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Pterygium

Pterygium

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Pterygium

  1. 1. Moderator: Dr. A.Y. Yakkundi Presentor: Dr. Arushi Prakash 1st January 2014
  2. 2. Contents: 08/22/15 1) Anatomy of Conjunctiva 2) Histology of Conjunctiva 3) Definition of Pterygium 4) Risk factors for developing Pterygium 5) Risk factors for predeliction of Pterygium Site 6) Pathophysiology 7) Clinical features 8) Classification of Pterygium 9) Differential Diagnosis
  3. 3. 08/22/15 10) Medical Managemement 11) Surgical Management 12) Adjunctive Therapy to prevent recurrence 13) Complications of current management options 14) Newer Modalities in Treatment of Pterygium
  4. 4. Anatomy of Conjunctiva
  5. 5. Anatomy of Conjunctiva
  6. 6. Palpebral conjunctiva 08/22/15  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
  7. 7. Palpebral conjunctiva 08/22/15 2. Tarsal Conjunctiva • Thin, transparent and highly vascular • In upper lid firmly adherent to whole tarsal plate • In lower lid adherent only to half width of tarsus
  8. 8. Palpebral conjunctiva 08/22/15 3. Orbital Part • Lies loose between the tarsal plate and fornix
  9. 9. Bulbar Conjunctiva 08/22/15 • Thin, transparent and lies loose over the underlying structures, hence can be moved easily. • Seperated from anterior sclera by episcleral tissue and Tenon’s capsule. • 3mm ridge of bulbar conjunctiva around the cornea is called limbal conjunctiva.
  10. 10. Bulbar Conjunctiva 08/22/15 • In the area of limbus, the conjunctiva, Tenon’s 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.
  11. 11. Conjunctival fornix 08/22/15 • Joins the bulbar conjuntiva with the palpebral conjunctiva. divided into 1) Superior fornix 2) Inferior fornix 3) Lateral fornix 4) Medial fornix
  12. 12. Histology of Normal Conjunctiva
  13. 13. Histology of Bulbar Conjunctiva 08/22/15
  14. 14. Histology of Bulbar Conjunctiva 08/22/15
  15. 15. Conjuntiva consists of- three layers 1)Epithelium 2)Adenoid Layer 3)Fibrous Layer 1.Epithelium of the bulbar conjunciva is 3 layered Superficial layer of cylindrical cells Middle layer of polyhedral cells Deep layer of cuboidal cells08/22/15 Histology of Bulbar Conjunctiva
  16. 16. Goblet cells are present in between the epithelial cells. Langerhans cells too are interdispersed in between the epithelial cells. 2.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. 08/22/15 Histology of Bulbar Conjunctiva
  17. 17. 3. 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 Tenon’s capsule. The adenoid layer and the fibrous layer are collectively called SUBSTANTIA PROPRIA of the conjunctiva. 08/22/15 Histology of Bulbar Conjunctiva
  18. 18. The triangular shaped encroachment from the bulbar conjunctiva onto the cornea is known as pterygium from the greek root “pterygos” meaning “little wing”
  19. 19. The base of the triangle lies within the interpalpebral conjunctiva and the apex of the triangle encroaches upon the cornea
  20. 20. Pterygium that is located at the nasal limbus is called nasal pterygium while pterygium located at the temporal limbus is called the temporal pterygium
  21. 21. Risk Factors Pterygium is commonly seen in people living in the Sunny lands of the equatorial region and it is Widely accepted that pterygium is caused by exposure to the UltraViolet B rays of sunlight
  22. 22. Risk Factors •The 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 p53 tumor suppressor gene, thus facilitating the abnormal proliferation of limbal epithelium
  23. 23. Risk Factors • Environmental 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
  24. 24. Risk factors for Pterygium Site Nasal 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. 08/22/15
  25. 25. Risk factors for Pterygium Site Light 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 08/22/15
  26. 26. Risk factors for Pterygium Site The 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 conjunctiva There 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. 08/22/15
  27. 27. Pathophysiology 08/22/15
  28. 28. Concepts of inheritence The detection of a potential tumor supressor gene involvement in pterygium has raised the possibility of a ‘two hit’ mechanism in it’s 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 08/22/15
  29. 29. 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. 08/22/15
  30. 30. Role of Ultra Violet (UV) Radiation But, 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. 08/22/15
  31. 31. Role of Ultra Violet (UV) Radiation It 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. 08/22/15
  32. 32. Role of Ultra Violet (UV) Radiation The presence of Stocker’s line along the head of a progressive pterygium may represent local iron metabolism which may be assosiated with free radical formation through biochemical reaction. 08/22/15
  33. 33. Angiogenesis factor A 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. 08/22/15
  34. 34. Ocular surface changes and Pterygium There 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. 08/22/15
  35. 35. Ocular surface changes and Pterygium There 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. 08/22/15
  36. 36. Oxidative Stress Increased 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. 08/22/15
  37. 37. Molecular genetic alterations p53 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. 08/22/15
  38. 38. Molecular genetic alterations This 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. 08/22/15
  39. 39. Molecular genetic alterations Telomerase 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. 08/22/15
  40. 40. Molecular genetic alterations Difference 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. 08/22/15
  41. 41. Role of genetically altered limbal stem cells It 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. 08/22/15
  42. 42. Role of genetically altered limbal stem cells A 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. 08/22/15
  43. 43. Role of genetically altered limbal stem cells Normal 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) 08/22/15
  44. 44. Role of genetically altered limbal stem cells The altered MMP expression of limbal basal epithelial cells (pterygium cells) enables them to invade and dissolute Bowman’s layer leading to firm adhesion of the lesion on the corneal surface. 08/22/15
  45. 45. 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. 08/22/15
  46. 46. Growth factors and Cytokines UV 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. 08/22/15
  47. 47. Growth factors and Cytokines UV radiation inducible cytokines include interleukin-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 receptors IL-8 displays mitogenic and angiogenic activity 08/22/15
  48. 48. Growth factors and Cytokines Growth factors involved include- • Epidermal growth factor (EGF) and heparin binding EGF, • Vascular endothelial growth factor (VEGF) • Basic fibroblast growth factor • Platelet derived growth factor • Transforming growth factor- beta • Insulin like growth factor proteins 08/22/15
  49. 49. Growth factors and Cytokines VEGF 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. 08/22/15
  50. 50. 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
  51. 51.  Malignant Pterygium: it is very rare and is a recurrent pterygium with restriction of ocular movements 08/22/15
  52. 52. Histologic changes in Pterygium Primary pterygium consists of stratified squamous epithelium of variable thickness 08/22/15
  53. 53. Histologic changes in Pterygium Subepithelial stroma consists of degenerated collagen fibrils, which are basophilic and can be stained by elastic tissue stain but do not get digested by elastase
  54. 54. Histologic changes in Pterygium this is termed as Elastotic Degereration
  55. 55. Histologic changes in Pterygium Recurrent pterygium does not exhibit elastotic degeneration.
  56. 56. 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 growth In the nek of the growth the blood vessels are connective tissue Also present are newly formed tubular glands and larger spaces lined with epithelium, both of which may result in formation of cysts. 08/22/15
  57. 57. CLINICAL FEATURES Symptoms- • Many small lesions are asymptomatic • Other symptoms may vary as- Discomfort Foreign body sensation Congestion Irritation Dryness Tearing (Lacrimation)
  58. 58. Diplopia on lateral gaze Aquired astigmatism For the cosmetically conscious patients painless area of elevated vascularized white tissue on the edge of the cornea may be a problem Impaired vision when growth extends onto the pupillary are of the cornea 08/22/15
  59. 59. Stages of Ptergyium- Progressive- 1) thick, fleshy with prominent vascularity 2) gradually increasing in size and encroaching towards the centre of the cornea 3) opaque infilterative spot (cap) seen just infront of the apex of the pterygium 4) deposition of iron as a line (Stocker’s line) is seen in corneal epithelium infront of the apex.
  60. 60. Parts of a Pterygium It has three zones A) Cap B) Head C) Body
  61. 61. A reddish brown line of iron deposition called Stockers line commonly seen at the apex Iron deposition line in the corneal epithelium, located at the corneal leading edge of a pterygium. Color may vary from yellow to golden brown. Causes no symptom or  clinical significance.
  62. 62. Atrophic- 1) thin, attenuated, with poor vascularity 2) no opaque spot (cap) is seen 3) it is stationary 4) ultimately it becomes membranous but never disappears
  63. 63. 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.
  64. 64. The head grows between Bowman’s layer and basement membrane of the corneal epithelium . Eventually the Bowman’s layer is pushed posteriorly and the pterygium invades the superficial stroma of the cornea.
  65. 65. Clinical Grades of a Pterygium Type 1: Extends less than 2mm onto the cornea.
  66. 66. Clinical Grades of a Pterygium Type 2: Involves upto 4mm of the cornea and may be primary or recurrent following surgery
  67. 67. Clinical Grades of a Pterygium Type 3: Encroaches onto more than 4mm of the cornea and involves the visual axis
  68. 68. Tan’s Classification 08/22/15 MILD PTERYGIUM clearly visible episcleral blood vessels under the body of the pterygium *given by Dr. Donald H Tan in 1997
  69. 69. Tan’s Classification 08/22/15 MODERATE PTERYGIUM partially visible episcleral blood vessels under the body of the pterygium.
  70. 70. 08/22/15 Severe pterygium Totally obscured episcleral blood vessels under the body of the pterygium Tan’s Classification
  71. 71. •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.
  72. 72. Pterygium Pseudopterygium Etiology • Degenerative process • May occur due to chronic exposure to sunlight and dust •Inflammatory process •May be secondary to chemical burns, trauma or surgery Age More commonly seen in the older age group May be seen in any age group
  73. 73. Pterygium Pseudopterygium Site Usually found at the 3o’clock or 9o’clock meridians May appear anywhere on the cornea Laterality Usually bilateral Will mostly be unilateral Stages Either progressive, regressive or stationary Always stationary Adherence to Limbus Adherent to limbus Does not adhere to the limbus, so a glass rod or muscle hook can be passed beneath it
  74. 74. 08/22/15
  75. 75. Differential Diagnosis 08/22/15 other important differentials include •Pingecula, •Nodular Episcleritis, •Phlycten , •Conjunctival carcinoma insitu (Bowen’s Disease), •limbal tumors like  Ocular Surface Squamous Neoplasia, Limbal Dermoid.
  76. 76. PINGUECULA 08/22/15 A pingueculum is limited to limbus and conjunctiva and does not encroach onto the cornea.
  77. 77. Nodular Episceleritis 08/22/15 It would be painful while a pterygium, unless inflammed is not painful
  78. 78. Phlycten A phlyctenule has microabscess-like appearance of the necrotic lesion, marked telangiectatic surrounding vascular pattern, and ulcerated surface, which stains with fluorescein.
  79. 79. Marginal Keratitis 08/22/15 •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.
  80. 80. Conjunctival carcinoma in situ/ Bowens epithelioma. 08/22/15 •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
  81. 81. 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.
  82. 82. Ocular surface squamous neoplasia May 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
  83. 83. Limbal Dermoid 08/22/15
  84. 84. Managemement Medical Management Symptomatic patients- Tear substitutes Inflammation- Topical steroids  Sunglasses- to reduce UV exposure and decrease growth stimulus 08/22/15
  85. 85. Indications for surgery 1.Extension to the visual axis and thus threatening it 2.Visual loss from induced astigmatism. 3.Recurrent irritation leading to intermittent inflammation 4.Restriction of occular movements due to pterygium 08/22/15 Managemement- Surgical
  86. 86. 5. Atypical appearance such as possible dysplagia 6. Cosmetic- patient should be explained there is fairly high risk of recurrence, which may be more unsightly. 08/22/15
  87. 87. Pterygium surgery today varies from the simplest procedure of bare sclera excision to complex surgery such as sclerokeratoplasty and amniotic membrane translaplantation. 08/22/15
  88. 88. OPERATIVE TECHNIQUE The eye is anesthetized Traction sutures may be used if necessary Conjunctival portion of Pterygium is marked
  89. 89. OPERATIVE TECHNIQUE 57 beaver blade is used to dissect the head & neck of pterygium back to limbus
  90. 90. OPERATIVE TECHNIQUE Head of the pterygium is avulsed from the cornea
  91. 91. OPERATIVE TECHNIQUE and residual attachment of tenon’s fascia and conjunctiva can be removed by scraping with a 15# blade which helps to minimize pos-top scarring and astigmatism Sharp dissection of conjunctival portion of pterygium
  92. 92. OPERATIVE TECHNIQUE Limbus polished/smoothed with beaver blade or diamond dusted burr
  93. 93. Wound Closure Options: Bare sclera Simple closure Sliding flap Rotational flap Conjunctival graft
  94. 94. Bare Sclera Closure No sutures or fine, absorbable sutures used to appose conjunctiva to superficial sclera in front of rectus tendon insertion Leaves area of “bare sclera” Relatively high recurrence rate with variable techniques of 5 – 68 % with primary / 35 – 82 % with recurrent)
  95. 95. Simple Closure Free edges of conjunctiva secured together Effective only if defect is very small Can be used for pingueculae removal Reported recurrence rates from 45 – 69 % Few complications (dellen)
  96. 96. Sliding Flap Closure An L-shaped incision is made adjacent to the wound to allow conjunctival flap to slide into place Reported recurrence rates from 0.75 – 5.6 % Few complications (flap retraction / cyst formation)
  97. 97. Rotational Flap Closure A U-shaped incision is made adjacent to the wound to form tongue of conjunctiva that is rotated into place Reported recurrence of 4 % Few complications
  98. 98. Conjunctival Graft Closure A free graft, usually from superior bulbar conjunctiva, is excised to correspond to wound and is then moved and sutured into place Can be performed with inferior conjunctiva to preserve superior conjunctiva
  99. 99. Harvested tissue should be approximately 0.5 – 1 mm larger than defect Most important aspect in harvesting is to procure conjunctival tissue with only minimal or no Tenon’s included Graft is transferred to recipient bed and secured with or without incorporating episclera Some 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
  100. 100. Conjunctival Graft Closure The 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 08/22/15
  101. 101. Conjunctival Graft Closure Tissue adhesive (fibrin glue) is another method of securing the graft. 08/22/15
  102. 102. Fibrin Glue  Contains two of the components that makes the blood clot: Fibrinogen and Thrombin 1. Sealant protein composed of human plasminogen, fibrinogen, fibrinonectin factor XIII reconstituted with human aprotinin. 2. Sealant setting solution composed of human thrombin reconstituted with calcium chloride.
  103. 103. Tisseel kit-2.Duplojet Injector Syringe
  104. 104. 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 graft  When the graft is inversted these two materials mix  The edges of the graft are then approximated using forceps and any excess graft tissue is excised  The graft adheres to the sclera with formation of fibrin clot 08/22/15
  105. 105. Advantages of Fibrin glue over Sutures 1. Decreased patient pain (operative and postoperative), 2. Reduced surgical time 3. Significant reduction in postop inflammation, 4. Recurrence rate=0% 5. Minor and correctable postoperative complications (conjunctival graft dislocation) 08/22/15
  106. 106. Conjunctival Graft Closure The 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. 08/22/15
  107. 107. Conjunctival Graft Closure The 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 08/22/15
  108. 108. Conjunctival Graft Closure Topical 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 present Reduces recurrence to 2 – 5 % (up to 40 % in some reports) Ameliorates the restriction of extraocular muscle function
  109. 109. Limbal Conjunctival Autografts It 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 perform  Recurrence rates of 0-15% have been reported
  110. 110. Amniotic Membrane Graft Closure Useful 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 pterygium  This method minimizes the risk of iatrogenic injury to the rest of the conjunctiva surface  However, it requires costly donor tissue  Reported recurrence rate between 3 – 64 % for primary cases and 0 – 37.5 % for recurrent cases
  111. 111. Lamellar Corneal TransplantLamellar 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.
  112. 112. Lamellar Corneal Transplant Can be used in conjunction with AMT for recurrent pterygia with corneal scarring and limited available conjunctiva Method involves increased surgical complexity, the requirement of donor tissue, and risk of infectious disease transmission 08/22/15
  113. 113. Adjunctive Beta Irradiation Most common dosage is 15 Gy in single or divided doses Reasonably acceptable recurrence rate 3- 11%) Risk of corneal or scleral necrosis and endophthalmitis
  114. 114. Adjunctive Thiotepa Mode of action by inhibition of vascular endothelial proliferation Most common dose is 1:2000 thiotepa given up to every 3 hours for approx. 6 weeks Usually used with bare sclera method Low reported recurrence rates of 0 – 16 %
  115. 115. Adjunctive Thiotepa Complications reported include early and later poliosis and periorbital skin depigmentation that can be permanent Sun exposure during therapy was suggested as a contributing factor in the skin and lash depigmentation. 08/22/15
  116. 116. Adjunctive Mitomycin C Most common dose is 0.02 % applied for 3 min during surgery  It has been recommended as o 1-2 mins application at the fornix edge in mild pterygium) o 2-3 mins for applicationModerate pterygium o 4-5 mins for application Severe pterygium (of MMC
  117. 117. Adjunctive Mitomycin C Risk of aseptic scleral necrosis / perforation and infectious sclerokeratitis Used more often for recurrent cases Rate of recurrence between 3 – 25 % for intra-op / 5 – 54 % for post-op with most studies showing < 10 % recurrence 08/22/15
  118. 118. Transplantation of Head of Pterygium In 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. 08/22/15
  119. 119. Recurrence rates of 30-75% were reported and therefore such procedures abandoned secondary to high recurrence rate and unsatisfactory cosmetic results. 08/22/15
  120. 120. Other Methods:  Pterygium head transplantation  Split skin grafts  Ruthenium adjunctive therapy  Laser or thermal cautery  Excimer laser treatment  Photodynamic thepapy ( verteporfin)  Intraoperative doxorubicin / daunorubicin  5-FU  Serum-free derived cultivated conjunctival graft  Recombinant epidermal growth factor ****Few studies with limited numbers of patients, poor follow-up, and variable recurrence rates
  121. 121. Complications of Pterygium Treatment Operative complications related to pterygium excision are uncommon, and are generally related to the surgical technique. These include Excessive bleeding Button hole of the conjunctiva graft Perforation of the globe with the suture needle Injury to medial rectus muscle08/22/15
  122. 122. Complications of Pterygium Treatment The main postoperative complication is recurrence Other postoperative complications like Pyogenic granuloma Dellen Persistent epithelial defects Are not uncommon, but these may be easily treated with no significant long-term sequelae 08/22/15
  123. 123. 08/22/15 Complications of Graft
  124. 124. 08/22/15
  125. 125. Graft Oedema may result secondary to inadequate debridement of the graft.  All tenon’s capsule remnants should be excised to avoid retraction and post operative oedema. Oedema usually subsides in the first week with topical steroid therapy 08/22/15
  126. 126. 08/22/15 Graft Retraction
  127. 127. Graft Necrosis is a rare complication occuring when the graft is misplaced with epithelial side down or if the recipient bed is avascular. 08/22/15
  128. 128. 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. 08/22/15
  129. 129. 08/22/15
  130. 130. 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. 08/22/15
  131. 131. Subconjunctival haematomas usually subside spontaneously without consequence, except for short term cosmetic appearance 08/22/15
  132. 132. Subconjunctival fibrosis may occur at the donor site. The fibrosis is triggered by the abnormal exposure of Tenon’s capsule and can cause problem that are usually cosmetic involvement of extra ocular muscle in the scar tissue may cause diplopia Corneoscleral thinning- more common in recurrent pterygia.08/22/15
  133. 133. Scleral thinning 08/22/15
  134. 134. Suture Granuloma 08/22/15
  135. 135. Other Complications Of 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 necrosis Infectious scleritis Severe secondary glaucoma Iritis 08/22/15
  136. 136. Secondary Cataract Corneal Oedema Corneal perforation Endophthalmitis 08/22/15
  137. 137. 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 08/22/15
  138. 138. 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 08/22/15
  139. 139. 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. 08/22/15
  140. 140. 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 08/22/15
  141. 141. 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. 08/22/15
  142. 142. 08/22/15 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
  143. 143. 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 08/22/15
  144. 144. 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 08/22/15
  145. 145. 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. 08/22/15
  146. 146. Texts Consulted 1) Anatomy and Physiology of Eye- A.K. Khurana 2) Comprehensive Opthalmology- A.K. Khurana 3 ) Clinical Ophthalmology- A Systemic Approach- Jack J Kanski 4) Surgical and Medical Management of Pterygium- Ashok Garg 5) Stallard’s Eye Surgery 08/22/15
  147. 147. Thankyou  08/22/15

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