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Moderator: Dr. A.Y. Yakkundi Presentor: Dr. Arushi Prakash 1 January 2014
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Pterygium

Jan 13, 2017

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Arushi Prakash
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  • Moderator: Dr. A.Y. Yakkundi Presentor: Dr. Arushi Prakash1st January 2014

    **

  • Contents:*Anatomy of ConjunctivaHistology of ConjunctivaDefinition of PterygiumRisk factors for developing PterygiumRisk factors for predeliction of Pterygium SitePathophysiologyClinical featuresClassification of PterygiumDifferential Diagnosis

  • *Medical ManagemementSurgical ManagementAdjunctive Therapy to prevent recurrenceComplications of current management optionsNewer Modalities in Treatment of Pterygium

  • Anatomy of Conjunctiva

  • Anatomy of Conjunctiva

  • Palpebral conjunctiva*It lines the lids.

    1. Marginal Conjunctiva Extends from the lid margin upto about 2mm on the back of the lid upto sulcus subtarsalis (a shallow groove)It is the transitional zone between the skin and conjunctiva proper

  • Palpebral conjunctiva* 2. Tarsal Conjunctiva Thin, transparent and highly vascularIn upper lid firmly adherent to whole tarsal plateIn lower lid adherent only to half width of tarsus

  • Palpebral conjunctiva* 3. Orbital PartLies loose between the tarsal plate and fornix

  • Bulbar Conjunctiva*

    Thin, transparent and lies loose over the underlying structures, hence can be moved easily.Seperated from anterior sclera by episcleral tissue and Tenons capsule.3mm ridge of bulbar conjunctiva around the cornea is called limbal conjunctiva.

  • Bulbar Conjunctiva*In the area of limbus, the conjunctiva, Tenons capsule and episcleral tissue fuse into a dense tissue which is stronly adherent to underlying corneo-scleral junction.At the limbus, the epithelium of conjunctiva becomes continous with that of cornea.

  • Conjunctival fornix*Joins the bulbar conjuntiva with the palpebral conjunctiva.

    divided into1) Superior fornix 2) Inferior fornix 3) Lateral fornix4) Medial fornix

  • Histology of Normal Conjunctiva

  • Histology of Bulbar Conjunctiva*

  • Histology of Bulbar Conjunctiva*

  • Conjuntiva consists of- three layers

    EpitheliumAdenoid LayerFibrous Layer

    Epithelium of the bulbar conjunciva is 3 layeredSuperficial layer of cylindrical cellsMiddle layer of polyhedral cellsDeep layer of cuboidal cells

    *Histology of Bulbar Conjunctiva

  • Goblet cells are present in between the epithelial cells.Langerhans cells too are interdispersed in between the epithelial cells.

    Adenoid Layer- also called the lymphoid layer and consists of connective tissue reticulum in the meshes of which lie lymphocytes. It is not present since birth but develops after 2-3 months of life.

    *Histology of Bulbar Conjunctiva

  • Fibrous Layer- consists of a meshwork of collagenous and elastic fibres. It is thicker than the adenoid layer and contains the vessels and the nerves of the conjunctiva.In the bulbar conjunctiva it blends with the underlying Tenons capsule.The adenoid layer and the fibrous layer are collectively called SUBSTANTIA PROPRIA of the conjunctiva.*Histology of Bulbar Conjunctiva

  • The triangular shaped encroachment from the bulbar conjunctiva onto the cornea is known as pterygium from the greek root pterygos meaning little wing

  • The base of the triangle lies within the interpalpebral conjunctiva and the apex of the triangle encroaches upon the cornea

  • Pterygium that is located at the nasal limbus is called nasal pterygium while pterygium located at the temporal limbus is called the temporal pterygium

  • Risk Factors

    Pterygium is commonly seen in people living in the Sunny lands of the equatorial regionand it is Widely accepted that pterygium is caused by exposure to the UltraViolet B rays of sunlight

  • Risk FactorsThe incidence increases as one gets closer to the equator. A pterygium belt has been mapped within the 30th parallels and is rare north or south of the 40th parallels. This geographic distribution has led to various theories of pterygium pathogenesis, which all emphasize the cumulative absorption of ultraviolet and infrared radiation from sunlight. The working hypothesis is that this radiation causes mutations in the p53tumor suppressor gene, thus facilitating the abnormal proliferation of limbal epithelium

  • Risk FactorsEnvironmental irritants and genetic predisposition are undoubtedly factors, too. There is also a chronic inflammation theory, which proposes that persistent ocular surface disease leads to transformation of limbal stem cells. Actively growing pterygia are more common in advancing age groups, and the incidence in men is nearly twice that of women

  • Risk factors for Pterygium SiteNasal part of bulbar conjunctiva more commonly affected than temporal part

    Various explanations have been given for this predilection.

    It is more exposed to direct irritation than the temporal conjunctiva.*

  • Risk factors for Pterygium SiteLight is reflected from the skin of the nose back on to the nasal limbus.Transcameral light focusing on the nasal limbus may expose limbal basal stem cells to increased amount of UV radiation thus causing genetic alterations in these cells.Longer temporal eyelashes of the upper eye lid and the greater downward bowing of the outer 2/3rds of upper eyelid shades and filters the light falling on the temporal conjunctiva and cornea*

  • Risk factors for Pterygium SiteThe normal flow of tears from temporal to nasal side towards the puctum carries with it any dust particles entering the conjunctival sac, thus further irritating the nasal conjunctivaThere are two anterior ciliary arteries on the nasal side while only one on the temporal side of the. Due to this fact presence of any irritant shall lead to greater hyperemia on nasal side.*

  • Pathophysiology*

  • Concepts of inheritenceThe detection of a potential tumor supressor gene involvement in pterygium has raised the possibility of a two hit mechanism in its pathogenesis.The first hit in the process of a tumor suppressor gene deactivation may be inherited whereas the second hit may be inflicted by environmental factors, such as a viral infection or UV radiation

    *

  • Role of Ultra Violet (UV) Radiation Strong epidemiological correlation between pterygium development and exposure to sunshine has lead to the assumption that some parts of the solar radiation may have direct pathogenic role.Early reports raised the possibility that solar light exposure acted in combination with exposure to dust or sand, thus leading to chronic ocular surface inflammation.

    *

  • Role of Ultra Violet (UV) RadiationBut, high prevelence rate of pterygia was detected in sailors or fishermen, who lived in environments devoid of dust but instead were exposed to increased amounts of scattered light from reflective surfaces such as the sea surface, or in eskimos as the light was reflected off the snow.

    *

  • Role of Ultra Violet (UV) RadiationIt has therefore been suggested that scattered light might follow alternative (transcameral) optical paths when entering the eye, thus hitting limbal stem cells from their inner surface.UV radiation is assosoiated with the creation of active free radicals which attack and deactivate various macromolecules.

    *

  • Role of Ultra Violet (UV) RadiationThe presence of Stockers line along the head of a progressive pterygium may represent local iron metabolism which may be assosiated with free radical formation through biochemical reaction.

    *

  • Angiogenesis factorA pterygium angiogenesis factor may exist which develops following repeated irritation at the limbus.

    This factor may produce vessel ingrowth and the formation of a pterygium.*

  • Ocular surface changes and PterygiumThere may be an assosiation between pterygium and dry eye changes, such as reduced tear film break up time.

    This indicates that pterygium may be a manifestation of a generalized ocular surface dysfunction, including a chronic inflammatory reaction.

    *

  • Ocular surface changes and PterygiumThere has been seen an up-regulation if Phospholipase D types 2, 3 and 4 in pterygium, compared with normal conjunctiva.

    PLD are involved in various processes, including inflammation, cell differentiation, apoptosis and wound healing.*

  • Oxidative StressIncreased UV Radiation oxidative stress has been reported in pterygium as comparerd to normal conjuntiva, leading to induction of proteins like survivin which has been correlated with DNA oxidation and down-regulation of p53.

    *

  • Molecular genetic alterationsp53 levels have been seen to be upregulated in pterygia which may reflect the increased exposure to UV radiation, since wild type of p53 is known to increase in normal tissues in response to DNA damaging agents.

    p53 expression in pterygia have been found to differ between epithelial layers- being higher in basal layers, compared to the more superficial layers.*

  • Molecular genetic alterationsThis finding could reflect increased exposure to UV radiation according to the proposed theory of transcameral exposure of limbal basal (stem) cells to solar light.Telomerase, a ribonucleoprotein participating in cell division is not expressed in normal conjunctiva. It is upregulated in many neoplasias and immortalized cell lines.

    *

  • Molecular genetic alterationsTelomerase is however expressed in pterygium, a finding attributed to neoplastic features of the lesion, or alternatively to induction by UV radiation.Epithelial cells in pterygium have an altered apoptotic potential, There is a disturbed balance between pro-apoptotic proteins (such as bax) and anti-apoptotic proteins (such as bcl-2) in the epithelium of pterygium, in favor of the latter.

    *

  • Molecular genetic alterationsDifference in the apoptotic status between different epithelial cell layers have been detected with apoptosis remaining active at the basal epithelium of pterygium but not at the more superficial epithelial layers.

    *

  • Role of genetically altered limbal stem cellsIt has been postulated that the initial biologic event in the pterygium pathogenesis may be a genetic alteration of limbal stem cells, due to chronic UVR radiation exposure.

    A breakdown of the corneoscleral limbal barrier results in subsequent conjuntivization resulting in pterygium.*

  • Role of genetically altered limbal stem cellsA disrupted balance between the populations of epithelial cells in cornea and conjunctiva could, result in advancement of conjunctival epithelium on the corneal surface resulting in the triangular (wing-like) shape of pterygium.*

  • Role of genetically altered limbal stem cellsNormal conjunctival, limbal, and corneal cells immunostain primarily for matrix metalloproteinase-1(MMP-1)whereas, limbal basal epithelial cells (pterygium cells)immunostain for multiple types of MMPs (MMP-1, MMP-2, MMP-3, MMP-9, membrane type1-MMP and membrane type2-MMP)

    *

  • Role of genetically altered limbal stem cellsThe altered MMP expression of limbal basal epithelial cells (pterygium cells) enables them to invade and dissolute Bowmans layer leading to firm adhesion of the lesion on the corneal surface.*

  • Viral Involvement It has been suggested that there may be a possibilty of an infectious origin of pterygium, viruses known to cause oculodermal infections like herpes simplex virus (HSV), and human papilloma virus (HPV) have been isolated from pterygium by Polymerase chain Reaction (PCR) technique but a correlation between them and pterygium formations has not been established.

    *

  • Growth factors and CytokinesUV radiation mediated genetic trauma may affect the expression of various cytokines, growth factors and growth factor receptors that participate in normal healing.

    Their altered expression in pterygium may indicate a response to ocular surface damage inflicted by the lesion.*

  • Growth factors and CytokinesUV radiation inducible cytokines includeinterleukin-1 (IL-1) system, acting in concert with tumor necrosis factor (TNG) which lead corneal keratocytes to adopt a repair phenotype.The IL-6 promotes epithelial cell migration through induction of integrin receptorsIL-8 displays mitogenic and angiogenic activity*

  • Growth factors and CytokinesGrowth factors involved include-

    Epidermal growth factor (EGF) and heparin binding EGF,Vascular endothelial growth factor (VEGF)Basic fibroblast growth factorPlatelet derived growth factorTransforming growth factor- betaInsulin like growth factor proteins*

  • Growth factors and CytokinesVEGF has been detected in increased amounts in pterygium epithelium, compared with normal conjunctiva by studies employing immunohistochemistry.TR- PCR assays have also revealed a correlation between VEGF expression and postoperative recurrence.*

  • Primary Pterygium is a triangular shaped fibrovascular tissue of bulbar conjunctiva that invades the cornea and occurs without any predisposing event like trauma or surgery. When fibrovascular tissue grows back across the limbus onto the cornea following the excision of primary pterygium it is referred to as recurrent pterygium

  • Malignant Pterygium: it is very rare and is a recurrent pterygium with restriction of ocular movements*

  • Histologic changes in PterygiumPrimary pterygium consists of stratified squamous epithelium of variable thickness

    *

  • Histologic changes in PterygiumSubepithelial stroma consists of degenerated collagen fibrils, which are basophilic and can be stained by elastic tissue stain but do not get digested by elastase

  • Histologic changes in Pterygiumthis is termed as Elastotic Degereration

  • Histologic changes in PterygiumRecurrent pterygium does not exhibit elastotic degeneration.

  • The body of the growth is made up of vascular, areolar tissue, which is compact in old case and is loose in the early stages in which there is rapid growthIn the nek of the growth the blood vessels are connective tissueAlso present are newly formed tubular glands and larger spaces lined with epithelium, both of which may result in formation of cysts.

    *

  • CLINICAL FEATURESSymptoms-Many small lesions are asymptomaticOther symptoms may vary as-DiscomfortForeign body sensationCongestionIrritationDrynessTearing (Lacrimation)

  • Diplopia on lateral gazeAquired astigmatismFor the cosmetically conscious patients painless area of elevated vascularized white tissue on the edge of the cornea may be a problemImpaired vision when growth extends onto the pupillary are of the cornea*

  • Stages of Ptergyium-

    Progressive- 1) thick, fleshy with prominent vascularity2) gradually increasing in size and encroaching towards the centre of the cornea3) opaque infilterative spot (cap) seen just infront of the apex of the pterygium4) deposition of iron as a line (Stockers line) is seen in corneal epithelium infront of the apex.

  • Parts of a PterygiumIt has three zones

    A) CapB) HeadC) Body

  • A reddish brown line of iron deposition called Stockers line commonly seen at the apexIrondepositionline in the corneal epithelium, located at the corneal leading edge of a pterygium.Color may vary from yellow togolden brown.Causesnosymptomorclinicalsignificance.

  • Atrophic-1) thin, attenuated, with poor vascularity2) no opaque spot (cap) is seen3) it is stationary4) ultimately it becomes membranous but never disappears

  • Body of the pterygium is adherent to underlying tenons capsule and spares the episclera, while the neck is adherent to episclera and slera at the limbus due to absence of the tenons capsule.

  • The head grows between Bowmans layer and basement membrane of the corneal epithelium .Eventually the Bowmans layer is pushed posteriorly and the pterygium invades the superficial stroma of the cornea.

  • Clinical Grades of a Pterygium

    Type 1: Extends less than 2mm onto the cornea.

  • Clinical Grades of a Pterygium

    Type 2: Involves upto 4mm of the cornea and may be primary or recurrent following surgery

  • Clinical Grades of a Pterygium

    Type 3: Encroaches onto more than 4mm of the cornea and involves the visual axis

  • Tans Classification*MILD PTERYGIUM clearly visible episcleral blood vessels under the body of the pterygium*given by Dr. Donald H Tan in 1997

  • Tans Classification*MODERATE PTERYGIUM

    partially visible episcleral blood vessels under the body of the pterygium.

  • *Severe pterygium

    Totally obscured episcleral blood vessels under the body of the pterygiumTans Classification

  • It is important to be able to distinguish a Pseudopterygium from a Pterygium

    A pseudopterygium is a fold of bulbar conjunctiva attached to the cornea. It is formed due to adhesions of chemosed bulbar conjunctiva to the marginal corneal ulcer.

  • PterygiumPseudopterygiumEtiology Degenerative process May occur due to chronic exposure to sunlight and dustInflammatory processMay be secondary to chemical burns, trauma or surgery AgeMore commonly seen in the older age groupMay be seen in any age group

  • PterygiumPseudopterygiumSiteUsually found at the 3oclock or 9oclock meridiansMay appear anywhere on the corneaLateralityUsually bilateralWill mostly be unilateralStagesEither progressive, regressive or stationaryAlways stationaryAdherence to LimbusAdherent to limbusDoes not adhere to the limbus, so a glass rod or muscle hook can be passed beneath it

  • *

  • Differential Diagnosis*other important differentials include

    Pingecula, Nodular Episcleritis,Phlycten ,Conjunctival carcinoma insitu (Bowens Disease),limbal tumors like Ocular Surface Squamous Neoplasia,Limbal Dermoid.

  • PINGUECULA*A pingueculum is limited to limbus and conjunctiva and does not encroach onto the cornea.

  • Nodular Episceleritis*It would be painful while a pterygium, unless inflammed is not painful

  • PhlyctenA phlyctenule has microabscess-like appearance of the necrotic lesion, marked telangiectatic surrounding vascular pattern, and ulcerated surface, which stains with fluorescein.

  • 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.

  • Conjunctival carcinoma in situ/ Bowens epithelioma.*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.

  • Ocular surface squamous neoplasia

    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.

  • Ocular surface squamous neoplasiaMay arise from a pterygium, carcinoma in situ, or de novo.On SLE surface may appear keratinized and friable

    On biopsy- well differentiated Squamous cell carcinoma with invasion of basal membrane

  • Limbal Dermoid*

  • ManagemementMedical Management

    Symptomatic patients- Tear substitutes Inflammation- Topical steroids Sunglasses- to reduce UV exposure and decrease growth stimulus

    *

  • Indications for surgeryExtension to the visual axis and thus threatening itVisual loss from induced astigmatism.Recurrent irritation leading to intermittent inflammationRestriction of occular movements due to pterygium*Managemement- Surgical

  • Atypical appearance such as possible dysplagiaCosmetic- patient should be explained there is fairly high risk of recurrence, which may be more unsightly.*

  • Pterygium surgery today varies from the simplest procedure of bare sclera excision to complex surgery such as sclerokeratoplasty and amniotic membrane translaplantation.

    *

  • OPERATIVE TECHNIQUEThe eye is anesthetized

    Traction sutures may be used if necessary

    Conjunctival portion of Pterygium is marked

  • OPERATIVE TECHNIQUE57 beaver blade is used to dissect the head & neck of pterygium back to limbus

  • OPERATIVE TECHNIQUEHead of the pterygium is avulsed from the cornea

  • OPERATIVE TECHNIQUEand residual attachment of tenons fascia and conjunctiva can be removed by scraping with a 15# blade which helps to minimize pos-top scarring and astigmatismSharp dissection of conjunctival portion of pterygium

  • OPERATIVE TECHNIQUELimbus polished/smoothed with beaver blade or diamond dusted burr

  • Wound Closure Options:Bare scleraSimple closureSliding flapRotational flapConjunctival graft

  • Bare Sclera ClosureNo sutures or fine, absorbable sutures used to appose conjunctiva to superficial sclera in front of rectus tendon insertionLeaves area of bare scleraRelatively high recurrence rate with variable techniques of 5 68 % with primary / 35 82 % with recurrent)

  • Simple ClosureFree edges of conjunctiva secured togetherEffective only if defect is very smallCan be used for pingueculae removalReported recurrence rates from 45 69 %Few complications (dellen)

  • Sliding Flap ClosureAn L-shaped incision is made adjacent to the wound to allow conjunctival flap to slide into placeReported recurrence rates from 0.75 5.6 %Few complications (flap retraction / cyst formation)

  • Rotational Flap ClosureA U-shaped incision is made adjacent to the wound to form tongue of conjunctiva that is rotated into placeReported recurrence of 4 %Few complications

  • Conjunctival Graft ClosureA free graft, usually from superior bulbar conjunctiva, is excised to correspond to wound and is then moved and sutured into placeCan be performed with inferior conjunctiva to preserve superior conjunctiva

  • Harvested tissue should be approximately 0.5 1 mm larger than defectMost important aspect in harvesting is to procure conjunctival tissue with only minimal or no Tenons includedGraft is transferred to recipient bed and secured with or without incorporating episcleraSome surgeons harvest limbal stem cells along with graft and orient graft to place stem cells adjacent to site of corneal lesion excision

    Conjunctival Graft Closure

  • Conjunctival Graft ClosureThe conjunctival autograft can be attached with sutures, fibrin glue, elctrocautery or autologous blood.

    While attaching the graft with sutures the 10- nylon or 8-0 vicryl interrupted sutures are used to anchor the graft first at the limbus and then on the nasal aspect*

  • Conjunctival Graft ClosureTissue adhesive (fibrin glue) is another method of securing the graft.

    *

  • Fibrin GlueContains two of the components that makes the blood clot: Fibrinogen and Thrombin

    Sealant protein composed of human plasminogen, fibrinogen, fibrinonectin factor XIII reconstituted with human aprotinin.Sealant setting solution composed of human thrombin reconstituted with calcium chloride.

    *

  • Tisseel kit-2.Duplojet Injector Syringe

  • The two components are applied seperately,

    Thrombin is applied sparingly to the bare sclera site and Fibrinogen is applied to the back or stromal side of the graftWhen the graft is inversted these two materials mixThe edges of the graft are then approximated using forceps and any excess graft tissue is excisedThe graft adheres to the sclera with formation of fibrin clot*

  • Advantages of Fibrin glue over SuturesDecreased patient pain (operative and postoperative),Reduced surgical timeSignificant reduction in postop inflammation, Recurrence rate=0%Minor and correctable postoperative complications(conjunctival graft dislocation)*

  • Conjunctival Graft ClosureThe autograft can also be attached with electrocautery pen.

    The autograft is placed on the bare sclera after excision of the pterygium and the tissue junction is wielded directly using electrocautery pen.At appropriate intervals the whole graft circumference is wielded to the surrounding conjunctiva. Usually 8-10 welds suffise.*

  • Conjunctival Graft ClosureThe latest method of securing the conjunctival graft in place is with use of autologous blood.

    After pterygium excision and fashioning of the autologous conjunctival graft, the recipient bed is encouraged to achieve natural haemostasis and then the conjunctival graft is placed over the scleral defect created after the pterygium excision.The autograft attaches to the sclera with the help of the fibrin clot formed by the oozing blood from the scleral vessels*

  • Conjunctival Graft ClosureTopical antibiotic-corticosteroid ointment used for 4 6 weeks post-operatively until inflammation subsides (compliance with this regimen decreases recurrence)Used when extensive damage or destruction of limbal epithelial stem cells is NOT presentReduces recurrence to 2 5 % (up to 40 % in some reports)Ameliorates the restriction of extraocular muscle function

  • Limbal Conjunctival AutograftsIt has been suggested that including the limbal stem cells in the conjunctival autograft may act as a barrier to conjunctival cells migrating onto the corneal surface and help prevent recurrence.

    The limbal- conjuntival graft includes approximately 0.5mm of the limbus and the peripheral cornea.This method is technically more demanding and time consuming to performRecurrence rates of 0-15% have been reported

  • Amniotic Membrane Graft ClosureUseful for very large conjunctival defects as in primary double-headed pterygium or to preserve superior conjunctiva for future glaucoma surgeries

    Amniotic membrane posseses antiscarring, antiangiogenic and anti-inflammatory properties, which may be useful for treating pterygiumThis method minimizes the risk of iatrogenic injury to the rest of the conjunctiva surfaceHowever, it requires costly donor tissueReported recurrence rate between 3 64 % for primary cases and 0 37.5 % for recurrent cases

  • Lamellar Corneal TransplantLamellar keratoplasty may be required is cases of recurrent pterygia with firm adhesion to the corneal stroma.

    It has been used to act as a barrier against pterygium recurrence and to replace thinned and scarred corneal tissue after pterygium excision.It does not offer any special advantage in precenting pterygium reccurence, with recurrence rates rangingt from 6 to 30%.Not performed often, and not a favored procedure for treating primary pterygium.

  • Lamellar Corneal TransplantCan be used in conjunction with AMT for recurrent pterygia with corneal scarring and limited available conjunctivaMethod involves increased surgical complexity, the requirement of donor tissue, and risk of infectious disease transmission

    *

  • Adjunctive Beta IrradiationMost common dosage is 15 Gy in single or divided dosesReasonably acceptable recurrence rate 3-11%)Risk of corneal or scleral necrosis and endophthalmitis

  • Adjunctive ThiotepaMode of action by inhibition of vascular endothelial proliferation

    Most common dose is 1:2000 thiotepa given up to every 3 hours for approx. 6 weeksUsually used with bare sclera methodLow reported recurrence rates of 0 16 %

  • Adjunctive ThiotepaComplications reported include early and later poliosis and periorbital skin depigmentation that can be permanentSun exposure during therapy was suggested as a contributing factor in the skin and lash depigmentation.

    *

  • Adjunctive Mitomycin C

    Most common dose is 0.02 % applied for 3 min during surgery

    It has been recommended as 1-2 mins application at the fornix edge in mild pterygium)2-3 mins for applicationModerate pterygium4-5 mins for application Severe pterygium (of MMC

  • Adjunctive Mitomycin CRisk of aseptic scleral necrosis / perforation and infectious sclerokeratitisUsed more often for recurrent casesRate of recurrence between 3 25 % for intra-op / 5 54 % for post-op with most studies showing < 10 % recurrence

    *

  • Transplantation of Head of PterygiumIn this procedure, head of pterygium is dissected and transplanted under the conjunctiva away from the limbus so that any future growth is innocous.The Head of the pterygium is not cut but fastened with suture near the insertion of the inferior rectus, beneath lower bulbar conjunctiva.

    *

  • Recurrence rates of 30-75% were reported and therefore such procedures abandoned secondary to high recurrence rate and unsatisfactory cosmetic results.

    *

  • Other Methods:Pterygium head transplantationSplit skin graftsRuthenium adjunctive therapyLaser or thermal cauteryExcimer laser treatmentPhotodynamic thepapy ( verteporfin)Intraoperative doxorubicin / daunorubicin5-FUSerum-free derived cultivated conjunctival graftRecombinant epidermal growth factor

    ****Few studies with limited numbers of patients, poor follow-up, and variable recurrence rates

  • Complications of Pterygium TreatmentOperative complications related to pterygium excision are uncommon, and are generally related to the surgical technique.These include

    Excessive bleedingButton hole of the conjunctiva graftPerforation of the globe with the suture needleInjury to medial rectus muscle

    *

  • Complications of Pterygium TreatmentThe main postoperative complication is recurrenceOther postoperative complications likePyogenic granulomaDellenPersistent epithelial defects

    Are not uncommon, but these may be easily treated with no significant long-term sequelae *

  • *Complications of Graft

  • *

  • Graft Oedema may result secondary to inadequate debridement of the graft.

    All tenons capsule remnants should be excised to avoid retraction and post operative oedema. Oedema usually subsides in the first week with topical steroid therapy*

  • *Graft Retraction

  • Graft Necrosis is a rare complication

    occuring when the graft is misplaced with epithelial side down or if the recipient bed is avascular.*

  • Sclerocorneal dellen occurs due to an oversized graft or persistent oedema.

    Excessive use of the diamond burr or blade to resect the head of the pterygium produces a rough surface with poor lubrication and subsequent dellen formation.*

  • *

  • Epithelial Inclusion Cysts are typically transparent and encapsulated.

    They appear 1 or 2 months postoperatively and may be produced by inclusion of epithelial debris beneath the conjunctival graft.Treatment includes excision of the involved conjunctiva and marsupialization of the cyst.*

  • Subconjunctival haematomas usually subside spontaneously without consequence, except for short term cosmetic appearance

    *

  • Subconjunctival fibrosis may occur at the donor site.

    The fibrosis is triggered by the abnormal exposure of Tenons capsule and can cause problem that are usually cosmeticinvolvement of extra ocular muscle in the scar tissue may cause diplopiaCorneoscleral thinning- more common in recurrent pterygia.

    *

  • Scleral thinning*

  • Suture Granuloma*

  • Other ComplicationsOf greater concern is the potentially serious sight-threatening complications that have been assosiated with the use of adjunctive mitomycin C and beta irradiations, such as

    Scleral necrosisInfectious scleritisSevere secondary glaucomaIritis

    *

  • Secondary CataractCorneal OedemaCorneal perforationEndophthalmitis*

  • Anti-VEGF in treatment of Pterygium As pterygia is composed of proliferating

    fibrovascular tissue and its formation and progression require neovascularization, it was postulated that there may be changed angiogenic stimulator-to-inhibitor ratio.many molecules that positively regulate angiogenesis have been identified of which is marked elevation of VEGF in pterygia in comparison to normal conjunctival samples has been documented

    *

  • Anti-VEGF in treatment of Pterygium With this finding, several trials of anti-VEGF drugs have been made in the treatment of both primary and recurrent pterygia

    *

  • Anti-VEGF in treatment of Pterygium Bevacizumab (Avastin) is a full-length, humanized, monoclonal antibody against all types of VEGF. It binds to and neutralizes the biologic activity of all types of human VEGF, so it prevents interaction with its on the surface of endothelial cells.

    *

  • Anti-VEGF in treatment of Pterygium Bevacizumab has been used to treat choroidal neovascularization due to age-related macular degeneration (ARMD), and more recently diabetic macular edema.Various clinical trials have shown that when administered intravitreally, it is well tolerated and associated with improvement in visual acuity, decreased central retinal thickness, and reduction in angiographic leakage

    *

  • Anti-VEGF in treatment of Pterygium Few studies have recently been undertaken to determine the clinical effect and safety of subconjunctival injection of bevacizumab for pterygium.

    *

  • *Results after a single dose of subconjunctival bevacizumab (0.2 ml/2.5 mg) in patients with recurrent pterygium

    * Alhammami H, Farhood Q, Shuber H (2013) Subconjunctival Bevacizumab Injection in Treatment of Recurrent Pterygium. J Clin Exp Ophthalmol 4: 267

  • Anti-VEGF in treatment of Pterygium Contradindications to Bevacizumab-allergy to bevacizumab, hypertension, proteinuria, bleeding tendencies, previous myocardial infarction or stroke, pregnant and lactating women *

  • Anti-VEGF in treatment of Pterygium No ocular-surface toxicity, persistent epithelial defects, corneal abrasion, infections, or uveitis were reported during the study. Occasional subconjunctival hemorrhage has been observed after injection and these resolved without intervention within 1-2 weeks

    *

  • Anti-VEGF in treatment of Pterygium Local application of bevacizumab, however, showed promise in inducing regression in pterygium vascularity and thickness.More research is still required in this area and this drug may later prove to be a boon for Pterygium inflicted patients who do not want to undergo surgery.

    *

  • Texts Consulted1) Anatomy and Physiology of Eye- A.K. Khurana2) Comprehensive Opthalmology- A.K. Khurana3 ) Clinical Ophthalmology- A Systemic Approach- Jack J Kanski4) Surgical and Medical Management of Pterygium- Ashok Garg5) Stallards Eye Surgery*

  • Thankyou *

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