Powerpoint presentation

1. Dr.Puneeth Isloor

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.  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. 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
- White ring of coats
STROMA ENDOTHELIUM AND
DESCEMET’S MEMBRANE
-Scarring with or without
vascularisation
-Lipid degeneration
-Polymorphic amyloid degeneration
-Crocodile shagreen
-Pre descemet’s 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.  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
- Descemet’s membrane – interstitial keratitis

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 Bowman’s layer –
Mechanical scraping or peeling can be done.
- Anterior 2/3 of stroma – Lamellar keratoplasty
- Full thickness scarring – Penetrating keratoplasty

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

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.  epithelial denudation as shown above (arrow
1), destruction of Bowman’s layer(arrow2)

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.  LIPID DEGENERATIONS
PATHOGENESIS
- Can be – Primary/Idiopathic
- - Secondary to corneal vascularisation
- It’s a Vicious cycle
Lipids leak from corneal vessels
Lipid phagocytosis
by keratocytes and
macrophages
Mild chronic inflammatory
response
Continued
Neovascularisat
ion

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.  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. - 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

22.  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

23.  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 Bowman’s
Membrane ,Superficial stroma.
ETIOLOGY
1) Abnormal Calcium and Phosphorus metabolism
-Hyperparathyroidism –primary & secondary
-Chronic Renal Failure
-Milk alkali syndrome
2) Keratoprosthesis and ocular prostheses

24. 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

25.  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

26.  PICTURE OF PATHOGENESIS FROM LEIBOWITZ

27.  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

29.  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

31. 3 types of clear zones in the band
-Discrete round holes within the opacity –
passage of nerves through BM
-Jagged intersecting fissures – corresponds to
breaks in Bowman’s layer
-Large clear geographic patches --- site of
sloughed plaques of calcium
- Early peripheral lesions are best seen ---on
sclerotic scatter
- Retroillumination highlights clear zones

32.  CLINICAL FEATURES - SYMPTOMS
 - Reduced Visual acuity
 - Foreign body sensation and grittiness –
conjunctival deposits can also contribute to
this in cases due to hypercalcemia

33.  Familial band shaped keratopathy
- X linked recessive ocular disease
-Affected 6 generations of Greek families
in Cyprus and Episkopi
-Produces a progressive,white opacity in
early life
-This later progresses to superficial stroma
Chronic Iridocyclitis
- Pauciarticular JRA-- few systemic symptoms
and 4 or less joints involved
-Children – 3-6 monthly review to detect the
iridocyclitis that cause BSK by 10yrs

34.  Tissue injury calcification in Corneal diseases
- Due to a combination of
superficial corneal ulceration + tear film
dysfunction
- Seen in RA , Ocular pemphigoid , Exposure
keratitis ,renal failure and systemic alkalosis
-Full thickness –corneal calcification – occurs
in severe dry eyes with persistent epithelial
defects – “ Calcareous degeneration”

35.  TOXIC CALCIFIC KERATOPATHY
- Phenyl mercuric nitrate – used in Pilocarpine
preparation
- Usually begins in the Inferonasal paracentral
cornea
-Topical steroid phosphate preparations can
cause deposits in pts with Keratitis

36. CALCIFIC DEPOSITS IN SYSTEMIC
DISEASES
CALCIFIC DEPOSITS IN
OCULAR DISEASES
Remain peripheral as moon
shaped arcs concentric to
limbus
Progress centrally over to the
pupillary area
Conjunctiva is also affected Usually limited to cornea
Disappear when the metabolic
disorder is corrected
Persist
CA * P product is elevated Normal

37.  TREATMENT
 - EDTA is used to chelate the calcium.
- Available commercially as a 150mg/ml
concentration.It should be diluted 1:10 with sterile
water .
- Topical anesthetic is instilled and lid speculum
placed
- Corneal epithelium is scraped from the corneal
surface with a scalpel
-EDTA can be applied by 3 methods
- Continuous irrigation
- Cotton tipped applicator
- Plastic or glass cylinder reservoir -10-12mm test
tube

38.  EDTA is applied for 15-20 minutes
 Topical anesthetic is reinstilled
 Corneal surface is gently rubbed with an
EDTA soaked microsponge until central
calcium is removed
 It is unnecessary to remove the peripheral
calcium
 Topical antibiotics, Cycloplegics and steroids
to be administered
 Soft contact lenses promotes epithelial
regeneration

39.  CLIMATIC DROPLET KERATOPATHY
- Synonyms – Labrador Keratopathy
-Bietti ‘s degeneration
-Spheroidal degeneration
-Actinic keratopathy
- Small to large ,refractile,yellowish droplets or spherules
in the subepithelial zone and in the superficial stroma
- Multiple and confluent lesions and usually bilateral
- Risk factors – Dry Arid conditions
- Extremes of temperature
- Microtrauma of blown sand
- Chronic UV radiation
-

40. - 4 categories
- Primary-Type 1 – No previous ocular disease/scar,
- bilateral
- Peripheral corneal deposits
- Secondary –Type 2 - Prexisting ocular pathology
- Paracentral and Central corneal deposits
- Conjunctival –type 3 – Spheroidal deposits over
- pinguecula
Familial –type 4 – Central corneal deposits
Strong family history

41.  CLINICAL SYSTEM FOR GRADING
Trace – Deposits in very small numbers
One eye affected
Only one end of interpalpebral strip in
each eye if bilateral
Grade 1 –Medial and lateral interpalpebral strips
Sparing of central cornea
Grade 2- Central cornea affected but visual acuity
spared
Grade 3 – Central cornea plus vision reduced
Grade 4 –Elevated nodules present + Grade 3

43.  PATHOLOGY
- Globular deposits contain proteins rich in
Tryptophan ,Tyrosine,Cysteine and Cystine
- Exact composition of the droplets is unknown
3 possibilities – Biochemical alterations in
cornea and conjunctiva
- Fibrocyte derived
- Plasma proteins that diffuse
Stains with Toluidine blue ,basic fuschin
- Globules elevate the epithelium and cause
erosions – Hence vision threatening

44.  CLINICAL FEATURES
- Primary – Droplets at 3o clock and 9 o clock
-Gradually spread centrally
-Confluent and coalesce
-Elevated epithelium
-Epithelial defects ----can cause
--sterile ulcers with corneal perforation
--secondary bacterial keratitis
--deep corneal scarring
--loss of corneal sensations

45.  Picture of climatic droplet keratopathy

46.  DIFFERENTIAL DIAGNOSIS
- Salzmann ‘s nodular degeneration
- Vogt s Limbal girdle – At 3 o clock and 9 o
clock position .Annular chalk –white ,well
defined appearance
- Calcific band keratopathy
Can coexist with spheroidal degeneration
Is not elevated.Has cracks ,holes and
geographic patches

47.  MANAGEMENT
- Prevention – Protection of the eyes from
climatic insults
-Excimer Laser phototherapeutic keratectomy
can remove climatic droplet keratopathy
For grades Trace to Grade 3 lesions
- Transepithelial phototherapeutic keratectomy
For grade 4 nodules and secondary degeneration
-Removal of nodules by scraping and peeling
- followed by Phototherapeutic keratectomy
Severe corneal scarring – Then PKP or Lamellar KP
If coexisting cataract is present – then it is treated
only after phototherapeutic keratectomy

48.  TERRIEN ‘S MARGINAL DEGENERATION
- Consists of Gradual thinning and ectasia of
superior peripheral cornea
-There is arcuate lipid deposition and
vascularisation in pts aged >40 yrs
-Bilateral and assymetric
- 2 types of terrien s marginal degeneration
TYPE 1 TYPE 2
Younger individuals older patients
Associated with
episcleritis
and scleritis
Asymptomatic gradual
thinning and ectasia

49.  Begins at the superior corneal limbus with
deposits of finely granular lipid material
separated from the limbus by a clear zone.
 Superior corneal thinning occurs and it forms a
gutter
 The gutter is centrally bound by an advancing
edge of dense lipid deposits
 Vascularisation can be observed across the
thinned out area
 Thinning progresses both centrally and
circumferentially

50.  With increased corneal thinning --- ectasia
 Can perforate after trauma
 Associated with
- VKC
- Pseudopterygium
D/D
1)Pellucid Marginal degeneration
- Occurs inferiorly
-No lipid deposits/scarring/vessels
2)Marginal thinning associated with RA and
autoimmune diseases
3) Late stages of Mooren’s ulcer
4) Age related marginal furrow- Lucid interval of
Vogt – becomes thinned out.

51.  HISTOPATHOLOGY
- Fibrillar degeneration -Bowman’s Layer and
stromal lamellae- responsible for thinning
- Cornea becomes thinner with appearance of
a subepithelial pannus

52.  MANAGEMENT
- Initial management includes correction of
astigmatism
- With spectacle lenses
-With contact lenses
- Surgical management in later stages
1)Lamellar keratoplasty in which a banana
shaped lamellar donor is placed on the host
bed

53.  POLYMORPHIC AMYLOID DEGENERATION
- Bilateral and Asymptomatic
-Detected Incidentally on slit lamp examination
-Amyloid deposits form discrete , punctate,
refractile ,glass like deposits in the cornea
in front of the Descemet’s Membrane
-They appear centrally and can spread from
posterior to anterior stroma
POLYMORPHIC AMYLOID
DEGENERATION
GUTTAE
Diffuse and Isloated Central and confluent
Posterior stroma and
Only indent the DM
Posterior surface of DM and
disrupt endothelial mosaic
Do not progress Slowly progressive
Normal appearing DM Thickened descemet’s
membrane

54.  PELLUCID MARGINAL DEGENERATION
- Bilateral disorder of unknown etiology
- Affects both sexes equally and seen in 20-40 yrs age
- Arcuate area of thinning in the inferior peripheral
cornea in the absence of inflammation
- The area of thinning is 1-2 mm in width
- Separated from inferior limbus by 1-2 mm of
normal thickness cornea.
- Cornea above the thinned area is normal in
thickness and protrudes downwards – irregular
astigmatism
- Believed to be a variant of Keratoconus

55.  MANAGEMENT
- Large amount of irregular astigmatism –
precludes treatment with spectacles and
contact lenses

56.  VOGT’S LIMBAL GIRDLE
- Arcuate opacity that appears in the interpalpebral
zone of corneal limbus at 3 o clock and 9 o clock
positions
- Symmetric
- Occurs in 100% of individuals over 80 years of age
- It is an epithelial elastotic degeneration of
collagen with particles of Calcium

57.  2 types
TYPE 1 TYPE 2
Concentric to limbus Nasal and temporal cornea
Clear Gap between it and the
limbus
Usually contiguous with the
conjunctiva
Less common
Has transparent Holes or
cracks
More common
Overlying epithelium is intact
and maybe hypertrophic

58.  Picture of vogt’s limbal girdle

59.  MOSAIC KERATOPATHY /CROCODILE SHAGREEN
- Anterior corneal Mosaic
- It is physiological
- Normal corneas exhibit a polygonal mosaic
pattern when fluorescein is instilled and
pressure is applied onto cornea
-When pressure is removed fluoresceins
pools to create a mosaic pattern
- Can also be seen in
---ocular hypotony
--keratoconus patients wearing hard contact lens
---after corneal trauma
- External pressure may change the normal tension of
Bowman s layer and throw it into folds or ridges that
indent the epithelium

60.  ANTERIOR CROCODILE SHAGREEN
- Gray polygonal corneal opacities that resemble
a crocodile’s skin.It is an incidental finding.
-The gray white opacities are separated by clear
lines at the level of Bowman’s membrane
-The pattern may be due to the way stromal
collagen fibrils insert into Bowman’s layer

62.  POSTERIOR CROCODILE SHAGREEN
- Polygonal opacities appear in the Posterior
stroma
-Bilateral and does not affect vision
-Does not involve descemet’s membrane or
endothelium
-Due to irregular alignment of stromal lamellae
with a saw-tooth pattern .
-0.5-2µm lacunae are present in stroma – represent
areas of glycoprotein that differ from normal cornea

63.  PRE-DESCEMET S DEGENERATION
CORNEA FARINATA
- Fine ,flour like ,gray white opacities distributed
in pre-descemet ‘s stroma in older individuals.
- Broad tangential illumination and retroillumination
- Does not affect vision
- These opacities are intracytoplasmic vacuoles
containing lipofuschin in stromal keratocytes.
-Pre –descemet’s opacities also occur in association
with Keratoconus
Posterior polymorphous dystrophy
Ichthyosis

64.  WHITE RING OF COATS
- Superficial stromal discrete round white ring
of dots around a clear centre
-0.1-0.2 mm in diameter
- Occurs after focal corneal injury
-Mostly in men who have been exposed to
occupational hazards
-Histologically the materials may represent
deposits of metallic foreign bodies
- Incidental observation.Vision not affected

66.  HASSAL HENLE BODIES
-Descemet’s warts
-occur with aging in the peripheral cornea
-Posterior non banded layer of descemet’s
membrane progressively thickens with age
- localised excrescences of Descemet’s
membrane produced by degenerating
endothelial cells – due to overproduction of
hyaline
-Non specific response of the endothelium to
injury

67.  DELLEN
- Depressions in the peripheral corneal surface
that occur most often at temporal limbus
-Transient – 24 -48 hours
-Usually occur adjacent to areas of conjunctival
elevation
- Adjacent to areas of chemosis from pterygia,
episcleritis,conjunctivitis,after ocular surgery
- Histopathologically shows thinning of corneal
epithelium,Bowman’s membrane and Stroma
-Treatment – use of ocular lubricants or pressure
patching

68. DEFINITION
Peripheral ulcerative keratitis is a group of
inflammatory destructive diseases involving
the peripheral cornea whose final common
pathway is characterized by corneal melting
ANATOMY AND PATHOGENESIS
- Peripheral corneal anatomy predisposes to
this condition
- Peripheral cornea extends 3.5-4.5 mm from
the visual axis and extends out to the junction
of limbus and sclera

69.  SPECIAL FEATURES OF PERIPHERAL CORNEA
- Greater thickness with tight collagen bundle
- Vascular arcades originating from anterior
ciliary artery extends 0.5 mm into clear
cornea
- Presence of more Langerhans dendritic cells
- High concentration of IgM and C1
-Proximity to the conjunctival vessels and
lymphatics provides the peripheral cornea
access to the immune system
- Limbus and other conjunctival vessels – source
of cytokines and collagenase and proteoglycanase

70.  ETIOLOGIES
- OCULAR NONINFECTIOUS
- Acne rosacea
-Mooren s ulcer
-Traumatic ,post surgical
-Exposure keratopathy
-Terrien’s Marginal degeneration
- OCULAR INFECTIONS
- Staphylococcal
-Viral – Herpes
-Acanthamoeba

71.  SYSTEMIC NONINFECTIOUS
- Rheumatoid Arthritis
- Wegener’s Granulomatosis
- PAN
- SLE
-Microscopic polyangiitis
-Relapsing polychondritis
-Churg strauss syndrome
-Systemic sclerosis and Sjogren’s syndrome
-Cicatricial pemphigoid/IBD/Sarcoidosis
SYSTEMIC INFECTIOUS – tuberculosis , Borreliosis
Gonorrhea,dysentery
Varicella zoster

72.  MOOREN ‘S ULCER
-Fewer than 300 cases in the world’s literature
- Mooren’s ulcer is idiopathic – occuring in the
absence of any systemic disorder
- Begins in clear cornea at the limbus and
progresses centrally,circumferentially and
posteriorly through the cornea
-The edge of the progressive ulcer is undermined
- Painful ulcer – Pain is out of proportion to the
signs
- Low grade Iritis may be present and spontaneous or
traumatic perforation can occur.
- Slow destruction of the entire cornea occurs

73.  PATHOLOGY
 It is believed to be a Type 3 hypersensitivity
The chief inflammatory cell is neutrophils
There is liberation of proteases and
collagenases
The conjunctiva adjacent to the destroyed
cornea has plasma cells ---which secrete
immunoglobulins

75.  MANAGEMENT
Mooren’s ulcer is mainly a diagnosis of exclusion
All other causes of Peripheral ulcerative keratitis
must be ruled out to arrive here
TREATMENT – Wide conjunctival resection to bare
sclera –
extending atleast 2 clock hours on either side of
the peripheral ulcer and 4 mm posteriorly
Then resection of the overhanging lip of ulcerating
cornea
Application of soft tissue adhesive and a soft
contact lens to promote healing

76.  Topical steroid therapy to be started – Prednisolone
sodium phosphate 1% qid
 Systemic tetracycline and 1%
medroxyprogesterone are believed to have
anticollagenolytic properties
 Bilateral progressive Mooren’s – Cytotoxic
chemotherapy – Systemic Methotrexate(7.5-15mg)
Azathioprine(2mg/kg/day)
Cyclophosphamide(2mg/kg/day)
 Therapy to be continued for 6 months before
tapering

77.  Rehabilitative Surgical therapy –
- To be done only after the disease process is
under control
- It needs 2 procedures
- Lamellar tectonic graft
-Followed by definitive penetrating graft
The lamellar graft is needed because the
peripheral corneal stroma is insufficient to secure
A penetrating graft.

78.  ROSACEA KERATITIS
- Rosacea is an inflammatory disorder of
unknown etiology – chiefly affecting the skin
- Affects forehead ,nose , cheeks
-More common in women in 4th decade
-More severe manifestations occur in men
-Believed to be a type 4 hypersensitvity reaction
to Demodex folliculorum
- Skin changes include Erythema,telangiectasia,
Papules,pustules and hypertrophic sebaceous
glands – causing Rhinophyma

79.  OCULAR MANIFESTATION
-Skin manifestations precede Corneal
manifestations except in 10% of cases
- Blepharoconjunctivitis can occur –
staphylococcal blepharitis
- Lid margins are thickened ,hyperemic with
telangiectatic blood vessels and meibomitis
CORNEA –Affects inferior quadrant of cornea
- Punctate epithelial erosions
-Vascular invasion of the peripheral cornea
with subepithelial infiltrates
- Progresses centrally and circumferentially –
ulceration ,scarring and perforation

80.  Limbal involvement – Nodular conjunctivits,
Nodular scleritis
TREATMENT
- Lid scrubs for blepharitis
- Oral tetracycline 250 mg QID for 6 – 8 weeks
- After that dosage to be tapered by 250 mg
per week
- Tetracycline 250mg OD for a year before
discontinuing

81.  PUK IN RHEUMATOID ARTHRITIS
- Usually develops in association with adjacent
necrotising scleritis
-PATHOGENESIS
- - Immune complex deposition in peripheral
cornea and limbal vessels and chemotaxis of
inflammatory cells

82. There are 2 types of PUK in RA
1)Paracentral
2)Peripheral
Paracentral keratolysis –presents in patients with
severe dry eye
Mechanism – Altered epithelium
Inflammatory mediators enter the stroma
Stimulate a sterile keratolysis and a T cell infiltrate
Progresses both centrally and circumferentially
and is unresponsive to topical therapy

83.  Peripheral keratolysis –
There is an obliterative Microangiitis at the level of
limbal vascular arcades
Deposition of Immune complexes in limbal vessels
Causes an immune microangiopathy and
obliterative microangiitis
leakage of inflammatory cells and proteins
collagenases and proteases are released by
neutrophils
corneal melting

85.  WEGENER ‘S GRANULOMATOSIS
- Peripheral ulcerative keratitis is the initial
ocular manifestation
- Sometimes maybe preceded by conjunctivitis
or episcleritis
- Crescentic peripheral corneal ulcer that
resembles Mooren’s ulcer
- Scleral involvement is invariably present
- this helps to differentiate it from Moorens

86.  HISTOPATHOLOGY – lymphocytes and plasma
cells predominate the substantia propria
- The sclera and episclera may show a
- Granulomatous reaction with epithelioid cells
and giant cells
- Areas of active collagen degradation can be
seen
- ANCA testing is positive
- MANAGEMENT – Systemic immunosuppression
with cyclophosphamide and steroids is highly
effective