Peripheral or Marginal keratitis_025603.pptx

Peripheral
or
Marginal Keratitis
Dr Sunil Kr “Parmar”
Asst. Professor, Department of ophthalmology, Patna Medical college,
Patna

Deceleration
• This power point presentation is only for teaching
purpose
• Presenter has no Financial interest concerned with
this presentation
• Pictures in this presentation has been collected from
by clinic, internet and Book ‘ Kanski's Clinical
ophthalmology’ 9th international edition

Mrs xxx Devi – seen on 23.4.22
Peripheral Epithelial defect Associated with vascularization and anterior uvitis

Mrs xx 36HF
on 11.05.22 on 18.05.22
Peripheral Epithelial defect Associated extreme stromal thinning

Peripheral Epithelial defect Associated extreme stromal thinning
Mrs xx 36HF
on 11.05.22 on 18.05.22

Peripheral or marginal keratitis
1. Marginal keratitis
2. Marginal keratitis ( Rosea)
3. Phlyctenular Keratitis
4. Mooren ulcer
5. Marginal Corneal degeneration
I. Pellucid II. Furrow III. Terrien
6. Dellen
7. PUK with Autoimmune disease
RA,WG,PAD,SLE
• RA- Rheumatoid arthritis
• WG- Wegener Glomerulitis
• PAD- Polyarteritis Nodosa
• SLE – Systemic Lupus Erythematosus

HYPOTHESIS behind this phenomenon
Hypersensitive reaction against Staphylococcal Endotoxin protein and
their cell wall protein .
Results in Attracting Antibody from peripheral blood vessels and tear
film
Formation of Ag- Ab complex
Results Secondary lymphocytic infiltration
However lesions are culture negative
But Staph. Aures is isolated from lid margin

1. Marginal Keratitis
Subepithelial marginal infiltrate at 10, 2, 4,
8 ‘o’clock, at Eye lid contact at limbus
Ulcerations are located in the marginal
zone and separated from the limbus by a
clear corneal zone.
Fluorescein staining often shows
epithelial defects that are smaller than the
infiltrate area

Marginal Keratitis
May 1 or >1
Coalesces
Overlying Corneal epithelial break

Marginal Keratitis
May 1 or >1
Coalesces
Overlying Corneal epithelial break
Circumferential spread

Marginal Keratitis Treatment
Topical steroid qid for 2 wk.
Oral tetracycline to take care of lid infection
Lid hygiene and Antibiotic ointment

Marginal Keratitis Rosea Acne
Common idiopathic
dermatosis
On sun exposed area
Facial telangiectasia
Facial Rhinophyma
Facial Flushing
* * Black head or white head
are absent as in Acne vulgaris

Rosea Acne
Ocular involvement
is
6- 18%
Eye lid telangiectasia

2. Marginal keratitis –
in Rosea with peripheral vascularization
•Marginal
•Limbal
Vascularization
Rosea Acne

Focal
•Corneal
thinning
Ocular involvement – 6-18%
Rosea Acne

•Severe Scarring
•and
•vascularization
Rosea Acne

Rosea Acne Marginal keratitis
Treatment
Topical antibiotic lid ointment – AZITHRO,ERYTHROMYCIN
Low potency steroid drop - minimize corneal thinning
 Oral Tetracycline – Lowers free fatty acid production from lid gland
a. Reduction in lid flora by anti inflammatory effect
b. Reduce activity of collagenase – minimize corneal thinning
c. Doxycycline 100 mg daily for 4 wk followed by 50 mg may be
continued for longer duration, C/I in pregnant, lactating mother
and children
 Severe case – immunosuppression by Azathioprine

Phlyctenular Kerato-conjunctivitis
• Small white limbal or
conjunctival nodule which may
extend to cornea
• Spontaneous resolution may
leave scar or can cause corneal
thinning and even perforation

Self limiting / Due to delayed hypersensitivity to Staphy.Ag
In developing country
T.B or helminth infestation may be a cause
Usually affect child and young
Short course of steroid and antibiotic accelerate healing
In recurrent cases – oral tetracycline is indicated

Mooren ulcer
• Superiorly 1/3rd thickness of cornea
• No clear zone
• It progress central
• No scleral progression
• Overhanging edge in epithelial defect
• Peripheral thinning
• Circumferential progression

Mooren ulcer
 Undermined and
infiltrating leading edge
is characteristic

Mooren ulcer
Recent Classification
• UM- unilateral Mooren's ulcer - Painful and progressive in elderly
• BAM- Bilateral Aggressive Mooren’s ulcer -Circumferential progression in younger
• BIM- Bilateral indolent Mooren’s ulceration Progressive peripheral in middle aged
Etiology
• It may be caused by an exaggerated immune response due to an autoimmune
dresponse to eye injury or infection.

Mooren ulcer
Treatment – if required
Topical treatments to keep tissue from degenerating
1. Moxifloxacin to prevent infections
2. Interferon a2b for hepatitis C infections plus minus antiviral
Ribavirin (Rebetron)
3. Conjunctival resection around ulcer
4. Cryotherapy
5. Tissue adhesion- adhesive materials near the ulcer to stop
spreading

Pellucid marginal degeneration
 Rare /idiopathic/
Degenerative
 BL , Painless
vision loss
 d/d keratoconus.
Clear thinning (ectasia) in the inferior
and peripheral region of the cornea,

Pellucid marginal degeneration
Diagnosed by
Corneal topography.
• Corneal pachymetry to
confirm.
Treatment
• Glass or contact lens
• Corneal cross linking
• corneal transplant surgery.
As the word "pellucid" means
clear that here retain clarity
Butter fly pattern

Furrow degeneration
• Also called as
1. Senile corneal furrow
degeneration of cornea
2. Corneal furrow degeneration, or
3. Age-related marginal corneal
degeneration
1. Safety spectacles (polycarbonate)
2. Contact lens to counter
astigmatism
3. Surgery – Annular excision of
Gutter with lamellar or full
thickness corneal transplantation

Terrien
Marginal degeneration
 Uncommon , idiopathic
 Asymptomatic Peripheral thinning
of cornea
 May be with episcleritis or scleritis
 Mainly male , BL
Visual deterioration due to
progressive astigmatism
 Outer slope of gutter is slopy and central steep
 Slowly progressive peripheral circumferential
thinning lead to Gutter
 A band of lipid is commonly present on corneal edge

Terrien
 Pseudo pterygium
may be seen

Terrien
Treatment
1. Safety spectacles
(polycarbonate)
2. Contact lens to counter
astigmatism
3. Surgery – Annular excision
of Gutter with lamellar or
full thickness corneal
transplantation
 Outer slope of gutter is slopy and central steep
 A band of lipid is commonly present on corneal edge

Dellen
• Dellen occur when the tear film
does not cover the eye. Here we
see
• subconjunctival hemorrhage that
has raised the Conuj. right at the
lumbus.

Dellen
Dellen Due to
Sub conjunctival
Hemorrhage

Dellen
• Post cataract surgery

Dellen
Nodular scleritis with
Dellen formation

Dellen
Chemosis
Long term
with Dellen formation

Dellen
Pingecula
Long term

Dellen
Pterygium
Stromal Elevation

What is PUK?
It is a group of inflammatory destructive disease of peripheral
cornea
Start with crescent shaped epithelial defect in epithelium
Juxta limbal within 2 mm from limbus
Invade deeper in stroma
melting of corneal stroma
corneal necrosis
ultimately lead to and perforation

What is PUK?
Mainly UL , may be BL
Age- affects older
 Gender- any
 Its prevalence is 3 persons per million per year.
 Spontaneous or induced by trauma( surgical / non surgical)
Present as– Redness, Pain, Photophobia, Tearing, D.V

Simultaneous partner of PUK
• 36-66%- Scleritis
most common necrotizing scleritis
• 9-67%- Anterior uveitis

I. Close to sclera
II. Limbal vascular arcade
III.Subconjunctival afferent lymphatics
Why in peripheral cornea?

a.Large number of Langerhans cells
b. Reservoir of inflammatory cells
c. More susceptible to immunological changes
Why in peripheral cornea?

Langerhans cell BIRBECK GRANULE
Tissue-resident macrophages of the Skin
Absent on cornea but present on limbus
Contain Tennis racket shaped specific granule
In case of infection local Langerhans cells uptake and process microbial Ag and transformed into a
fully functional Ag presenting cell.

Pathogenesis of PUK
• PUK is an immunologic condition mediated by both abnormal T-cell and
antibody-mediated pathways
• It is hypothesized that:
 an abnormal T-cell pathway may produce Ab that result in Ag-Ab
complex deposition in the cornea
Later on that activate the complement system and recruit harmful
inflammatory cells to the area.
 Neutrophils and macrophages then secrete local collagenases and
other proteases which cause destruction of the corneal stroma.

Localized conjunctival injection adjacent to the ulcer
supply inflammatory mediators to surrounding infiltrate
Pathogenesis of PUK

PUK – along with perforation

PUK association with systemic diseases
Non infectious disease
• RH Arthritis- commonest
Prevalence 2-3% in adult population
• WG
• SLE
• Poly arteritis nodosa
• Sjogren syndrome
• Leukemia
• Giant cell Arteritis
Infectious disease
• STD
Gonorrhea/ Syphilis/ HIV
• TB
• Salmonella, shigella
gastroenteritis
• Helminthus

Course of disease
The disease generally begins with
 Intense limbal inflammation
 Swelling in the Episcleral
 Swelling in Conjunctiva
 Later on Corneal involvement
 2-3 mm from the limbus
 Appears as grey swellings
 That rapidly furrow
 Affect superior 1/3rd of stroma

PUK presentation and stage
Crescentic ulceration at limbus
 with stromal infiltration and thinning
Spread Circumferentially and occasionally central to cornea
End stage result in ‘Contact Lens Cornea”
May be associated with Limbitis, Scleritis or Episcleritis

PUK in autoimmune disease
This may precede or follow the onset of systemic disease or collagen
vascular disorder
I. Rheumatoid arthritis-
 Commonest association- 30 % cases develop PUK in late vasculitis phase
 May also present as non ulcerative type where
a. gradual resorption of peripheral stroma leaving epithelium intact
b. Gradual thinking and opacification of corneal stroma around
Scleritis
c. Severe dry eye and central corneal melting

PUK in autoimmune disease
This may precede or follow the onset of systemic disease or collagen
vascular disorder
II. Wegener granulomatosis -
 Second commonest association- 50 % cases develop PUK in Early
phase
iii. Relapsing polychondritis- More with episcleritis or scleritis rather PUK
iv. Systemic Lupus erythematosus- (SLE)- Rare association

Crescentic ulceration at limbus with stromal
infiltration and thinning

CRESCENTIC ULCERATION AT LIMBUS
WITH STROMAL INFILTRATION AND THINNING

End stage PUK – ‘Contact Lens’ cornea

PUK treatment - Medical
• Medical
 Therapeutic or Prophylactic appropriate antibiotics
 to dilute cytokinin in precorneal tear film Enhance Lubrication
Patching and bandage contact lens
Topical collagenase inhibitors
Sodium citrate 10%, Acetylcysteine 20% , Medroxy progestron 1%
Systemic Collagenase inhibitor - Tertacycline
Topical steroid –useful in initial stage
Not effective in WG, PAN rather it enhance collagenase effect

PUK treatment
• Medical
 Oral corticosteroid
Methyl prednisolone 1m/kg/day is commonly used
Severe progressive cases – pulsed 0.5 to 1gm methylprednisolone consecutive for 3 days
Immunosuppressive –
immunomodulatory
I. Methotrexate
II. Azathioprine
III. cyclosporine A
Cytotoxic like
Cyclophosphamide

PUK treatment - medical doses
Immunosuppressive –
 in Idiopathic PUK – Cyclosporin A 2.5mg/kg/day
In severe PUK with necrotizing scleritis
First line therapy
Cytotoxic cyclophosphamide 2mg/kg/day with oral or IV methyl
prednisolone
Maintainace by Methotrexate or oral or subcutaneous 7.5 to 12.5 mg
/week

PUK treatment - Surgical
 Conjunctival resection
 Tissue Adhesive – cyanoacrylate glue
Keratoplasty if perforation is larger to be sealed
Surgical lamellar keratectomy to arrest progress
Lamellar tectonic grafting if 7-8 mm cornea unaffected
ulcer more than 1/3rd of periphery – crescent shaped lamellar graft
Ulcer more than 2/3rd of periphery – doughnut shaped lamellar graft

PUK treatment - Surgical
 Amniotic membrane transposition
Conjunctival flap reposition – not in immune mediated PUK

PUK treatment
A. Topical Steroid are warranted increase thinning of sclera
Exception is in Relapsing polychondritis – frequent instillation of
steroid drop is helpful
B. Oral tetracycline 100 mg bd may be helpful as they retard
thinning by anti- collagenase property.
C. Conjunctival excision
D. Corneal Gluing
E. Emergency keratoplasty( lamellar) in Perforation
F. Elective keratoplasty( lamellar or PK) To restore vision

PUK treatment
Because PUK is associated with life threatening systemic vasculitis
The must be treated with immunosuppressive agents on onset
Rheumatologist advise or association should be hired.
I. High dose steroid to control disease
II. Cytotoxic drug for log term for maintenance and counter steroid
side effects
Cyclophosphamide is useful in Wegener granulomatosis
Other are Methotrexate, Azathioprine, Mycophenolate mofetil

This Photo by Unknown Author is licensed under CC BY-SA

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