pterygium and its management

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PTERYGIUM AND ITS MANAGEMENT MODERATOR: DR SURESH.H.H PRESENTER:DR ANJALI

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Page 1: Pterygium and its management

PTERYGIUM AND ITS MANAGEMENT

MODERATOR: DR SURESH.H.H PRESENTER:DR ANJALI

Page 2: Pterygium and its management

Anatomy of conjunctiva

Page 3: Pterygium and its management

Histology of normal conjunctiva

Page 4: Pterygium and its management

Derived from Greek word ‘pterygion’ means wing.

It is a non malignant slow growing proliferation of wing shaped fibrovascular tissue.

Arises from subconjunctival tissue. May extend over the cornea thus disturbing

the vision.

DEFINITION- PTERYGIUM

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World wide distribution.

More common in warm and dry climates.

Prevalence : 22% equatorial areas.

<2% in latitudes between

28-38degree.

Direct relation with amount of UV exposure.

EPIDEMIOLOGY

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Sex: male : female= 2:1

Age:>40years high prevalence

20-40years high incidence.

In India prevalence is 9.5%.

Morbidity: causes significant alteration in

visual function in advanced cases.

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Strong association between UV light exposure and formation of pterygium.

More common- in patients who worked outdoors.

In welders than other factory workers. Also associated with basal cell carcinoma,

porphyria cutanea tarda, polymorphous light eruptions, xeroderma pigmentosa.

ETIOPATHOGENESIS.

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ANGIOGENESIS FACTOR:Prolonged UV

exposure causes biological changes in the

bowmans membrane.

Altered protein so formed could act as

angiogenic/ pterygiogenic factor.

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UV Exposure: May induce hyperplasia in limbal

cells. These altered cells invade the cornea and

limbus which moves centripetally with them.

This explains wing shape of the pterygium.

UV radiation causes depletion of langerhan

cells at limbus.(stocker’s line).

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Exposure to UVB+altered tear film

Injury and susceptibility

Loss of collagenase and dehydration

Accumulation of Extracellular matrix

Antigenic,type1 HS Pinguecula Fibroblastic reaction Inflammation PTERYGIUM PTERYGIUM

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Light entering the temporal limbus at

90degree is concentrated at medial limbus.

Related to corneal curvature.

This explains the predominance of medial

pterygium.

ALBEDO HYPOTHESIS

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Dry and dusty environment.

Drying of the tear film by wind devitalizes

tissue of medial 3rd of the palpebral

aperture.

This allows the actinic radiation to damage

the conjunctival, corneal epithelium and

bowmans membrane.

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MICROTRAUMA: mechanical irritation by dust particles, enhanced by tear flow from lateral to medial.

IMMUNOLOGY: Cell bound IgE irritant complexes initiate the release of inflammatory mediators from mast cells.

Release of stimulatory factors. Development of pterygium.

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Expression of vimentin. P53 mutation leads to decreased

apoptosis and increased TGF-b which leads to increased growth.

RECURRENT PTERYGIUM- stem cells are more scattered and expression pattern is more denser.

Genetic predisposition

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HYPOXIA: increase in non perfusion areas and attenuated vessels in nasal limbus during early stage of pterygium causes recruitment of progenitor cells.

Viral markers: infection with HPV and herpes virus is considered as risk factor(rare).

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Elastotic degeneration of collagen.(Not a true elastic tissue)

Fibro vascular proliferation with an overlying covering of epithelium-characterized by Cellular proliferation.

Tissue remodeling. Neovascularisation.

Subepithelial tissue shows basophilic degeneration.

PATHOLOGY

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Destruction of bowman’s membrane in the cornea.

So there is residual corneal scarring when these growth are removed.

Epithelium shows secondary changes like orthokeratosis,acanthosis,dyskeratosis.

Mast cells occur in increased number.

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Histology

Normal conjunctiva Pterygium

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Histology

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CLINICAL STAGING PATHOLOGICAL STAGING

Stage I Exposure conjunctivitis

Size and number of Conjunctival vessels Mild – moderate congestionS/S of drynessNo formed lesions

Altered tear filmMild vascular response

Stage II Pinguecula and pterygium

Distinct raised lesion on bulbar conjunctivaWith or w/o abnormal vascularization and inflammation

Cell injuryInflammatory response

Clinical staging of pterygium

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Stage III Limbal pterygium

Head is on or across the limbus with or w/o an iron line at the conjunctival corneal interface

Vascularization and fibrous proliferationSymptoms more pronounced

Lesion organization

Mixed proliferation and degeneration

Stage IV Corneal pterygium

Lesion 2mm or more into corneaInvasion of granulation tissueZone of dellenStocker’s lineInfiltration of corneal nerves- pain

Lesion b/w epithelium and bowman

Mixed proliferative and degeneration

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Stage V

Compound pterygium

Induced astigmatismSymptoms more frequent and severe

Lesion extended into stroma

Mixed proliferative and degeneration

Proliferation- Small lymphocytes and plasma cellsDegeneration- Swirls of type I collagen

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Fuch’s patches. Stocker’s line. Hood. Head. Body. Base. Superior edge. Inferior edge.

Parts of pterygium

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Parts of pterygium

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Progressive: thick fleshy marked vascularity.It has opaque infitrative spot known as cap.Stocker’s line.

Atrophic/stationary: thin attenuated poor vascularity no cap.

Clinical types of pterygium

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Clinical types

Progressive pterygium Atrophic pterygium

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Stocker’s line

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Primary double pterygium.

Recurrent pterygium.

Pseudopterygium.

Malignant pterygium(rare):recurrent

pterygium with restriction of ocular

movements.

Other types

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Double pterygium involving the visual axis

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Asymptomatic Foreign body sensation Discomfort Congestion(redness) Irritation and grittiness-interference with

precorneal tear film. Interference with vision-obscuring visual axis -inducing astigmatism

Cosmesis.

Signs and symptoms

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Type 1: extends <2mm on the cornea.

Type 2: 4mm of cornea is involved.

Type 3: encroaches onto >4mm of cornea and involves visual axis.

Signs

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Pseudopterygium

Most often hx of previous infective, chemical, thermal, or traumatic injury to the cornea.May occur at multiple locations and is not restricted to the 3 and 9 o'clock (interpalpebral) positions.

-Slit-lamp examination: reveals lesion to be adhesion of a fold of conjunctiva, which has occurred as a response to a previous peripheral corneal ulcer/inflammation.-Lesion typically only fixed at its apex to the cornea so that a probe may be passed underneath its body at the limbus, while a true pterygium adheres to the underlying cornea throughout its length. Thinning of the underlying cornea may be seen at its head.

Differential diagnosisCondition Signs and symptoms Tests

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Pinguecula Does not encroach on the cornea.

Slit-lamp examination: reveals exact extent and nature of lesion. A pingueculum is limited to limbus and conjunctiva and does not encroach onto the cornea.

Marginal keratitis Associated with blepharitis. Infiltrate on corneal surface is separated by a clear zone from the limbus. Occur at 2, 4, 8, and 10 o'clock position. Does not have typical pterygium shape. Often superior and inferior.

Corneal swab/scraping: microscopy and culture positive for infecting organism, but infecting organisms are often not detected, as many cases are due to an inflammatory reaction to staphylococcal proteins

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Corneal micropannus Hx of trachoma or lack of corneal oxygenation due to excessive contact lens wear.

Slit-lamp examination: reveals encroachment of fine blood vessels onto corneal surface.

Conjunctival carcinoma in situ/ bowens epithlioma.

Rare. Does not have typical pterygium shape. Not restricted to the 3 and 9 o'clock (interpalpebral) positions and can occur at any position on the cornea.

Slit-lamp examination: gelatinous-appearing mass.Biopsy: cytological features of a squamous cell carcinoma, but the basal membrane of the epithelium remains intact.

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Squamous cell carcinoma

Rare. Does not have typical pterygium shape. Not restricted to the 3 and 9 o'clock (interpalpebral) positions and can occur at any position on the cornea. May arise from a pterygium, carcinoma in situ, or de novo.

Slit-lamp examination: surface may appear keratinised and friable.Biopsy: well-differentiated squamous cell carcinoma with invasion of the basal membrane.

Limbal dermoid Benign choriostomatous tissue. MC site:inferior temporal quadrant.

Histology contains abberant tissue like epidermal appendages,connective tissue,skin,fatmuscle teeth.

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Symptomatic patients- Tear substitutes Inflammation- Topical steroids

Sunglasses- to reduce UV exposure and decrease growth stimulus

Medical Treatment

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1. Extension to the visual axis and induced astigmatism.

2. Recurrent irritation.

3. Cosmetic- patient should be explained there is fairly high risk of recurrence, which may be more unsightly.

Indications for surgery

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Free conjunctival autograft for primary and recurrent pterygium.

Pre op evaluation:

1. Evaluation of pterygium.

2. Evaluation of superior bulbar conjunctiva.

3. Pre op preparation.

4. Anaesthesia and sedation.

Surgical technique

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Preparation and drape.

Place anaesthetic drops or topical vasoconstrictor.

Ask patient to look opposite side of pterygium.

Surgical technique

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Pterygium Excision Goal: Achieve a normal, topographically

smooth ocular surface Dissect a smooth plane toward the

limbus Preferable to dissect down to bare

sclera at limbus Bare sclera = remove loose Tenon’s

layer and leave episcleral vessels intact

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Mechanism of action: it acts forming a fibrin clot between graft and host tissue.

Advantages : decreases the post op pain. reduces the surgical time as

well as recurrence rate.Disadvantage : not FDA approved. graft dehiscence. infection, discomfort.Recurrence rate: less as compared to suture.

Fibrin sealant and conjunctival auto graft

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Avoid exposure to sunlight.

Use of dark sun glasses.

Topical steroid antibiotic drops, topical NSAIDS, artificial tears.

POD3/5 graft acquires redness.

Post operative care

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Complete healing expected between 6-8weeks.

Topical medications should be tapered. Lubricants should remain for 3months.

Instruction to patient: avoid exposure to sunlight.

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Graft failure. Granuloma formation. Conjunctival infection. Suture detachment. Delayed healing. Recurrence.

Complications

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Bare sclera technique:-recurrence:5-68%(primary)35-82%(recurrent)

Other surgical methods

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Simple closure: recurrence 45-69%

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Sliding flap: recurrence 45-69%

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Rotational flap: recurrence 4-6%

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Subconjunctival scarring limitation of movements diplopia.

Disinsertion of medial rectus muscle.

Scleral perforation.

Corneal irregularity due to deep stromal excision.

Complications

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Pterygium Recurrence Growth of fibrovascular tissue across the

limbus onto cornea after initial removal.

Excludes persistence of deeper corneal vessels and scarring which may remain even after adequate removal.

Bunching of conjunctiva and formation of parallel loops of vessels, which aim almost like an arrowhead at the limbus, usually denotes a conjunctival recurrence.

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Proposed Recurrence Grading System

Grade 1 – normal appearing operative site.

Grade 2 – fine episcleral vessels in the site extending to the limbus.

Grade 3 – additional fibrous tissues in site.

Grade 4 – actual corneal recurrence.

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AIM: To reduce recurrence.1. Corticosteroids- post operative use of

topical steroids can reduce inflammatory reaction and revascularization at the operative site.

2. No significant role in prevention of recurrence.

Adjunctive therapy

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Antibiotic and antineoplastic properties.

Blocks the DNA synthesis.

Concentration: 0.02%

Use: intraoperative to the area of resection

with sponge for 2min followed by irrigating

with balanced salt solution.

Mitomycin C

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Side effects: pyogenic granuloma dellen of sclera. perforation of eye. glaucoma. cataract. corneal edema. Recurrence: 3-25% (intraoperative) 5-54%(postoperative)

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Post operative period LCAG MMC 3 month 1 - 6 month 1 2 12 month - 1 18 month - - Total 02 (4%) 03 (6%)

Comparison of recurrence rate

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Nitrogen mustard alkylating agent. antimitotic property. Radiomimetic- obliterates vascular

endothelial cells. Dose:1:2000 every 3 hours for 6 weeks. Used in bare sclera method. Complication: scleral thinning. Recurrence:10-16%

Thiotepa

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Antiproliferative Inhibits thymidylate synthetase, thus

inhibits DNA. Only cells in the synthesis phase are

affected, allowing the remaining cells to continue to proliferate after exposure to 5-FU.

5-fluorouracil

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Immunosuppresant drug. Dose: 0.05% topical for 3 months following

pterygium excision.

Safe and effective.

Low recurrence rate(3.4%)

Cyclosporine A

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Inhibit neovascularisation. Stop the progression or prevent the

recurrence.

Case reported by Wu and co workers.Topical bevacizumab eye drops 25mg/ml

4times for 3weeks. No recurrence in 1year follow up period.

Bevacizumab

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Reduces mitosis in rapidly dividing vascular endothelial cells.

Dose : 15Gy units in single or divided doses.

Recurrence: 4.3%-35% with bare sclera or simple conjunctival closure.

Complications: scleral necrosis endophthalmitis cataract formation. conjunctival telangiectasia.

Beta radiation

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The area of bare scleral was covered with amniotic membrane, which was oriented with the basement membrane side up.

The amniotic membrane was sutured through the episcleral tissue to the edge of the conjunctiva along the bare sclera border with 7-8 interrupted 8-0 Vicryl sutures.

The eye was patched.

Amniotic membrane.

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Amniotic membrane application after pterygium excision

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Useful in:

very large conjunctival defects. To preserve superior conjunctiva for future

glaucoma surgery.

Advantages: faster healing rate less discomfort. lower recurrence rate(2% in 1year follow up)

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ANECORTANE ACETATE:

Angiostatic steroid: Inhibits the blood vessel’s.

Topical 1% have inhibitory effect on pterygium regrowth following recurrenr pterygium excision.

Under trial

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Surgical and medical management of pterygium-Ashok garg.

Pterygium-a practical guide to management,L. Alfred andeze.

Kanski clinical ophthalmology.

References

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THANK YOU