This document provides an overview of pterygium, including:
1. The anatomy and histology of the conjunctiva where pterygium develops.
2. Risk factors for pterygium include ultraviolet light exposure, which may cause genetic mutations in limbal stem cells through oxidative stress and altered expression of growth factors.
3. Pterygium is believed to develop from these genetically altered limbal stem cells, disrupting the normal balance between corneal and conjunctival epithelium and allowing conjunctiva to grow onto the cornea.
2. Contents:
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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
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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
6. Palpebral conjunctiva
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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. Palpebral conjunctiva
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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
9. Bulbar Conjunctiva
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• 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. Bulbar Conjunctiva
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• 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. Conjunctival fornix
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• Joins the bulbar conjuntiva with the palpebral
conjunctiva.
divided into
1) Superior fornix
2) Inferior fornix
3) Lateral fornix
4) Medial fornix
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. 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.
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Histology of Bulbar Conjunctiva
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.
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Histology of Bulbar Conjunctiva
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. The base of the triangle lies within the
interpalpebral conjunctiva and the
apex of the triangle encroaches upon
the cornea
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. 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. 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. 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. 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.
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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
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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.
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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
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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)
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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.
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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.
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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.
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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
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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.
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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. Malignant Pterygium: it is very rare and
is a recurrent pterygium with restriction of
ocular movements
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54. 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
59. 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.
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60. CLINICAL FEATURES
Symptoms-
• Many small lesions are asymptomatic
• Other symptoms may vary as-
Discomfort
Foreign body sensation
Congestion
Irritation
Dryness
Tearing (Lacrimation)
61. 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
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62. 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.
63. Parts of a Pterygium
It has three zones
A) Cap
B) Head
C) Body
64. 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.
65. 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
66. 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.
67. 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.
68.
69. Clinical Grades of a
Pterygium
Type 1: Extends less than 2mm onto the
cornea.
70. Clinical Grades of a
Pterygium
Type 2: Involves upto 4mm of the cornea
and may be primary or recurrent following
surgery
71. Clinical Grades of a
Pterygium
Type 3: Encroaches onto more than 4mm of
the cornea and involves the visual axis
75. •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.
76.
77. 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
78. 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
83. Phlycten
A phlyctenule has microabscess-like
appearance of the necrotic lesion, marked
telangiectatic surrounding vascular pattern,
and ulcerated surface, which stains with
fluorescein.
85. Conjunctival carcinoma in
situ/ Bowens epithelioma.
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•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
86. 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.
87. 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
90. 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
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Managemement- Surgical
91. 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.
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92. Pterygium surgery today varies from the
simplest procedure of bare sclera excision
to complex surgery such as
sclerokeratoplasty and amniotic membrane
translaplantation.
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93. OPERATIVE TECHNIQUE
The eye is anesthetized
Traction sutures may be
used if necessary
Conjunctival portion of
Pterygium is marked
96. 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
99. 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)
100. 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)
101. 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)
102. 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
103. 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
104. 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
105. 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
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107. 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.
109. 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
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110. 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)
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111. 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.
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112. 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
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113. 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
114. 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
115. 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
116. 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.
117. 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
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118. 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
119. 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 %
120. 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.
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121. 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
122. 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
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123. 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.
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124. Recurrence rates of 30-75% were
reported and therefore such procedures
abandoned secondary to high recurrence
rate and unsatisfactory cosmetic results.
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125. 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
126. 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
127. 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
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130. 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
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132. Graft Necrosis is a rare complication
occuring when the graft is misplaced with
epithelial side down
or if the recipient bed is avascular.
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133. 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.
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135. 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.
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137. 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
140. 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
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142. 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
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143. 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
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144. 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.
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145. 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
146. 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.
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147. 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
148. 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
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149. 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
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150. 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.
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151. 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
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