPEROPIC VISUAL CHANGES

• ASTIGMATISM• PERIPHERAL CORNEAL VASCULARISATION- ASSOCIATED

WITH NODULES THAT ARE MORE DIFFICULT TO REMOVE

TREATMENT

LUBRICATION WITH CONTROL OF CAUSETO IMPROVE VISUAL ACUITY AND TO DECREASE THE IRREGULAR ASTIGMATISM A SUPERFICIAL KERATECTOMY WAS RECOMMENDED TO REMOVE THE SALZMANN’S NODULES.• SUPERFICIAL KERATECTOMY, BY MANUAL DISSECTION OR

WITH PHOTOTHERAPEUTIC KERATOABLATION, MAY BE USED FOR LESIONS NEAR THE VISUAL AXIS.

• FOR LESIONS EXTENDING TO THE MID STROMA, LAMELLAR OR PENETRATING KERATOPLASTY MAY BE NECESSARY. RECURRENCE IS POSSIBLE AFTER KERATOPLASTY

TERRIEN’S MARGINAL DEGENERATION

• TERRIEN’S MARGINAL DEGENERATION IS NON-ULCERATIVE THINNING OF THE MARGINAL CORNEA.• PERIPHERAL

DEGENERATIVE CONDITION

TERRIEN MARGINAL DEGENERATION DISPLAYING SUPERIOR STROMAL THINNING WITH INTACT EPITHELIUM, OVERLYING PANNUS, AND LIPID AT THE LEADING EDGE.

• DISEASE IS BILATERAL AND SYMMETRIC, BUT MAY BE ASYMMETRIC.

• THE LESION USUALLY BEGINS SUPERONASALLY WITH FINE PUNCTATE OPACITIES IN THE ANTERIOR STROMA WITH A LUCENT AREA TO THE LIMBUS

• LESION RESEMBLES ARCUS SENILIS• A GUTTER THEN FORMS BETWEEN THE OPACITY AND

LIMBUS. THE STROMA PROGRESSIVELY THINS. OVERLYING EPITHELIUM REMAINS INTACT.

• THE GUTTER BECOMES MORE VASCULARIZED AND WIDER OVER TIME. THE LESION MAY EVENTUALLY EXTEND CIRCUMFERENTIALLY OR CENTRALLY.

• BAND OF LIPID PRESENT AT CENTRAL EDGE

• TWO TYPES OF TERRIEN’S DEGENERATION HAVE BEEN CLASSIFIED.

• THE MORE COMMON QUIESCENT TYPE IS SEEN IN OLDER PATIENTS.

• THESE PATIENTS MAY BE ASYMPTOMATIC FOR A LONG TIME BECAUSE THE LESION PRODUCES NO PAIN.

• INFLAMMATORY TERRIEN’S DEGENERATION USUALLY OCCURS IN THE YOUNGER AGE GROUPS.

• ASTIGMATISM MAY BE PRODUCED FROM THE MARGINAL THINNING

ETIOLOGY

• IT TYPICALLY OCCURS IN MEN WHO WORK OUT-DOORS ESPECIALLY IN HOSTILE CLIMATE.

• ITS OCCURRENCE HAS BEEN RELATED TO EXPOSURE TO ULTRAVIOLET RAYS AND /OR AGEING AND/OR CORNEAL DISEASE.

• BOWMAN’S LAYER IS FRAGMENTED OR ABSENT. BREAKS IN DESCEMET’S MEMBRANE MAY BE SEEN IN THINNED AREAS.

• WHEN THINNING OCCURS, AQUEOUS POCKETS OCCASIONALLY CAN BE SEEN CLINICALLY. AQUEOUS POCKETS MAY EVEN CONNECT TO THE SUBEPITHELIAL SPACE, CAUSING A FILTERING BLEB AND HYPOTONY

DIAGNOSIS

• CLINICALLY• DIFFERENTIATED FROM OTHER CORNEAL THINNING

DISORDERS- SUPERFICIAL VASCULARISATION PRESENT, LACK OF EPITHELIAL DEFECT AND SLOW PROGRESSIVE COURSE

• NO LAB TEST REQUIRED

DIFFERENTIAL DIAGNOSIS

• MARGINAL FURROW DEGENERATION(IS B/L, ASVASCULAR AND MINIMAL THINNING)

• DELLEN• COLLAGEN VASCULAR DISEASE(NO SYSTEMIC

ASSOCIATIONS)• PELLUCID MARGINAL DEGENERATION• INFECTIOUS CORNEAL ULCER• MOORENS( TERRIENS-NO PAIN, NO INFLAMMATION, NO

EPITHELIAL DEFECT)

COMPLICATION

• COMPLICATION SUCH AS PERFORATION (DUE TO MILD TRAUMA) AND PSEUDOPTERYGIUM MAY DEVELOP.

TREATMENT

• EARLY REFRACTIVE TREATMENT INCLUDES:

• SPECTACLES (POLYCARBONATE)- FOR PROTECTION IF THINNING IS SIGNIFICANT

• CONTACT LENS IS AN OPTION THOUGH DIFFICULT TO FIT DUE TO IRREGULAR ASTIGMATISM

• ALTHOUGH THERE IS NO TREATMENT TO PREVENT THE DISEASE FROM ADVANCING, PROGRESSION IS SLOW.

• PATIENTS MAY BE TREATED WITH CRESCENTIC OR ANNULAR EXCISION OF GUTTER WITH LAMELLAR OR ECCENTRIC PENETRATING GRAFTS IN CASES OF HIGH ASTIGMATISM, IMPENDING PERFORATION, OR PERFORATION

SPHEROIDAL DEGENERATION /LABRADOR KERATOPATHY/CLIMATE DROPLET KERATOPATHY/BIETTI’S NODULAR CORNEAL DEGENERATION• THIS RELATIVELY

COMMON CONDITION FEATURES CHARACTERISTIC OIL DEPOSITS AT THE LIMBUS WHICH ARE CHARACTERIZED HISTOLOGICALLY AS MAUVE GLOBULAR DEGENERATION AND ARE STRONGLY ASSOCIATED WITH UV EXPOSURE.

• SPHEROIDAL DEGENERATION IS CLASSIFIED INTO THREE BASIC TYPES.

• TYPE 1• OCCURS BILATERALLY IN THE CORNEA WITHOUT EVIDENCE

OF OTHER OCULAR PATHOLOGY .• TYPE 2• SECONDARY SPHEROIDAL DEGENERATION, OCCURS IN THE

CORNEA IN ASSOCIATION WITH OTHER OCULAR PATHOLOGY.• TYPE 3 • CONJUNCTIVAL FORM OF THE DEGENERATION AND MAY

OCCUR WITH TYPES 1 OR 2.

• ETIOLOGIES FOR THE PRIMARY AND CONJUNCTIVAL FORMS ARE THE SAME AS THOSE FOR PTERYGIUM AND PINGECULA .

• HISTOPATHOLOGICALLY, DEPOSITS OF HYALINE-LIKE MATERIAL ARE FOUND IN THE CORNEAL STROMA, BOWMAN’S LAYER, AND SUBEPITHELIUM.

• BOWMAN’S LAYER IS DISRUPTED, AND IN ADVANCED CASES THE EPITHELIUM IS ELEVATED AND THINNED.

• THE SOURCE OF THE DEGENERATIVE MATERIAL IS CONTROVERSIAL.

• IT IS SUGGESTED THAT THE MATERIAL ORIGINATES FROM1. CORNEAL STROMA WHERE IT IS ASSOCIATED WITH

ABNORMAL COLLAGEN.2. SECRETED BY CORNEAL AND CONJUNCTIVAL FIBROBLASTS. 3. TO BE OF PLASMA ORIGIN-EXPERIMENTS HAVE SUGGESTED

THAT PLASMA PROTEINS DIFFUSE INTO THE CORNEA.THESE PROTEINS ARE THEN PRECIPITATED WITHIN THE SUPERFICIAL CORNEA AFTER ALTERATION, PRESUMABLY DUE TO ULTRAVIOLET RADIATION.

SYMPTOMS

• SPHEROIDAL DEGENERATION IS ASYMPTOMATIC IN MAJORITY OF THE CASES.

• VISUAL ACUITY MAY BE AFFECTED IF THE DEPOSITS EXTEND TOWARDS THE CENTER OF THE CORNEA, THEREBY, BLOCKING THE VISUAL AXIS.

• OCULAR (EYE) SYMPTOMS IN ADVANCED CASES MAY BE:• IRRITATION.• DISCOMFORT.• FOREIGN BODY SENSATION.• DIMINUTION OF VISION.

CLINICAL FINDINGS •  0.1-0.6 MM YELLOW OIL

DROPLETS DEPOSIT NEAR THE LIMBUS  IN THE 3 AND 9 O’CLOCK POSITIONS IN OLDER INDIVIDUALS.

• THE AREAS MAY APPEAR BAND SHAPED AND OFTEN ARE ASSOCIATED WITH PINGUECULAE

• AMBER-COLOURED SPHEROIDAL GRANULES ACCUMULATE AT THE LEVEL OF BOWMAN’S MEMBRANE AND ANTERIOR STROMA IN THE INTERPALPEBRAL ZONE.

 GRADING OF THE CONDITION DEPENDING ON THE SEVERITY IS:

• TRACE: • TRACE IS CHARACTERISED BY SMALL NUMBER OF DEPOSITS IN ONE EYE, OR ONLY

AT THE END OF THE INTERPALPEBRAL STRIP IN EACH EYE (IF BILATERAL).• GRADE 1:•  IN GRADE 1, THERE IS SPARING OF CENTRAL CORNEA WITH INVOLVEMENT OF

MEDIAL AND LATERAL INTERPALPEBRAL STRIPS.• GRADE 2: • GRADE 2 AFFECTS CENTRAL CORNEA BUT THERE IS NO EFFECT ON VISUAL ACUITY.• GRADE 3:•  IN GRADE 3, CENTRAL CORNEA IS AFFECTED WITH REDUCED VISION.• GRADE 4: • GRADE 4 SHOWS ELEVATED NODULES IN ADDITION TO THE FINDINGS OF GRADE 3. 

SPHEROIDAL DEGENERATION MAY BE DIFFERENTIATED FROM:

• THERE DO NOT APPEAR TO BE OTHER CORNEAL CONDITIONS THAT RESEMBLE SPHEROIDAL DEGENERATION OF THE CORNEA. HOWEVER, CONDITIONS WHICH MAY BE CONSIDERED ARE:

• BAND SHAPED KERATOPATHY:•  BAND SHAPED KERATOPATHY SHOWS DEPOSITION OF

CALCIUM WITH ‘SWISS CHEESE’ APPEARANCE.• PSEUDO-ENTRAPMENT OF EYE OINTMENT:. THESE

RESULTING DROPLETS ARE NOT CHARACTERISTIC OF SPHEROIDAL DEGENERATION. THE DROPLETS DO NOT AUTOFLUORESCE. ONCE THE PRESSURE DRESSING IS REMOVED THE PSEUDO-ENTRAPMENT OF OINTMENT DISAPPEARS.

TREATMENT • THE MAJORITY OF PATIENTS OF SPHEROIDAL DEGENERATION ARE

ASYMPTOMATIC.• MANAGEMENT OF PATIENTS WITH SPHEROIDAL DEGENERATION IS MAINLY

SYMPTOMATIC. THERE IS NO SPECIFIC TREATMENT AVAILABLE FOR THE RESOLUTION OF SPHERULES.

• MOST OF THE TIME, SPHEROIDAL DEGENERATION PATHOLOGY IS LOCATED NASALLY AND TEMPORALLY, AND OBSERVATION ALONE IS REQUIRED.

• GENERAL MEDICAL THERAPY:• ULTRAVIOLET LIGHT PROTECTION: PATIENTS WITH SPHEROIDAL

DEGENERATION SHOULD HAVE PROTECTION AGAINST ULTRAVIOLET LIGHT DAMAGE WITH SUNGLASSES, TO AVOID FURTHER DAMAGE DUE TO EXPOSURE.

• TOPICAL ARTIFICIAL TEARS: PATIENTS WITH MILD DEGENERATION MAY REQUIRE LUBRICATION WITH TOPICAL ARTIFICIAL TEARS. LUBRICATION CAN SLOW THE PROCESS, IF THE TEAR FILM IS DECREASED.

• SURGICAL THERAPY:• PATIENTS WITH CORNEAL SCARRING AND GLOBULES

INVOLVING ANTERIOR CENTRAL PART OF CORNEA COMPROMISING VISION, OR CAUSING PAIN, MAY REQUIRE SURGICAL INTERVENTION.

• EXCIMER LASER ASSISTED PHOTOTHERAPEUTIC KERATECTOMY (PTK): PHOTOTHERAPEUTIC KERATECTOMY WITH EXCIMER LASER MAY BE USED TO GAIN USEFUL VISION.

• LAMELLAR OR PENETRATING KERATOPLASTY: LAMELLAR OR PENETRATING KERATOPLASTY MAY BE USED IN PATIENTS WITH IRREGULAR CORNEAL SURFACE.

LIPID KERATOPATHY- CAN BE PERIPHERAL, CENTRAL OR DIFFUSE

PRIMARY LIPID KERATOPATHY RARE AND OCCURS APPARENTLY SPONTANEOUSLY, BILATERALYELLOWISH, CRYSTALLINE ELEMENT, STROMAL DEPOSITS CONSISTING OF CHOLESTEROL,PHOSPHOLIPIDSNOT ASSOCIATED WITH VASCULARISATIONSECONDARY LIPID KERATOPATHYMORE COMMONPREVIOUS OCULAR INJURY OR DISEASE THAT RESULTED IN CORNEAL VASCULARISATION THE MOST COMMON ASSOCIATIONS ARE HERPES SIMPLEX AND HERPES ZOSTER KERATITISOTHER ASSOCIATIONS- INTERSTITIAL KERATITIS, TRAUMA, CORNEAL HYDROPS, CORNEAL ULCERATION, AND MUSTARD GAS INJURIES DUE TO ITS THROMBOSING PROPERTIES

TREATMENT

• TREATMENT IS USUALLY UNSATISFACTORY. AIMED AT MEDICAL CONTROL OF UNDERLYING DISEASE • IN SOME CASES SLOW RESORPTION OF LIPID

INFILTRATE CAN BE INDUCED BY ARGON LASER PHOTOCOAGULATION OF THE NEW BLOOD VESSELS. • PENETRATING KERATOPLASTY IN ADVANCED

CASES BUT QUISCENT DISEASE , THOUGH VASCULARISATION AND THINNING MAY PREJUDICE THE OUTCOME.

AMYLOID DEGENERATION • AMYLOID DEGENERATION OF CORNEA IS CHARACTERIZED BY

DEPOSITION OF AMYLOID MATERIAL UNDERNEATH EPITHELIUM.

• IT IS VERY RARE CONDITION AND OCCURS IN PRIMARY (IN A HEALTHY CORNEA) AND SECONDARY FORMS (IN A DISEASE CORNEA).

• ACQUIRED (SECONDARY LOCALIZED) CORNEAL AMYLOIDOSIS MAY BE ASSOCIATED WITH

CORNEAL INFLAMMATION (SUCH AS TRACHOMA, KERATOCONUS, HANSEN DISEASE [LEPROSY], OR PHLYCTENULOSIS) OR INTRAOCULAR DISEASE (SUCH AS UVEITIS, RETINOPATHY OF PREMATURITY,OR GLAUCOMA) OR MAY BE SECONDARY TO TRAUMA.

• CLINICALLY, AMYLOID DEPOSITS USUALLY OCCUR AS RAISED, YELLOW-PINK NODULAR MASSES IN THE CORNEA.

• IN MOST CASES, CORNEAL VASCULARIZATION IS ASSOCIATED WITH THE AMYLOID. THE DEPOSITS MAY BE REFRACTILE WITH RETROILLUMINATION.

FURROW DEGENERATION

• SENILE MARGINAL DEGENERATION• THINNING PERIPHERY– FURROW• IN PRESENCE OF ARCUS SENILIS, FURROW IS IN LUCID INTERVAL OF VOGT• FIBRILLAR DEGENERATION OF STROMA• DEFECTIVE VISION DUE TO ASTIGMATISM• TREATMENT USUALLY NOT NECESSARY

• THANK YOU

REFERENCES

• CORNEA-KRACHMER,3RD EDITION• COMPREHENSIVE OPHTHALMOLOGY KHURANA, 5TH EDITION• KANSKI’S CLINICAL OPHTHALMOLOGY,8TH EDITION• PARSONS-DISEASES OF EYE 22ND EDITION• PICTURES- INTERNET