Pterygium

PTERYGIUM
A PRACTICAL GUIDE TO MANAGEMENT

PTERYGIUM
A PRACTICAL GUIDE TO MANAGEMENT
Alfred L Anduze MD MH
PO Box 3019
Island Medical Center
Kingshill, US Virgin Islands 00851
Foreword
John C Merritt
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Pterygium: A Practical Guide to Management
© 2009, Jaypee Brothers Medical Publishers
All rights reserved. No part of this publication should be reproduced, stored in a retrieval system, or transmitted in any form or by any
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First Edition: 2009

ISBN 978-81-8448-725-1
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Dedicated to
My colleagues and scholars who believe in good basic

medical and surgical principles for pterygium
management and set out to diagnose and treat in the most
effective manner.
and
My wife and family for putting up with my “practice” of
medicine for so long.
Foreword
On my first work day within the Surgery Department at Howard Universty College of Medicine in Washington,
DC, I was introduced to Alfred Anduze, MD, MH, Leon Reid, MD and Ghaleb Hatem, MD as first year residents in
the Ophthalmology Residency Program of July 1975. All the three residents were easy to teach as they were good
listeners, avid readers and compassionate physicians. Fred returned to his home St Croix, Virgin Islands, to begin
his ‘maiden voyage’ with the disease ‘pterygium’. During his first 15 years of busy practice, he maintained the
commitment to elevate both standards of patient care and continuing medical education within the Caribbean
nations. To this end, he engaged in the Continuing Medical Education (CME) Department at Howard University
College of Medicine to provide educational seminars dealing with the common diseases (diabetes, glaucoma, cataract)
within the Virgin Islands. These CME ventures were closely followed by the formation of the Ophthalmic Society of
the West Indies (OSWI). During one of our early OSWI scientific sessions, Dr Hugh Vaughn of Kingston, Jamaica
and one of its first 4 ophthalmologists, made the comment:”Fred, everybody in the Caribbean is an expert on
pterygium.” It is true that every practicing ophthalmologist may “see” a lot of pterygium patients, but a few are
hardly “experts.” Only Alfred L Anduze MD, MH has separated himself by refusing to blend into the “treat as usual
routine”. The ophthalmic world has ‘thereafter’ been blessed by his relentless desire to remain a student of (constantly
learning) and physician for preventing and treating this disease.
Physicians interested in disease prevention will appreciate the ocular and systemic therapies described in the
‘Prevention’ chapter. Essentially informative is the simple approach to understand sunglasses, hydration (local and
systemic) and the avoidance of maximum sunlight exposure times (10 am to 2 pm). The Chapter that correlates the
clinical staging of pterygium with its histopathologic characteristics is critical to understand early preventive therapy.
Finally, the surgery section, with the appropriate pre- and postoperative regimes in lace, provides established surgical
techniques with low recurrence rates. Thank you, Fred, for being the physician, teacher/educator and humanitarian
(family and the world) that we know and for finally sharing a 30-year pterygium experience with the world.
John C Merritt MD
Prevention for the People, Inc.
Clinton, North Carolina, USA
Preface
A pterygium (Gk), as its name suggests, is a wing-like, fleshy mass of tissue usually located in the medial palpebral
fissure and commonly affects both eyes with differing severity. In the Caribbean, it is also known as el pterygio and
le ptérygion. Colloquially, it is referred to as a ‘fish scale’ in the eye, ‘unio’ and simply, as a ‘flesh’. This book is
intended to provide a detailed clinical layout for general and specific pterygium cases. It is a guide for students,
residents and practitioners who encounter classical as well as unusual cases. It is a manual of clinical situations and
deals with how to approach and get the best results. It is based on 35 years of experience with some basic lesions and
some of the most complicated cases seen in extreme tropical conditions. It is my hope and expectation that it will be
translated and distributed in the regions of the world where pterygium is endemic and becoming more common.
Alfred L Anduze
Acknowledgments
James V Kasin MD Jean-Christophe Joyaux MD
Chapter four on Pathology, preparation and interpreta- For encouragement, support and the conjunctival
tion of histological sections (Australia and Virgin Islands). autograft technique and photos.
(Martinique and Bordeaux, France)
Eduardo Alfonso MD
For features of a corneal lesion and everything there is to John C Merritt MD

know so far about external diseases. For inspiration, motivation, unwavering support and
(Miami, Florida) repeated reminders to get this work done.
(Clinton, North Carolina)
Juan Batlle MD Basil Morgan MD
For developing the Ambiodry technique and sharing his For continued interest and suggestions on VEGF research.
knowledge of pterygium with others. (Baltimore, MD)
(Santo Domingo, Dominican Republic)
Raymond Richer MD
Alfonso Equiguieren MD For sharing conjunctival autograft cases and exposing the
For his questioning mind and unquestioned loyalty. May positives and negatives of our various techniques.
he rest in peace. (Fort-de-France, Martinique, France)
(Georgetown, Guyana)
Cyril Reifer MD
Of Barbados: First to use conjunctival flaps technique

Khalil Fakim MD
when it was the merest sclera and stick with it, with good
For the mucosal graft surgery protocol and complications.
results. (Bridgetown, Barbados)
(Mauritius)
Michel Sickenberg MD
Sam Jones (Artist) For the complicated cases and FRAS and anti-
Surgical Technique Illustrations inflammatory treatments prior to and after surgery.
(St Croix, Virgin Islands) (Lausanne, Switzerland)
xii Pterygium: A Practical Guide to Management
Garth Taylor MD Hugh Vaughn MD
For his solid support and incredible wisdom to see the For disagreeing (often) and offering alternative solutions
value of trying new techniques. We will never forget him. such as transposition and bare sclera with beta radiation.
(Toronto, Canada) (Kingston, Jamaica)
William Trattler MD The Ophthalmic Society of the West Indies (OSWI)

For trying the conjunctival flaps technique with …for providing a forum in which to discuss controversial
mitomycin C, realizing its value, expanding on it and findings, and its members for being so resistant as to make
sharing his knowledge with others. defining and refining the work a necessity.
(Miami, Florida) (West Indies)
Sheffer Tseng MD, PhD Doctors in Hungary, Tunisia, Libya, Egypt, the
Genius of the ocular surface; for the amniotic membrane Netherlands and Mexico, who showed enough interest
graft technique and video and your timely advice with in the treatment of pterygium to share their views and
complicated cases. (Miami, Florida) cases and provide a forum for discussion.
Contents
Chapter 1 Features ................................................................................................................................................ 1
Chapter 2 Epidemiology ................................................................................................................................... 11
Chapter 3 Pathogenesis ..................................................................................................................................... 15
Chapter 4 Pathology ........................................................................................................................................... 23
Chapter 5 Prevention ......................................................................................................................................... 37
Chapter 6 Surgery ............................................................................................................................................... 47
Chapter 7 Complications .................................................................................................................................. 81
Appendix ........................................................................................................................................... 107
Index .................................................................................................................................................. 117

Introduction
Most books and articles on pterygium focus on Most of the information, suggestions and deductive
outcomes. This practical guide identifies the features findings in this manual are based on empirical data in
of a particular case and the reasons for using a the forms of direct and indirect observation of results
particular method. as well as research studies and is to be used for clinical
All of the management strategies are the surgeon’s interpretation and management of the individual case.
preference and are based on more than 30 years of Much of the content is based on articles written over
experience with large, active, tropical pterygia. The the years by the author and others from regions in
repeated themes of protection from UV radiation, which pterygium is prevalent. Some of the information
inflammation control and restoration of tear film is anecdotal and will be designated as such. The ideas
refer to the elements of pathogenesis which have been and suggestions presented are based on logic and
observed as leading directly to prevention and experience. Some are controversial and may appear
successful medical and surgical management. Clinical to be circumstantial. This is a clinical, practical guide.
situations involving preoperative treatments, intra- It is comprised of management strategies that work.
operative techniques and postoperative care are However, when the decision on management of a
derived from actual patient cases. By following the particular case is made, the practitioner should do
basic principles and practices of good medicine, initial what is the most appropriate and effective in his/her
growth and recurrence of pterygia can be prevented. hands.
For the practitioners who see and do 4 or 5 cases a I did my first pterygium operation in 1978, upon
year as well as those who do more than 100 cases, the my return to the Virgin Islands.
most effective approaches with the lowest acceptable There was a backlog of cases, half of which were
recurrence rate (<1%) will be highlighted. Recommen- recurrences done elsewhere. I used the bare sclera
dations and suggestions are based on observed and technique which was merely suggested in the textbook
documented results of over 5000 pterygium cases without any detailed management and was rewarded
managed by the author. with the customary 50% recurrence rate. On the timely,
For an excellent reference on historical and in-depth advice from a doctor in Puerto Rico with more
perspectives, the textbook, Pterygium Surgery by Lucio experience than I, phenol 30% was tried as an adjunct.
Burratto and associates is a comprehensive anthology It reduced the recurrence rate to about 20% but left
with excellent information and references and should the eyes white with thin scleras and poor corneal
be used as such. healing. From that time, prevention made more sense
xvi Pterygium: A Practical Guide to Management
than the endless repeated surgeries and dissatisfied the endemic regions. Newer techniques have been
patients. Shortly after, my own pterygium had made included and indications for use specified accordingly.
an appearance and was responding positively to low The surgical correction of pterygium has always
dose decongestants and tear film replacement, a commanded all the glory. Likewise, a recurrence
regimen that I still use today. receives the shame and stigma of something done
The modified conjunctival flaps technique incorrectly. The section on recurrence, how to prevent
developed out of common sense and successful it and how to fix it, is highlighted in Complications.
outcomes. If you cover the sclera, control inflammation It includes explicit examples and how to avoid them
and restore the tear film, you remove the stimulus for as well as how to fix them. In Clinical Correlations,
the pterygium to grow back. It works. The statements routine cases are provided so that the practitioner can
and conclusions that appear in this manual that could apply some of the techniques in management directly
seem controversial or circumstantial are derived from to clinical practice. Unusual cases with successful
solid observations of improvement in structure and outcomes can be used to compare with your own.
function of the eye following appropriate pterygium Finally, Summary includes a wrap-up of highlights
management. and pearls.
Pertaining to the layout of the book, note that the During the early years of my experience with
themes of Epidemiology and Pathogenesis are closely pterygia, while on a celebratory trip to London,
related to Pathology. Understanding the pathology is I encounterd a set of ancient surgical eye instruments
essential to the demonstration of behavior of the lesion in the Egyptian section of the British museum. These
which determines its character. By identifying its instruments along with the alleged words of the 16th
character, a classification and staging can be directly Century French surgeon, Ambroise Paré, (in a different
applied to determine the most appropriate surgical section) pertaining to pterygium that “it always grows
treatment. back”… set me to thinking and trying and striving to
A chapter on Prevention has been included in this arrive at the perfect (or near perfect) solution to the
manual in response to the many statements in the pterygium “problem”.
medical literature that there is no prevention except
for the “possible use of sunglasses”. This is perhaps
the most important section as pterygium is a
preventable lesion and all the sequences need not occur
if a few basic measures are adopted. Early cases have
been presented and before and after photos have been
provided.
The chapter on Surgery has been simplified to give
step by step methods of pterygium treatment to make
the patient comfortable and confident in a positive
outcome. The conjunctival flap method has been
detailed more than the others as this gives the best
results by far and has been corroborated by worldwide Surgical eye instruments: British museum of
agreement of those surgeons doing the most cases in Egyptian artifacts, c. BCE 1000
Introduction xvii
The ultimate purpose of this work is to stimulate 5. What can I do to prevent a pterygium from
interest in pterygium research and publication of growing?
journal articles particularly from practitioners and 6. What are the indications for pterygium surgery
scholars in areas of the tropics where it is endemic. and when can it be left alone?
Better methods of prevention should be investigated 7. What is the best technique for a specific type of
and more convenient and effective techniques of pterygium?
handling difficult cases should be established. 8. What is the best way to do surgery to prevent
Moreover, those who are presented with challenging recurrence?
cases should consult with those who have been there 9. What is the best way to gain patient confidence,
and are willing to share the experience. ensure the most comfort and get the best results?
In following some of the suggestions included in 10. What is the most important factor in preventing
this guide, it is my sincere conviction that your complications?
outcomes will be successful. 11. What is the basic pathology of the average
pterygium?
Second Disclaimer 12. Is mitomycin C as bad as the early articles
portrayed? What is the most effective and safest
The author has no financial interest in any of the
dose?
products mentioned in this book.
13. Is cosmetic pterygium surgery practical?
“When you see multiple viewpoints, you are less attached
14. Why should bare sclera never be done?
to your own.”
15. What are the main causes of postoperative
inflammation and how do I avoid them?
Questions Most Often Posed by Visiting
Ophthalmologists 16. How much astigmatism does pterygium cause and
how do I treat it?
1. What is the pathogenesis of a pterygium? 17. When do you use adjunctive therapy?
2. Which eyes are most susceptible to pterygium 18. What are the causes of recurrence and how do you
formation? prevent them?
3. Which environment has the highest incidence of 19. What are some of the vision threatening
pterygium? complications of pterygium surgery?
4. How does a pingueculum become a pterygium? 20. Who is to blame when there is a recurrence?
Features
2 Pterygium: A Practical Guide to Management
The hallmarks of pterygium formation are UV radiation exposure, altered tear film and inflammation. Duke-
Elder defines a pterygium as a triangular shaped degenerative and hyperplastic process, occurring medially
and laterally in the palpebral aperture, in which the bulbar conjunctiva encroaches onto the cornea.1 Since this
description was made in 1954, much work has been done in identifying the cause and development of pterygium.
The general consensus proposes that a pterygium arises in response to mechanical injury and/or chemical
irritation which then results in the alteration of the eye’s defenses, thus further perpetuating the growth of the
lesion. The chief goal of pterygium management is to minimize the deleterious effect of the lesion by restoring
the anatomy and physiology to normal or near normal conditions.
Several myths have circulated that a pterygium never crosses the midline and never crosses arcus senilis
(Figures 1.1 and 1.2). Other speculations claim that a pterygium always occurs in the palpebral fissure, they
are always preceded by a pingueculum, they do not occur in animals, they only occur in people who live in the
tropics and they only occurs in people with outdoor occupations. The facts indicate that pterygia do occur
outside the medial and lateral palpebral fissure and they can be located inferiorly when present in cases of
incomplete blinking and subsequent changes in the inferior cornea or when due to focal trauma as shown in
Figure 1.3.
Figure 1.1: Pterygium crossing the midline
Figure 1.2: Pterygium crossing arcus senilis

Features 3
Figure 1.3: Inferior pterygium due

to chemical burn
A pterygium does occur de novo (Figure 1.4) in the absence of pingueculum and it does occur in sawmill
workers and watch factory workers due to dryness, chronic irritation and abnormal blinking patterns. My
personal observations have revealed the presence of pterygium in computer workers suffering from dry eyes
and little exposure to outdoor influences. They do occur in the eyes of horses, cattle and dogs as a result of
focal trauma. With respect to locations outside the Tropics, there are reports of pterygium cases in
Newfoundland with an incidence of 30% and in the Eskimo population across Canada with a 9% incidence.2
The Pingueculum and the Pterygium
A pingueculum (Figure 1.5) is a mass of fatty degenerative deposits in the subconjunctival layers of the eye
which raises it above the surface of the sclera. Though having a similar pathogenesis, histology and pathology
as a degenerative pterygium, it consists only of a body. The limbal border (proximal, head) is usually wider
than the canthal border (distal, body). It is usually avascular, stationary, and only becomes red when irritated.
The symptoms are similar to those of dry eye and consist of fatigue and a gritty, foreign body sensation.
Figure 1.4: Pterygium de novo

Figure 1.5: Pingueculum
Figure 1.6: Pterygium
A pterygium (Figure 1.6) has a morphology that is organized into head, neck and body. The canthal body is
usually wider than the limbal head. It is usually vascularized and dynamic. The head grows onto and into the
cornea with a definite horizontal pattern of radial vessels in fibrous tissue. This fibrovascular arrangement
gives it the “wing-like” appearance characteristic of its name. The symptoms are similar to those of pingueculum
with the addition of burning and pain when inflamed.
When the lesion becomes inflamed and red, acquires a fibrovascular architecture and moves toward or
touches the cornea, in my opinion, it is a pterygium (Figure 1.7).
Visual Disturbances
With a pterygium the earliest and most common visual symptoms in eyes with pterygium begin as the result
of anatomical and physiological changes in the tear film. These changes are subtle at first. In a clinical situation
involving the observation of the tear film of a 10-year-old compared to that of an 18-year-old, both of which
Features 5
Figure 1.7: Pingueculum in evolution to

pterygium
have been exposed to similar intensities and duration of UV radiation, there is a perceived difference in thickness
and texture. The 18-year-old often reports a foreign body sensation and occasional blurred vision due to protein
debris and threads in the oily layer and a decreased aqueous level and shows signs of early stage pterygium
formation. The 10-year-old has a normal looking tear film and offers no complaints.
Once established, the lesion that rises above the surface limit of the tear film, is further exposed to the
elements, loses its defenses and exhibits faster growth. At this point it may interfere with the eyelid coverage
of the ocular surface leaving pockets of dryness (dry spots) as the result of reduced or incomplete blinking
(Figure 1.8). The raised uneven surface initiates a decrease in immune defenses and an increase in irritation
which leads to further inflammation.
Anatomical obstruction of the pupil by a large corneal mass is a late finding and indicates an advanced
pterygium. A lesion in the papillary axis will also have passed deep enough to occupy the corneal stroma and
cause mechanical contractions which will greatly affect the vision (Figure 1.9).
Corneal distortion due to changes in the stromal collagen will lead to an induced astigmatism.
Figure 1.8: Raised degenerative lesion may

cause blink interference
Figure 1.9: Stage IV pterygium may cause blink

interference with pupil interference
Astigmatism occurs when Bowman’s membrane is destroyed by the advancing pterygium head and the
stroma is contracted by the invading fibrous tissue which results in warping of the corneal curvature. The
degree and direction of the astigmatism is dependent on the following factors: Size and invasiveness of the
pterygium, the corneal elasticity, the inherent resistance to the mechanical forces and the duration of exertion
of those forces. The force of the pterygium flattens the cornea in the horizontal meridian and the force of
contracture steepens it in the vertical meridian at 90º away. This results in with the rule, plus (+) cylinder
astigmatism on the side of the pterygium. More often the astigmatism occurs between 6º and 120º due natural
distortion and variation in the forces of exertion. There is a significant correlation between the size and extension
of the pterygium onto and into the cornea and the degree of astigmatism present. Surgical excision of the
pterygium will reduce the amount of astigmatism in most cases but the outcome is dependent on the former
mentioned factors concerning size, shape and age of the lesion.3
Figures 1.10A and B show the eye of a 30-year-old male with pterygium induced with-the-rule astigmatism
which responds well after surgery.
Figure 1.10A: Stage V pterygium with 3.5 D Figure 1.10B: Corneal topography with
cylinder in a 30-year-old male induced astigmatism
Features 7
Figure 1.11A: Stage V pterygium with 3.0 D

cylinder in a 60-year-old male
Figure 1.11B: Corneal topography with irregular

astigmatism
Figures 1.11A and B show the eye of a 60-year-old male with a more irregular with-the-rule pterygium
induced astigmatism which is less responsive after surgical removal.
Differential Diagnosis
Pingueculum
The size, shape and orientation usually distinguishes a pingueculum from a pterygium. Unless it is symptomatic
or cosmetically displeasing, it can be left alone.
Pseudopterygium
Results from a corneal injury or ulceration at or near the limbus.

A probe can usually be passed beneath the body. It is self-limited and may be easily removed for cosmetic
reasons.
Conjunctival Hemangioma
It is an irregular cluster of blood vessels in the subconjunctival layer (Figure 1.12). Caution is suggested when
removing this lesion due to the likelihood of excessive bleeding.
Foreign Body
Foreign body in the conjunctiva and especially at the limbus elicits an inflammation response with the rapid
proliferation of fibrovascular tissue which is pterygious in appearance and behavior (Figure 1.13).
Papilloma
It resembles a bunch of grapes but is hiding a very vascular core. It usually has a pedicle.
Granuloma
It is a raised, smooth lesion that arises rapidly following a history of recent surgery or injury.
Figure 1.12: Conjunctival hemangioma
Figure 1.13: Foreign body

Features 9
Phlyctenule
It is a flat, fibrovascular, thin and is characterized by a history of infection. It usually appears in childhood or
infancy and is associated with a hypersensitivity reaction.
Nodular Episcleritis
It is superficial, hyperemic, flat, rounded lesion consisting of irregular conjunctival and episcleral vessels
which blanch with the application of decongestants. In the early stages it is often associated with localized
pain.
Limbal Catarrh
It is known as vernal keratoconjunctivitis in temperate zones and is associated with allergy and atopy. The
follicles are usually arranged around the limbus and are often in the palpebral fissure associated with exposure.
Dermoid
It has a history of congenital origin, is yellowish-red in color and has no abnormal blood vessels.
Squamous Cell Carcinoma
It is the most common neoplasm mistaken for pterygium. It often has irregular tiers and hard white calcifications.
Definitive diagnosis by appearance only is difficult and must be made by histological examination. Bowen’s
epithelioma, malignant melanoma, malignant epithelioma, amelanotic melanoma and carcinoma in situ are
all variants of serious lesions that occur on the ocular surface. Surgical removal and submission to pathology
is mandatory with a suspected neoplasm4 (Figure 1.14).
Figure 1.14: Squamous cell carcinoma
REFERENCES
1. Duke-Elder S. Textbook of Ophthalmology. St Louis: Mosby 1954;7:57086.
2. Peckar CO. The aetiology and histo-pathogenesis of pterygium. Documenta Ophthalmologica. Springer. Netherlands.
1972;31(1);141-57.
3. Lindsay RG, Sullivan L. Pterygium-induced corneal astigmatism. Clin Exp Optom 2001 Jul;84(4):200-3.
4. Buratto L, Phillips RL, Carito G. Pterygium Surgery. Thorofare NJ. Slack, inc 2000;10:33-4.
Epidemiology
The myth claims that pterygia only occur in the darkly pigmented eyes of persons who reside in the tropics.
The fact is that pterygia also occur in temperate zones with humid conditions and in lightly pigmented eyes.
The incidence and prevalence are more closely related to environmental factors than to genetics.
Geographic Location (Figure 2.1)
A pterygium occurs with higher frequency (above 10%) in warm, sunny areas between 30 degrees latitude
north and south of the equator.1 Excessive sun exposure in the teenage and early adult years is the primary
risk factor for pterygium formation. The associated risk of UV-B exposure and the pterygium was reported as
43.6% in one study.2 Small islands with elevations less than 2000 feet have a high cloud ceiling (blue skies), low
density forests (less UV radiation absorption) and white sandy beaches (more reflection). By my observation,
people living on these small islands have a higher prevalence of pterygium than those living on larger islands
with more tree coverage, darker volcanic sand and higher elevations. Similarly, those individuals living on the
coastal areas have more pterygia than those living in the mountainous areas. Hence, the population of a small
island in the Bahamas at 35 degrees latitude will have a higher frequency than a population at 10,000 feet in
Ecuador at the equator. Following the destruction of the forests by hurricanes in the Caribbean, the incidence
of pterygium formation increases and there is reactivation of those that were dormant due to less absorption
of UV radiation as well as more exposure of laborers while doing repairs. The highest cumulative exposure is
in fishing and sea sports as the salt crystals seem to act as tiny magnifiers of UV and white sand grains offer the
best reflective surfaces. It is a well known fact that the best way to “tan” (and burn) is to swim first in the ocean
then bask on a white sandy beach.
Environment
It has been suggested that a dominant gene with variable penetration is associated with a tendency to pterygium
formation. However, there is no scientific evidence for this assertion. The inherited characteristics would still
be phenotypic and would be consistent with prominence of the eye in the orbit; variation in the amount and
quality of the tear film; variations in blink rate; and varying sensitivity to UV radiation. The structure of the
Figure 2.1: World distribution of pterygium

(adapted from Pterygium Around the World by
ME Cameron)
Epidemiology 13
orbit may play a role in that an eye that protrudes from the orbit is more likely to be affected by UV radiation
than an eye that is recessed in the orbit and protected by the large superior orbital bone. If the nasal conjunctiva
is more exposed, it receives a depleted tear from the temporal conjunctiva with each blink, it is drier, and it
receives more reflected UV radiation from the nasal skin, thereby making this area more susceptible to the
formation of a pterygium.3
Many people residing in the tropics tend to be dehydrated due to inadequate water intake, high rate of
perspiration and high surface evaporation. Eyes with darker pigmentation tend to absorb UV radiation better
than lightly pigmented eyes. The latter receive surface burns through reflection and tend to form a pterygium
at a faster rate. Light skin burns in the sun due to reflection, and dark skin absorbs and suffers less burn.
Individuals with darkly pigmented eyes are indigenous to the tropics and are more likely to be exposed in
outdoor occupations for a longer period of time and will therefore show a greater prevalence of pterygium
especially in the older age groups. However, when sensitivity is considered, the darker pigmented eyes develop
more degenerative Type Ib as in Figure 2.2 and the lighter pigmented eyes develop fibrovascular Type IIa as
in Figure 2.3.4 People with “red” pigmented skin, freckles and lightly pigmented eyes appear to be the most
sensitive to UV radiation and form aggressive, inflammatory, vascular lesions which have a high rate of
Figure 2.2: Pingueculum in a pigmented eye

after 56 years’ exposure
Figure 2.3: Pterygium in a blue eye after 6 years’

exposure
complications. This is possibly due to the presence of pheomelanin, a type of photosensitizing melanin thought
to be causally related to susceptibility to the harmful effects of ultraviolet radiation. By my observations, those
individuals with oily skin who are sufficiently exposed to UV radiation over a substantial period of time will
develop pterygia regardless of ethinicity or degree of pigmentation.5
The age of onset corresponds well with the onset of exposure as seen in teenagers involved in outdoor
sports, while undergoing hormonal changes. Many in the 14-20-year-old age group have stage I to II conjunctival
lesions. The incidence of new established cases in the Caribbean, which tend to be fibrovascular (stage III and
IV) in the Caribbean coincides with the 25-30-year-old age group. The 40-70-year-old age group tends to show
degenerative pterygia suggesting a key role of the aging immune system. In Asia, pterygium is found in the
20-30-year-old age group with a predominance of males as well as in those with allergies, dry eyes and exposure
to chronic irritation. Prevalence was higher in factory workers than in office workers, higher in rural areas
than in the city and highest in fishermen.6
Perhaps the largest, most comprehensive epidemiological study done to date in the tropics to date is the
Barbados Eye Study. The prevalence of pterygium in darker skin people (94.1% of the population) was found to
be 23.4%; in the mixed group (3.5% of the population) it was 27.8% and in the lightly pigmented group (2.4%
of the population) it was 10.2%. But the majority of outdoor occupations occurred in the first group. Those
persons wearing prescription spectacles and sunglasses had a lower prevalence. There was a higher frequency
with increasing age as this correlated with increased exposure time.
There was no difference with regards to gender. One would expect a higher incidence in males. However,
in the US Virgin Islands, there was a high incidence of pterygium formation in female watch factory workers
who were indoors during the peak exposure times of the day. It may be suggested that a relationship exists
between work-related dry eyes possibly due to reduced blinking and/or workplace dryness and pterygium
formation despite limited exposure to UV radiation may be suggested. This incidence was greatly reduced in
subsequent years by employee education in maintaining the tear film and further limiting exposure to UV
radiation.
The Barbados Eye Study concludes that having darker skin and wearing sunglasses are protective factors.7
There are other lifestyle attributes that contribute to pterygium formation and by examination we can determine
which measures can be taken to reduce the incidence and improve the clinical management.8
REFERENCES
1. Cameron ME. Pterygium throughout the World. Springfield Il, Charles C Thomas, 1965.
2. McCarty CA, Fu CL, Taylor HR. Epidemiology of Pterygium in Victoria, Australia Br J Ophthalmol 2000;81:289-92.
3. Walsh JE, et al. Quantification of the ultraviolet radiation (UVR) field in the human eye. Br J Ophthalmol 2001;85:1080-5.
4. Anduze AL, Biscoe BW. Pterygium Staging in the Caribbean Ann Ophthalmol 1998 Aug;30(2):92-4.
5. Rees J, Oh C, Hennessy A, et al. Pigment Cell Research 2005;18(3);220-3.
6. Wong TY, et al. The prevalence and risk factors for pterygium in an adult Chinese population in Singapore. Am J Ophthalmol
2001;31(2):176-83.
7. Luthra R, Leske MC, et al. Frequency and risk factors for pterygium in the Barbados Eye Study. Arch Ophthalmol 2001;119:1827-
32.
8. Saw SM, Tan D. Pterygium: prevalence, demography and risk factors. Ophthalmic Epidemiology 1999;6(3):219-28.
Pathogenesis
In his classic monograph of 1965, Pterygium throughout the World, ME Cameron describes a pterygium as
“an ingrowth of subconjunctival tissue whose stimulus to growth is ultraviolet light.”1 This latter term should
be modified to read “radiation”, as UV-B (320-286 nm) is not visible as light.2 Though it is certainly more
prevalent in the tropical regions, residents of temperate zones with dry eyes and increased exposure to chronic
irritants are susceptible to the development of pterygia as well.
The primary causative factor of the pterygium is excess exposure to UV-B radiation.3 This exposure is
cumulative and dose-related:4 it can be occupational such as occurs with fishermen, construction workers,
landscapers or sailors; it can be recreational, as occurs with surfers, tennis players, and those who frequent the
beach. The first observable changes in the eye appear to be associated with the characteristics of the tear film.
Drying of the tear film alone will lead to exposure keratitis. Ultraviolet radiation burn alone will cause
conjunctival and corneal punctuate erosions, which appear as dry spots on fluorescein staining (Figure 3.1).
Put them together, add inflammation and a pterygium forms.
Figure 3.1: Dry spots on fluorescein stain
Examination at the slit lamp of the eyes of children of varying ages suggests that there is an “alteration“ in
the tear film that appears around the ages of 10 - 12 in those exposed to UV radiation and other irritants (wind,
dust, chemicals). There is a decrease in tear volume (reduced tear lake in the inferior fornix). Through both
external evaporation and internal dehydration, the aqueous level in the tear film is reduced (Many of these
children drink very little water, opting for sodas and juices instead). Additionally, a decrease in the mucus
level through direct damage to medially located goblet cells, results in a relative and compensatory increase in
the oil layer. This occurs well before the appearance of a lesion and leaves the cornea at risk for irritants.
Figure 3.2 shows an eye that is relatively “normal” in appearance, but has some of the early “pre-pterygium”
features of an oily tear film, sparse aqueous and a reduced tear lake. Concurrent with the appearance of a
small fatty lesion (pingueculum) which may or may not become vascularized (pterygium), is the increase in
tear break-up time which is a sign of lid blinking dysfunction. A raised lesion leads to further reduction in
ocular surface defenses which prompt the blood vessels to respond by dilating, where the leakage of protein
thickens the tears even more.
Pathogenesis 17
Figure 3.2: Early tear film and ocular surface

changes
Ultraviolet radiation is mutagenic for the suppressor gene p53 in limbal cells, which leads to loss of collagenase
and deregulation of apoptosis, so that collagen is overproduced. Direct stress from UV-B and other irritants
further lowers the immune response and adversely affects healing. A weakened immune system in an altered
tear film cannot respond adequately so there is reduced tear film renewal. Focal changes at the limbus that
consists of corneal edema and cell destruction encourages a pterygium to form.5
Figure 3.3 shows an eye before exposure to intense tropical sunlight. Figure 3.4 shows the same eye three
years after windsurfing without several times a week without the use of protective eyewear.
Table 3.1 lists the electromagnetic spectrum of which visible light is only a small part.
The formation of pterygium is attributed to the effects of ultraviolet B (320 - 286 nm).
Table 3.1*: The Electromagnetic Spectrum
Infrared C 10,000-3000 nm (retina RPE)

Infrared B 3000-1400 nm (lens, thermal cataract)
Infrared A 1400-780 nm (corneal superficial burns, skiing)
Visible light 1200-400 nm (red to violet)
Ultraviolet A 400-320 nm (lens, cataract)
Ultraviolet B 320-286 nm (cornea, pterygium)
Ultraviolet C 286- 0 nm (absorbed by ozone layer)
(*adopted from Isaac Asimov’s Book of Facts. Hasting house. Daytrips Publ.,1992.pg 389)
How does a Stage I Pingueculum become a Stage IV Pterygium?
Dehydration and alteration in the tear film leads to loss of protection which leaves the corneal and conjunctival
surface tissues vulnerable to injury by thermal and chemical irritants. Initially the integrity of epithelial cells is
compromised as seen with a positive stain with 1% rose bengal solution and lissamine green. Further damage
to the surface epithelium leads to loss of cells and the affected area stains with fluorescein 0.5% solution. The
subepithelial cells are bared and respond by proliferating fibroblasts which produce an additional extracellular
Figure 3.3: Patient IH in 2004
Figure 3.4: Patient IH in 2007
matrix which results in the irregular swirls of Type I collagen that can be seen on histological slides. This
“lesion” (pingueculum) is now raised and further susceptible to additional drying and direct injury.
A stage II lesion may remain in the pingueculum stage until it degenerates and atrophies with age. There is
a critical point at which this same lesion may incur and respond to further injury by releasing antigenic factors
and inflammatory cells and becomes a pterygium. Given the right conditions, the pingueculum becomes a
pterygium.6 By observation, it appears that these conditions are altered tear film, excessive exposure and
inflammation.
Inflammation in the conjunctiva arises from antigenic stimulation from environmental factors (UV-B and
irritants). The resulting increase in cell bound IgE complexes stimulates the release of reactive mediators like
platelet activating factor, from mast cells which then release antigenic factor X which produces epidermal
growth factors. Ultraviolet radiation-activated fibroblasts appear in the subconjunctival tissues and the
inflammatory reaction, mainly lymphocytes, pushes into the corneal epithelium, and proceeds to damage
Bowman’s membrane and leads to fibrosis and contracture of subconjunctival tissue onto and into the cornea.
Inflammation is the key factor in the fibrovascular proliferation process. It leads to the formation of a complete
pterygium, either from a pre-existing pingueculum or from normal conjunctiva. In other words, it is the fire
Pathogenesis 19
Figure 3.5: Pingueculum in evolution
Figure 3.6: Pterygium in situ
that creates the stew. Figure 3.5 shows an inflamed pingueculum encroaching on the limbus. Figure 3.6 shows
an inflamed vascular pterygium in the process of crossing the limbus into the cornea.
Limbal stem cell destruction has been implicated as a cause of pterygium. However, studies reveal that
VEGF levels are similar in limbal and conjunctival pterygium cells.7 Replacement of the limbal epithelium
with amniotic membrane tissue or conjunctival autograft from superior or inferior non-limbal conjunctiva
gives successful results without stem cells. Likewise, cell proliferation patterns of primary and recurrent pterygia
are not significantly different, thereby implying a similar mechanism.
Closely linked to the relatively slow pathogenesis steps of an environmental pterygium is a direct injury to
the cornea or bulbar conjunctiva (including foreign body) which stimulates the acute proliferation of
subconjunctival fibroblasts. The acute pterygium can grow to maturity within a few weeks to months.
The cause and mechanism of pterygium formation are related to and dependent on inflammation. Figure
3.7 shows a small seemingly insignificant subconjunctival hemorrhage. The resulting inflammatory response,
Figure 3.7: Early inflammation in the

subconjunctiva
Figure 3.8: Advancing head of an inflamed

lesion
when prolonged by environmental factors, may induce the formation of pterygium at this site. Figure 3.8
shows the advancing head of an inflamed pingueculum in the process of crossing the limbus.
Figure 3.9 shows an active pterygium that has converted from a pingueculum and has just crossed the
limbus into the cornea. Figure 3.10 shows a classic advancing corneal pterygium most likely with visual
disturbances.
Table 3.2 is a schematic outline of the possible pathogenesis of a pterygium.
If we can interrupt the pathway at any juncture, we may be able to prevent the formation of the lesion.
Pathogenesis 21
Figure 3.9: Active pterygium onto the cornea
Figure 3.10: Classic corneal pterygium
Table 3.2: Pathogenesis of Pterygium Pathway
Exposure to UV-B radiation + Altered Tear film

↓ ↓
Injury and Susceptibility
↓ ↓
Loss of collagenase and Dehydration
↓ ↓
Accumulation of extracellular matrix (lesion formation)
↓ ↓
Inflammation Pingueculum
↓ ↓
Antigenic stimulation Inflammation
Type I hypersensitivity
fibroblastic reaction ↓
Pterygium Pterygium
Pterygium formation occurring in regions with relatively low levels of ultraviolet radiation exposure may
involve other factors. Cumulative exposure and intensity of the welder’s arc, fluorescent lighting, high intensity
mercury lamps, xenon arc lamps, bilirubin lights as in some operating rooms and possibly video display and
computer terminals may be associated. Chronic irritants like cigarette and cigar smoke and indoor fires with
poor ventilation, salt water, “caliche” dust (limestone) at many construction sites, chlorine in swimming pools,
air conditioning which removes moisture from the air and motorized fans, which contribute to drying of the
eyes. Photosensitizing medications include some sedatives like diazepam and chlordiazepoxide, diuretics,
oral hypoglycemics, antihypertensives, oral contraceptives, antibiotics like sulfacetamide and tetracycline,
artificial sweeteners with cyclamates and most antihistamines have also been implicated.
Likewise, some other ocular effects associated with ultraviolet radiation exposure are listed in Table 3.3.
Table 3.3: Other Ocular Effects of Ultraviolet Radiation
1. Macular degeneration
2. Solar retinitis
3. Corneal dystrophies
4. Solar keratosis
5. Limbal catarrh (vernal keratoconjunctivitis)
6. Malignant melanoma
7. Basal cell carcinoma
REFERENCES
1. Cameron ME. Pterygium through the World. Thomas, Springfield, 1965.
2. Anduze AL. Ultraviolet radiation and cataract development in the US Virgin Islands. JCataract Refract Surg, 1993;Vol 19:
298-300.
3. Elliott R. The aetiology and pathology of pterygium. Trans Ophthal Soc Aust and NZ 1966;25:71-4.
4. Threlfall TJ, English DR. Sun exposure and pterygium of the eye: a dose-response curve. Dept Pub Health, Univ Western
Australia, Perth 2006.
5. Ochoa-Tabares JC. Génesis del Pterigión. Una aproximación desde la biología Molecular. Rev Mex Oftalmol 2006;80(6):318-
24.
6. Hill JC, Maske R. Pathogenesis of pterygium. Eye 1989;3,218-26.
7. Gebhardt M, et al. Differential expression of vascular endothelial growth factor implies the limbal origin of pterygia.
Ophthalmology 2005;112(6):1023-30.
Pathology
Morphologically, a pterygium consists of an advancing head, connecting neck and a wider body. Most often it
has an arrowhead-like shape. Histologically, it is characterized by a combination of elastotic degeneration of
collagen and fibrovascular proliferation of inflammatory cells. The specific pathology of each lesion is dependent
on the pattern of growth. The degenerative type may be slow and the inflammatory type may be fast. Both
reveal altered collagen and epithelial hyperplasia, but in differing degrees. There is no increase in number of
structural cells. Degeneration (clinical stages III, IV, class Ib, IIb) will show a thickened conjunctival epithelium,
greater degrees of stromal collagenization and hyalinization, with closed vascular channels and fibrosis.
Proliferation (clinical stages III, IV, V, class Ia, IIa) will show greater degrees of infiltration of inflammatory
cells like lymphocytes and plasma cells with high levels of IgG and IgE, which is indicative of Type 1
hypersensitivity. It features open vascular channels, loose fibrous connective tissue covered by fairly normal
conjunctival epithelium, replacement of Bowman’s membrane by collagen and active proliferation of vascular
buds.
While normal conjunctiva stains pink with hematoxylin and eosin (H&E), the collagen in sun-damaged
conjunctiva stains blue as it resembles the basophilic degeneration of old elastic tissue. This blue staining is
also be seen in the cellular tissue of actinic keratosis, melanoma, basal cell and squamous cell carcinomas of
the same area.
The increase of goblet cells in the medial conjunctiva correlates well with the finding of increased mucus
and decreased aqueous in the altered tear film discussed earlier.
A pingueculum also shows degeneration of the collagen fibers of the conjunctival stroma with thinning of
the overlying epithelium and occasional calcification. When it adopts a fibrovascular component, it will advance
and be considered as a pterygium.
The gross morphology of the degenerative pterygium (Figure 4.1) shows a white collagenous head, a
pigmented limbal neck and a thin vascular body. This pterygium is largely asymptomatic and inactive, but is
cosmetically unattractive. The histology (Figure 4.2) shows empty vascular channels and thickened collagen.
The proliferative pterygium (Figure 4.3) shows an advancing edematous head, vascular channels in the cornea,
a wide vascular congested body with irritation, discomfort and probable visual disturbances. The histology
(Figure 4.4) shows inflammatory lymphocytes and plasma cells, extensive basophilic degeneration and patchy
hyalinization with a well vascularized intervening stroma.
Figure 4.1: Degenerative pterygium

Pathology 25
Figure 4.2: Stromal collagenization
Figure 4.3: Proliferative pterygium
Figure 4.4: Inflammatory cells

Classification (Table 4.1) is used to identify and possibly predict the behavior of the lesion based on its
appearance, activity and symptoms. The pterygium appears as either inflamed, vascular or opaque,
degenerative or a combination of both. The earliest symptoms are dryness of the eyes and a sandy feeling
often described as “gravelly”or “gritty”.
The management for class Ia and class IIa is surgical excision.1 Class Ib is usually inactive but symptomatic
in relation to tear film dynamics and induced astigmatism. It is usually found in the older age groups and may
be unpleasant in appearance. As recurrences after surgery are rare, it is usually managed surgically. Class IIb
can be observed and probably will recede and fade with time.
Table 4.2 contains a suggested clinical staging of pterygium based primarily on size and location of the
lesion. Patients may be placed into several categories depending on the stage and classification of the lesion.
Those eyes at risk because of environmental exposure, susceptible skin type, conducive lifestyle, but with no
lesion may be placed in category I, stage I and need no treatment. Those at risk, with a small lesion, mild
symptoms and no visual disturbances should be in category II and receive medical treatment. Those with an
established lesion, active symptoms and impending or evident visual disturbances should be in category III
Table 4.1: Classification of Pterygium
Primary active (Class Ia) (Figure 4.5)

Highly vascular, inflamed, symptomatic lesion with or without an iron line, corneal edema at the head with positive1% rose
bengal stain; no prior surgery.
Primary passive (Class Ib) (Figure 4.6)

Raised, hyalinized, degenerative, fibrosis with or without pigmentation and tear film defect; little or no vascular channels.
Secondary active (Class IIa) (Figure 4.7)

Raised, vascular, symptomatic regrowth with 2 mm or more corneal involvement; recurrence.
Secondary passive (Class IIb) (Figure 4.8)

Flat, avascular, asymptomatic re-growth with 2 mm or more corneal involvement; atrophic.2
Figure 4.5: Active vascular primary Class Ia

Pathology 27
Figure 4.6: Degenerative quiet primary Class Ib
Figure 4.7: Active recurrence Class IIa
Figure 4.8: Inactive recurrence Class IIb

Table 4.2: Clinical Staging of Pterygium
Stage I: Exposure conjunctivitis

Increase in size and number of conjunctival vessels; mild to moderate congestion coinciding with periods of exposure, signs
and symptoms of dryness; no formed lesion.
Stage II: Conjunctival pingueculum and pterygium

Presence of a distinct raised lesion in the bulbar conjunctiva, with or without abnormal vascularization and inflammation;
symptoms of burning and itching; foreign body sensation.
Stage III: Limbal pterygium

Leading edge of the lesion (head) is on or across the limbus, with or without an iron line at the conjunctival-corneal interface,
vascularization and fibrous proliferation; symptoms more pronounced.
Stage IV: Corneal pterygium

Lesion is 2 mm or more onto and into the cornea; may be degenerative or vascular; granulation tissue invades the cornea
between the epithelium and Bowman’s membrane; a zone of dellen, edema or iron staining cells may be present at the
advancing head of the lesion; can be painful as it affects the corneal nerves directly or due to inflammation. See Figure 4.12.
Stage V: Compound pterygium

Lesion has extended through Bowman’s membrane into the corneal stroma; astigmatism is induced and vision is compromised;
symptoms are more frequent and more severe; these lesions include bilateral pterygia (medial and lateral, same eye), secondary
recurrences and rapidly progressive traumatic and chemical lesions.3
and receive surgical treatment. The best use of staging and classification is to assist the practitioner in
determining the most appropriate and effective management.
Figures 4.9 to 4.13 are examples of the clinical stages.
Stages I and II can be managed medically with great success in retarding the progression and even reversal
of the lesion in some cases. Stage III should be surgically removed if it is symptomatic or cosmetically
unattractive. Stages IV and V should be excised and adjunctive therapy used to prevent recurrence.
Figure 4.9: Stage I exposure conjunctivitis

Pathology 29
Figure 4.10: Stage II conjunctival pterygium
Figure 4.11: Stage III limbal pterygium
Figure 4.12: Stage IV corneal pterygium

Figure 4.13: Stage V compound pterygium
Figures 4.14A and B are examples of the eye of a 45-year-old male with a Stage III, Class Ia, symptomatic,
limbal pterygium which showed active clinical fibrovascular proliferation.
Figure 4.14A: Active limbal stage III Class Ia
Figure 4.14B: Inflammatory cells and collagen

Pathology 31
Figure 4.15A and B is the eye of a 27-year-old male with a history of intense exposure to ultraviolet-B
radiation and chronic irritants in his occupation as a construction site mason. He had a large active corneal
pterygium with extensive vascularity, impediment of abduction and impairment of visual acuity due to induced
astigmatism. The histology shows non-specific chronic inflammation and a fibrovascular stroma, with increased
hyalinization, full vascular channels and increased subepithelial lymphocytes.
Figure 4.16A and B is the eye of a 65-year-old female with a corneal pterygium composed of almost equally
mixed degenerative and proliferative changes.
The histology shows the presence of fibrovascular stroma and dense collagenization with partial
hyalinization. There are patchy infiltrates of chronic inflammatory cells, where lymphocytes give way to
neovascularization, then normal collagen and scattered fibroblasts.
Figure 4.17A and B is the eye of a 71-year-old male with a history of alcohol abuse and poor health. He
exhibits a degenerative pterygium occupying the medial aspect of the corneal surface and crossing his arcus
senilis. The histology shows a thinned epithelium, thickened fibrotic stroma, heavy collagen and few cells.
Figure 4.18A and B is the eye of a 72-year-old female with a second recurrence after bare sclera surgery
with mitomycin C drops, which resulted in impaired vision due to deeply scarred cornea and induced
astigmatism. This advanced lesion has lost its vascular appearance due to destruction of Bowman’s membrane
Figure 4.15A: Active vascular stage V Class Ia
Figure 4.15B: Inflammatory cells and full

vascular channels
Figure 4.16A: Degenerative and proliferative

pterygium
Figure 4.16B: Lymphocytes and fibroblasts
Figure 4.17A: Degenerative pterygium Stage IV,

Class Ib
Pathology 33
Figure 4.17B: Less cells, more collagen
Figure 4.18A: Stage V, class IIa fibrovascular

recurrence
Figure 4.18B: Basophilic degeneration

caused by the advancing pterygium and the reactive hyperplasia of squamous epithelium. There is underlying
actinic elastosis of connective tissue with basophilia, prominent hyalinization and central degeneration of
collagen fibrils in the histological slide.
Figure 4.19A and B is the eye of a 28-year-old male with a rapidly progressive lesion. In the histological
specimen the thickened epithelium (left) exhibits severe dysplasia and carcinoma in-situ. Invasive nests (right)
of malignant squamous cells have breached the basement membrane and irregularly infiltrate the underlying
stroma. Note the collagen hyalinization and degenerative changes of pterygium formation as well as the
lymphocytic host response to the tumor. This is an example of why any specimen that looks suspicious must
be submitted to pathology for analysis.
Figure 4.19A: Squamous cell carcinoma
Figure 4.19B: Mixed pathology

Pathology 35
Table 4.3 is derived entirely from the pathology slides presented above and is a suggested staging.
Table 4.3: Pathology Staging
I. Exposure altered tear film, mild vascular response

II. Conjunctival.. cell injury, inflammatory response
III. Limbal lesion organization, mixed proliferative-degenerative
IV. Corneal lesion between epithelium and Bowman’s membrane mixed proliferative-degeneration ( A and B)
V. Compound lesion into stroma, mixed proliferative-degenerative (A and B) destruction of Bowman’s membrane
Proliferation A vs Degeneration B
small lymphocytes, swirls of type I collagen
plasma cells
REFERENCES
1. Buratto L, Phillips RL and Carito G. Pterygium Surgery.Thorofare, NJ: Slack, Inc. 2000;5:15-6.
2. Anduze AL and Merritt JC. Pterygium: clinical classification and management in the Virgin Islands. Ann Ophthalmol
1985;17(1);92-5.
3. Anduze AL and Biscoe BW. Pterygium staging in the Caribbean. Ann Ophthalmol 1998;30(2):92-4.
Prevention
Most of the literature on pterygium has managed to avoid the concept of prevention. Though it is unclear
whether prevention is successful or what actions may actually be preventive measures, there are several
precautions and measures that have shown promise. For example, the protection to the ocular surface tissues
offered by sunglasses appears to be a viable remedy. The implication for prevention of pterygium is that
ocular protection is beneficial at all ages.1 Although, there is no known method or specific drug for preventing
a pingueculum or a pterygium, its symptoms and progression can be addressed.2
Through my observation of reliable patients in a stable community, the formation and systematic progression
of a pterygium can be prevented by using a series of measures by way of protecting the eyes from excess
ultraviolet radiation, maintaining an adequate tear film and reducing localized and frequent inflammation of
the ocular surfaces. The small seemingly innocent lesion in Figure 5.1 can be prevented from becoming the
large destructive lesion in Figure 5.2.
Ultraviolet Protection
The formation of a pterygium involves an injury to the ocular tissues from chronic and cumulative exposure
to excessive ultraviolet-B radiation exposure. UV-B is not seen as “light”but is felt as a “burn” on the skin and
Figure 5.1: Early active stage I
Figure 5.2: Late active stage V

Prevention 39
ocular tissues. UV400 wrap-around, antireflective-coated medium-gray tinted lenses appear to be best suited
for the tropics. They reduce light intensity without altering the color of objects and are the preferred lenses of
the majority of Caribbean residents. Green-blue tint is also acceptable. Brown tint increases depth perception
and is more suited to desert conditions, while yellow and amber tints are suited for conditions with low
contrast sensitivity. Polarized lenses are most effective for blocking glare but they reduce general visual acuity
especially for outdoor sports. Photo-chromatic, transition, lenses which change in response to intensity of
sunlight tend to become discolored in the tropics and are not as reliable or enduring as the UV coated lenses.
Mirrored lenses (gray-green) offer the least distortion of color vision and when coupled with a UV coating is
effective in reducing up to 99% of the harmful radiation. Most sunglasses come in three lens types, plastic,
polycarbonate and glass. Crown glass is a natural blocker of UV-B but is heavier, often thicker than plastic and
more expensive. Cheap plastic lenses from the rack may distort the vision and should be avoided.
Polycarbonate lenses are safest for extreme conditions of work and play as they are practically unbreakable.
They are reasonably priced but may not be readily available. It has been observed that even prescription
glasses without tint will provide similar relief from ultraviolet radiation as will UV400 Lite and that there is
very little difference between prescription sunglasses and nonprescription sunglasses with regards to protection.
Degree of tinting should depend on degree of iris pigmentation, pupil sensitivity, occupation and environment.
In general, the lighter the iris color of the eye, the darker the tint should be.4
Figures 5.3A and B show the same eye before and after sunglass wear without any other treatment. Adequate
protection may have reduced the reactive inflammation and allowed the tissues to heal.
Avoidance of exposure in the peak sunlight hours between the times of 10 a.m. and 2 p.m. is a good idea,
but ultraviolet exposure being invisible can be all day long. Since ultraviolet-B damage to the tissues is
cumulative, decrease the frequency of exposure as well. A brimmed hat or visor or an umbrella blocks up to
half of the ultraviolet-B radiation from reaching the eyes.
Avoidance of chronic irritants like chlorine in swimming pools, chemical pollutants from factories and
engine exhausts, and cigarette smoke is also necessary. Wind and dust also contribute to acute and chronic
irritation and should be avoided or exposure minimized. Direct patient and public education through various
available channels is essential to getting the message across. UV radiation and chronic irritants are harmful to
Figure 5.3A: Before sunglass wear

Figure 5.3B: One month after sunglass wear
the eyes. The prominent glare and probable high intensity of ultraviolet radiation is shown in Figure 5.4. A
simple pair of ultraviolet protecting lenses is shown in Figure 5.5.
Maintaining a Healthy Tear Film
An abnormal tear film may affect susceptibility of the tissues to ultraviolet radiation exposure damage.
Examination of the tear film of children in the 10 to 12 years age group usually reveals a healthy three layers of
aqueous, oil and mucus, with normal break up time and full integrity. In the 14 to 16 years age groups this
integrity appears to begin disintegrating. There is a distinct reduction in the aqueous layer which coincides
with the early signs of a pterygium. It is noted that injury to the eye, either mechanical or chemical in the
younger/pre-teen age groups will lead to an earlier and sometimes more acute pterygium formation. It is
possible that pterygium formation may be associated with tear film disruption.
Figure 5.4: UV-B radiation and glare

Prevention 41
Figure 5.5: UV400 tinted sunglasses
Anatomically, since the aqueous enters the tear film from the lacrimal gland located at the lateral aspect of
the eye and travels across the width of the eye, it is most sparse at the medial aspect. The medial aspect is also
the wider, most exposed area of the eye. Goblet cells in this area may also be injured (burned) by exposure and
the mucus layer may be affected. This exposure leaves a tear film with predominantly an oil layer for protection
and in a dehydrated state with low aqueous and mucus layers. With the tear film compromised and practical
loss of protective tear enzymes, the eye tissues will be more susceptible to damage.
If we restore and maintain the tear film, protection of the eye tissues may be possible. Furthermore, by
drinking more water and adding artificial tears to the eye, adequate hydration may be achieved. Be aware that
lubricants reduce the friction between two surfaces and may not offer adequate hydration, so the increased
intake of water systemically is a necessity. It should be noted that the excessive intake of alcohol leads to
further dehydration. Juices and sodas are not suitable replacements for water and should be avoided (For
every glass of juice imbibed, a glass of water should be taken to neutralize the effect).
The use of cyclosporine to produce tears and provide an anti-inflammatory effect may also be of some
benefit. The use of punctum plugs to increase tear film availability is also an effective option. Increased blinking
frequency can help to distribute the tear film more evenly. Figures 5.6A and B show the probable decongestive
effects of tear film substitutes and systemic hydration on the eye.
Figure 5.6A: Before tear film restoration

Figure 5.6B: One week after tear film restoration
Controlling Inflammation
Pterygium formation appears to be associated with acute, frequent and prolonged inflammation. Ocular surface
irregularities and exposure to irritants are linked to inflammation. Control or elimination of inflammation
may lead to control of the pterygium. With acutely inflamed lesions, immune suppression with NSAIDs like
diclofenac sodium, and topical steroids, like loteprednol and dexamethasone phosphate are appropriate for
short term use. Fluorometholone may be more appropriate for long term use. A decongestant and/or cold
eyewash may be added to reduce surface blood vessel activity and constrict the blood vessels. Figure 5.7A
shows a raised, vascular, inflamed pterygium before treatment with dexamethasone phosphate 0.1% and
naphazoline hydrochloride 0.012% drops three times daily. Figure 5.7B shows the eye with a shrunken lesion
Figure 5.7B and reduced inflammation.
Once the acute inflammatory condition has improved, then maintenance with decongestants, hydration
and immune enhancement can be used to control the inflammatory response. Various studies show that a diet
high in antiinflammation omega-3 essential oils and low in inflammation producing omega-6 fatty acids may
be appropriate in reducing inflammation throughout the body. The avoidance of all junk food, including
Figure 5.7A: Before topical treatment

Prevention 43
Figure 5.7B: One month after topical with

steroids treatment
trans-, partially hydrogenated- and saturated-fats and the use of a low protein diet will further enhance the
immune system to protect against acute episodes of inflammation.5-8 By adding vitamin C to the daily diet for
its positive role in wound healing, turmeric and ginger for their antiinflammatory activity and flaxseed oil for
dry eyes, many of my patients showed a marked improvement in the status of their pterygia.9 Though
supplements were taken in some cases, whole foods appeared to be more effective.
New Medical Treatments
Since pterygium is a vascular growth of the conjunctiva onto and into the cornea and exhibits inflammatory
characteristics, it is probably initiated and maintained by VEGF (vascular endothelial growth factor).
Antivascular compound now in use for inflammatory skin disorders and diabetic retinopathy may have an
effect on endothelial cell function and inflammatory reaction of the conjunctival blood vessels. Though the
angiogenic process may vary due to the vast diversity of inducers and mediators at different sites, perhaps the
basic pathophysiology can be applied to pterygium. In a study done in Zurich, Switzerland, the application of
the compound NVP-BAW2881 inhibited proliferation, migration and tube formation by human umbilical vein
endothelial cells and lymphatic endothelial cells in vitro. In a mouse model of psoriasis, the same compound
reduced the number of blood and lymphatic vessels and infiltrating leukocytes in the skin and showed strong
anti-inflammatory effects. Topical application of the anti-VEGF compound reduced the inflammatory response
elicited in pigskin by ultraviolet radiation and by contact hypersensitivity reactions.10 Specific studies are
needed to see if topical application or injection of anti-VEG F factors in the early stages of a pterygium would
inhibit blood vessel growth and prevent formation and progression, and during or after excision, prevent
recurrence.
Preoperative Management of Pterygium Using Surgeon’s Preferences
Patient preparation is essential in getting the best possible outcome from pterygium surgery. The primary
concern before surgery should be the reduction of inflammation, which is a major cause of postoperative
complications. Figure 5.8 shows an inflamed eye that should be treated medically preoperatively before doing
Figure 5.8: Inflamed preoperative eye
surgery. Topical decongestants like naphazoline 0.012% and tetrahydrozaline, tear film substitutes preferably
with a high aqueous content, topical anti inflammation medications like dexamethasone phosphate 0.1% or
loteprednol drops q.i.d or a combined compound like cyclosporine and protective UV-B sunglasses should be
used over a period of one to two weeks or as long as it takes to achieve a “quiet”eye (Figure 5.9).
Inflammation is the first response of the immune system to trauma, irritation and infection. It involves the
release of prostaglandin E2 and leucotriene C4, histamines, bradykinins, platelet activating factor, interleukins
and many more. We treat this response by immune suppression and inhibition. Once this is achieved, measures
may be considered to enhance the immune system prior to surgery. Vitamin C 300-500 mg has a positive role
in wound healing.9 I also recommend 1000 mg of omega-3, 500 mg of ginger and 700 mg of turmeric to reduce
and/or prevent inflammation preoperatively.
As there are no definitive or exact dose/response guidelines for these supplements, cold water fish, raw
ginger and curry powder may be added to food when possible. Known immunosuppressants like tobacco,
Figure 5.9: Quiet preoperative eye

Prevention 45
excessive oral steroids, smoking, excessive alcohol intake, refined sugar and narcotic drugs should not be
used.*
REFERENCES
1. Threlfall TJ and English DR. Sun Exposure and Pterygium of the Eye: A dose-response curve. Dept Pub Health, Univ Western
Australia, Perth, 2006.
2. Health Encyclopedia. Diseases and Conditions. Prevention of Pterygium and Pingueculum 2001. The Health Central Network,
Inc.
3. Anduze AL, Biscoe BW. Pterygium staging in the Caribbean. Ann Ophthalmol 1998;30(2):92-4.
4. Fiore M. Five Reasons to wear Sunglasses. Am Optometric Assn, 2007.
5. Ariza-Ariza R, Mestanza-Peralta M, Cardiel MH. Omega-3 fatty acids in rheumatoid arthritis: an overview. Semin Arthritis
Rheum 1998;27(6):366-70.
6. Coates P, Blackman M, Cragg G, et al (Eds) Encyclopedia of Dietary Supplements. New York: Marcel Dekker 2005:241-48.
7. Blumenthal M, Goldberg A, Brinckman J (Eds) Herbal Medicine: Expanded Commission E Monographs. Newton, MA:
Lippincott Williams & Wilkins 2000:379-84.
8. Weeks BS, Perez PP. A novel vitamin C preparation enhances neurite formation and fibroblast adhesion and reduces xenobiotic-
induced T-cell hyperactivation. Med-Sci Monit 2007;13(3):BR51-8.
9. Ringsdorf and Cheraskin. Vitamin C and human wound healing: Oral Surg 1982.
10. Halin C, Fahrngruber H, Meingassner JG, et al. Inhibition of chronic and acute skin inflammation by treatment with a
vascular endothelial growth factor receptor tyrosinase kinase inhibitor. Am J Pathol 2008 Jun 5; Zurich, Switzerland.
* Studies on the immune enhancers can be found in the Cochrane Review 2000 and the German Commission E monographs.
Surgery
When preventive measures and topical treatments fail to control the progression of a pterygium, surgery may
be necessary to restore the architecture and function of the eye.
Proper preoperative care is required to maximize the success of the surgery. There is no better or only
technique for removing a pterygium. It is more practical to utilize the technique that is most comfortable for
your hands and that gives the best result.
Patient education is an important part of pterygium management. Pain and pain management are the most
important concerns of most patients who are about to experience a surgical procedure. The presence or absence
of pain and its degree determines whether the patient has a positive or a negative experience. Fear of pain is
evident before fear of a poor outcome. It is important to communicate the anticipations and fears and give
adequate reassurances. Use open ended questions in an attempt to determine the individual’s pain threshold
and then address it appropriately. Explain the procedure with special emphasis on the anesthesia aspect and
what to expect postoperatively. Be honest. Cite the experiences of others and perhaps yourself. Discuss and
choose the setting, whether it is in the office or the hospital. Some people are more comfortable in an office
setting. Others need the full services of the hospital because of anxiety and/or systemic concerns such as
diabetes, hypertension, cardiac condition which need to be monitored. If planning to use oral sedatives like
phenergan, diazepam and lorazepam, a history of previous use and reactions as well as current supplemental
products should be elicited.
A discussion of the possible complications and how they would be handled should include special reference
to recurrences. The low rate of recurrence with adjunctive therapy and good surgical technique is a positive
highlight of patient preparation.
The percentage of patients who return for the second eye surgery increases with a comfortable pain-free
experience and adequate information.1 In 2002, in our practice, of 142 pterygium cases, 48 returned for the
second eye; 29 were patient-to-patient referrals and only 15 patients reported noticeable discomfort. Severe or
debilitating pain was not encountered.
The suggested indications for surgery include the early cosmetically apparent lesions shown in Figures
6.1A and B. The patient in Figure 6.1A wishes to use contact lenses and is concerned about the increased
Figure 6.1A: Stage II raised mixed

Surgery 49
Figure 6.1B: Heavily pigmented stage II

pterygium pinguculum-nevus with fibrous
components
redness of her eyes when she uses them. The patient in Figure 6.1B has 20/20 vision without correction but is
concerned about the appearance of his eye. Both lesions are relatively low risk for complications and could be
removed by simple excision with conjunctival flaps or autograft without adjunctive therapy.
Stage II and stage III symptomatic pterygia should be pretreated and then removed. Eyes with raised lesions
which are uncomfortable due to recurrent bouts of inflammation, may be treated with topical NSAIDs and
decongestants for 7 to 10 days before surgery. Conjunctival flaps or autograft with adjunctive mitomycin-C,
0.05 cc at 0.02% strength, single dose intraoperatively is the suggested technique (Figures 6.2A and B) .
The same technique is suggested for stage IV primary degenerative pterygia (Figure 6.3A) which are
asymptomatic or fibrovascular after reduction of the inflammation as in Figure 6.3B. A degenerative pterygium
in an aged eye with a mature cataract (Figure 6.3C) can be done first as full visualization is preferred for safe
and uncomplicated cataract surgery (Figure 6.3D).
Figure 6.2A: Inflamed stage II

Figure 6.2B: Inflamed stage III
Figure 6.3A: Degenerative stage IV
Figure 6.3B: Stage IV “preoperative” pterygium

Surgery 51
Figure 6.3C: Degenerative pterygium with

cataract
Figure 6.3D: Postoperative eye at 8 weeks with

cataract
This technique has a very high success rate for good results as in Figure 6.3D.
A large stage V pterygium (Figures 6.4A and B) with mixed fibrovascular and degenerative components,
impaired vision due to pupil obstruction and/or induced astigmatism and multiple risk factors, can be done
with conjunctival flaps, autograft or amniotic membrane graft. The technique should include the application
of a higher dose (0.1 cc of 0.04%) of mitomycin C.
Double-headed pterygia have better results when done with bilateral conjunctival flaps and 0.05 cc of 0.04%
mitomycin-C under each flap. There is insufficient conjunctival tissue available for two autografts on the same
eye and it is preferable not to disturb the fellow eye (Figures 6.5A and B). Sufficient undisturbed limbal
conjunctiva would remain should the need for filtration surgery arise. Amniotic grafts requiring the re-
epithelialization of both sides of the same eye would be the second choice.
Figure 6.4A: Stage V pterygium with induced

astigmatism
Figure 6.4B: Stage V pterygium with obstructed

pupil
Figure 6.5A: Double-headed pterygium

fibrovascular
Surgery 53
Figure 6.5B: Double-headed pterygium

degenerative
Table 6.1 is a summary of the basic instrumentation recommended for pterygium surgery.
The operating microscope should be situated at the temporal aspect for easier access to the palpebral fissure
and better visibility.
The preoperative anesthesia begins at the reception desk with the patient and staff interaction. Sincere
efforts must be made to put the patient at ease. In the holding area, preoperative oral medicines and topical
anesthetic drops are started. We use Tetracaine 0.5% one drop to the designated eye. This gives the patient a
chance to compare the sensation or lack of sensation between the two eyes. The patient is then escorted to the
Table 6.1: Suggested Instruments for Pterygium Surgery
Wire lid speculum

Westcott scissors (sharp tips)
Colibri forceps or 0.12 forceps with teeth
Tying forceps (X2)
# 64 Beaver blade
Needle holder (fine tip)
Disposable cautery or bipolar
3X3 sterile gauze sponges
Cotton tip applicators (sterile)
9-0 or 10-0 nylon sutures
BSS 15 or 30 cc
Phenylephrine 2.5% drops
Mitomycin-C 0.02% and/or 0.04%
1 cc syringe with 25 gauge cannula
Carbocaine or xylocaine 2% injectable anesthetic
3 cc syringe with a 30 gauge needle
operating table and made comfortable with headrest and appropriate sheets. The patient’s preferred music is
played. We operate either early in the morning or late in the afternoon when there are no other distractions or
companion noises or need to rush to the next patient. A second dose of topical anesthetic is instilled. This
second dose is with Xylocaine 4%, which is considerably stronger and excellent for advancing anesthesia to
the conjunctiva prior to the injection of carbocaine. The upper face is prepped with betadine solution and the
designated eye draped. Care must be taken to ensure adequate breathing space under the drape as there is
usually no assisted oxygen provided in the office setting.
A third dose of topical anesthetic (Xylocaine 4%) is instilled and the surgeon separates the lids with the
fingers. The syringe with 1 cc of carbocaine 2% is brought slowly from the side, to minimize visibility by the
operated eye. The 30 gauge needle is slipped gently into the subconjunctival space at the point where the
pterygium head meets the limbus. A very small bolus is injected and tamponaded with a Q-tip. This provides
preliminary subconjunctival anesthesia. The lid speculum is then inserted and the remainder, usually less
than 1 cc., of the Carbocaine can be injected into the subconjunctival space to balloon the body of the pterygium.
The raised lesion is tamponaded with a Q-tip to spread the anesthetic around just past the involved tissue to
ensure complete anesthesia.
Surgical Techniques
1. Conjunctival flaps for pterygium surgery: L Hirst MD Australia “the majority of surgeons use rotating Flaps”
Conjunctival flaps are the most successful and most used procedure for pterygium surgery worldwide.2-9
This simple technique is the surgeon’s preference and is recommended for all primaries, small
recurrences and especially double-headed lesions. It features the same attached blood supply, blood vessels
oriented vertically away from the limbus, ease of performance, fast healing, a single wound and reports an
average recurrence rate of 1-3%. The procedure consists of six steps.
a. Initial incision (Figures 6.6A and B) is made into the body at a point 2-4 mm from the limbus. This isolates
the head for better visibility, easier access and safer excision of the head. It allows the rest of the conjunctiva
to retract and leaves enough tissue for the flaps to cover the sclera. Only light cautery should be applied
to minimize scleral injury. Excessive use causes postoperative pain and inflammation. Phenylephrine
2.5% drops may be used to assist with hemostasis. Only a moderate tenonectomy is suggested with the
excision comprised of involved fibrovascular tissue closest to the cornea. Avoid the muscle sheath entirely.
Take less tissue not more. Less trauma to the tissues results in minimal postoperative inflammation.
b. Excision of the head (Figures 6.7A and B) is done with a #64 Beaver blade or equivalent and from the limbal
side. While hemostasis was being addressed, the pterygium head should have shriveled and the
conjunctival tissue should have retracted toward the canthus thereby allowing full view of the entire
head for a safer excision. Start the incision superficially (either superiorly or inferiorly, whichever gives
the better access) and engage the subepithelial fibers of the cornea at the edge of the head. Avoid starting
the dissection too far away from the head or it will be too deep into the stromal lamellae. Lift the pterygium
head upward with the forceps to keep it taut and provide a good cleavage plane. This achieves minimal
damage to the cornea, less chance of dellen formation and better healing.
c. Conjunctival flaps (Figures 6.8A and B) are fashioned by making superior and inferior relaxing incisions
in the conjunctiva at its juncture with the limbus. Continue the incisions vertically 5-6 mm in each direction
Surgery 55
Figures 6.6A and B: Initial incision into the body

B of a primary stage IV pterygium
A B
Figures 6.7A and B: Excision of the head
B Figures 6.8A and B: Conjunctival flaps
to create easily opposable flaps with which to cover the sclera at or up to 1 mm from the limbus (i.e.relaxing
incisions). Undermine to loosen the flaps so that they slide and move easily with minimal tension. These
flaps should cover the sclera entirely, keep the blood supply intact and serve as a barrier between the
cornea and the remainder of the retracted pterygium body. The semilunar fold is the landmark for the
proper resting position of the conjunctiva.
d. Initial closure (Figures 6.9A and B) is done with 9-0 non-absorbable suture, starting from the distal canthus
or from the proximal limbus. Use short bites (3 or 4) to put the flaps in place, then long bites (2 or 3) to
minimize tension and prevent traction, so that the sclera remains covered throughout the healing period.
A single counter-traction suture may be placed at one o’clock or 5 o’clock at the apex of the relaxing
incision in order to stabilize the flaps. The remaining knots should be in the midline or pulled inferiorly
and trimmed accordingly. Do not bury as they may irritate the sclera and subconjunctival tissue which is
the source of the pterygium in the first place. Nylon holds better and longer than vicryl, and there is less
inflammatory response and less chance of wound dehiscence.
Surgery 57
Figure 6.9A: Initial closure at the limbus
Figure 6.9B: Initial closure at the canthus
e. Completed closure (Figures 6.10A and B) is achieved with the conjunctival flaps oriented so that the blood
vessels are directed vertically, away from the cornea. Closure should be neat and flat and cover the sclera
no less than 2 mm from the limbus. This serves as a barrier, orients the blood vessels vertically and
reduces the area of stimulus for recurrence.5,6
f. Adjunctive therapy (Figures 6.11A and B) should be done with mitomycin-C in a single low dose, given
subconjunctivally (0.05 cc of 0.4 mg/ml (0.04%) or 0.1 cc of 0.2 mg/ml (0.02%). This dosage range is
effective and free of serious side effects. Tamponade with a Q-tip done at the time of instillation will
localize the mitomycin-C at the site where it is needed, the subconjunctival tissue. A rinse can be done
after 3 minutes for priaries and 5 minutes for recurrences. Note that a few drops of Mitomycin-C applied
directly to the sclera just after the initial incision and tenonectomy will assist with hemostasis.
(Complications may occur with too high a dosage, with the use of multiple drops, with cautery damage
to the sclera and with bare sclera technique. See adjunctive therapies).
Figure 6.10A: Completed closure
Figure 6.10B: Long and short sutures
A B
Figures 6.11A and B: Subconjunctival mitomycin C application

Surgery 59
2. Conjunctival autograft for pterygium surgery: The instruments and anesthesia are the same as for conjunctival
flaps except for the addition of calipers. The technique is the surgeon’s preference for primary degenerative
pterygia in older eyes with thin conjunctiva and no glaucoma and for degenerative recurrences. It involves
two wounds, tissue glue or/and many sutures which may cause additional inflammation. The
revascularization is somewhat unpredictable and the new blood vessels may reorient and regrow toward
the cornea. The recurrence rate averages 5-15%. It should be used judiciously in the Tropics, where many of
the people are of African origin and are at high risk for developing glaucoma which may need filtration
surgery at some time. Many of the pterygia are double headed (both sides on the same eye) and there may
not be enough tissue available for the required two wounds. In the absence of these situations, the procedure
is considered by many surgeons to be the gold standard.
This procedure consists of five basic steps.
a. Initial incision (Figure 6.12) can be made into the body at a point 2-4 mm distal to the limbus which would
generally involve most of the pterygium, then dissected back toward the cornea or it can be started in the
cornea at the apex or at either juncture with the limbus, taking care not to cut too deeply or remove too
much of the corneal tissue.
b. Excision of the head (Figure 6.13) should be done carefully in order to avoid taking too much corneal
tissue. Corneal injury accounts for delayed healing and reactive inflammation which leads to greater risk
of recurrence. Continue the incision into the body and remove only the affected tissue. In a large primary
pterygium, some of the distal body tissue may be left in place. The conjunctiva will retract to a comfortable
position. Measure the area to be covered only after the conjunctiva has settled into position with the
semilunar fold. When the area to be covered is less than 1.5 cm square, the more successful the graft will
be. Often the semilunar fold has been pulled toward the cornea by the pterygium. When the semilunar
fold retracts to its original position, this is a good guide for how much tissue to use to cover the sclera.
c. Harvesting the free graft (Figure 6.14) should be done from the superior or inferior aspect of the conjunctiva.
(Avoid the palpebral fissure on the contralateral side as this tissue is exposed to UV radiation and the
formation of another lesion is highly likely at the site). Use blunt dissection to avoid button-holing the
graft. Copious amounts of BSS must be used to keep the tissues hydrated throughout the procedure.
Note that this second wound should granulate in without sutures.
Figure 6.12: Initial incision into the head

Figure 6.13: Excision of the head
Figure 6.14: Harvesting the free graft from the

superior aspect of the conjunctiva
d. Positioning the free graft (Figure 6.15) should be done without it losing contact with the host surface. It is
imperative to lay it flat on the moistened cornea with the subconjunctival side down and then slide it into
position on the scleral bed. The original limbal edge should be apposed to the cornea at the corresponding
limbus. Stretch the graft at the limbus so it maintains contact. It should cover the exposed sclera entirely
and slightly overlap the cut edges of the conjunctiva. This position will reduce the chance of graft
contracture and subsequent wound dehiscence which would convert to bare sclera and eventual graft
failure.
e. Suturing the free graft (Figure 6.16) in place should be done with 10 - 0 non-absorbable sutures. Use only
the number of sutures that will stabilize the graft in position (about 7 or 8). Excess sutures may lead to
increased inflammation. The knots can be buried to reduce irritation on the lids. Tissue glue may be used
instead and will be discussed in the section on new techniques.
* Conjunctival autograft photos provided courtesy of Dr. Jean-Christophe Joyaux, technique is from Dr KR Kenyon’s
1985 article.10
Surgery 61
Figure 6.15: Positioning the graft
Figure 6.16: Graft sutured in position
3. Amniotic membrane graft for pterygium surgery: This procedure is indicated for a large primary pterygium,
large and multiple recurrences, large double headed, pterygium with symblepharon, corneal epithelial
defect, and chemical injuries. Sufficient amounts of donor tissue are available for transplant. It features an
average recurrence rate of 10 - 25% which is partly due to the severity of the lesion, a high inflammation
response and relatively slow reepithelialization during wound healing. The graft is a single layer of cuboidal
epithelial cells from the placenta. It has a thick basement membrane and avascular stromal matrix loosely
attached to the chorion. It provides a new basement membrane to which the new epithelial cells can migrate
and grow. We have used two types, amniotic biotissue (cryo-preserved wet glass vial storage) and ambiodry
(dehydrated box storage). Both have been quite successful and are useful especially for large and multiple
recurrences (Figures 6.17 and 6.18). The limitations consist of the fact that it is used in the most complicated
cases in which there is extensive damage to the host tissues. This results in severe inflammation, high incidence
of postoperative bacterial infection and difficult healing due to extreme secondary complications. The
relatively high cost and regional availability of the material precludes use in all primaries especially in third
world tropical areas.
Figure 6.17: Third recurrence with medial

symblepharon
Figure 6.18: Amniotic membrane graft sutured in

place
The instruments are the same as for autograft with the addition of a muscle hook. A more extensive
anesthesia consisting of xylocaine 2% with epinephrine for local infiltration and marcaine 0.75% for a
peribulbar deposit.
The procedure is in five basic steps.
a. The initial incision should be made in the body at the distal limit of the area to be removed. Dissecting
toward the head affords better visibility and ensures less damage to the underlying sclera.
b. The excision of the lesion should involve the affected scar tissue as far back as possible since the healing
will depend on the migration of new epithelial cells and their growth onto the new substrate. Care should
be taken not to injure the sclera further with deep dissection and excessive cautery. The sclera should
retain some vascularity (but not hemorrhage) in order to sustain the graft tissue. A conjunctival pedicle
flap should be created on three sides to which the graft will be attached.
Surgery 63
c. Preparation of the amniotic membrane graft should be carefully planned and executed. Measurements
should be taken and the graft must be cut and trimmed to cover the entire area of bare sclera. The basement
membrane side must be in the “up” position. Place and manipulate it with the muscle hook. In some
cases the graft may be folded to provide more bulk in which case both sides will be basement membrane.
Hydrate well with BSS throughout the procedure.
d. Secure the edges of the graft beneath the cut edges of the host conjunctiva with 10 - 0 non-absorbable
sutures which will allow the host epithelium to slide over the graft tissue (If tissue glue is used, secure in
the same location under the conjunctiva).
e. Mitomicin-C, 0.1 cc of 0.4 mg/ml (0.04%) is instilled under the graft and a steroid/antibiotic ointment is
applied twice daily for 4 to 10 weeks.11,12
4. Mucosal graft technique for pterygium surgery: The indications for this procedure are large or multiple
recurrences with or without symblepharon, inadequate amounts of autologous conjunctival and when
amniotic tissue is not available. The technique is limited due to difficulty harvesting the mucosal tissue, the
requirement of two wounds for healing, possible infection due to bacterial content, postoperative pain and
high incidence of granuloma.
Excision of the lesion is done in the conventional manner described for conjunctival flaps and autograft.
The large bare sclera area obtained should be free of bleeders but contain some visible viable vascularity.
After sufficient anesthesia with a local subepithelial injection of 2% lidocaine or equivalent, a split
thickness (thin) mucosal graft is obtained from the internal face of the lower lip. No cauterization or sutures
are necessary at the donor site. This minimizes postoperative pain and/or infection.13
Positioning of the graft on the scleral bed is done with a muscle hook and smooth forceps and should
be with subepithelial side down. The graft should be slightly smaller than the area to be covered and 1 to 2
mm of bare sclera may remain at the limbus.
The graft should be secured flush with the edges of the cut conjunctiva with non-absorbable suture in
a tensionless way by leaving the loop slightly loose before tying the knots. Buccal mucosal tissue will usually
stretch to fill the gaps.
Mitomycin-C in a single low dose of 0.1 cc of 0.2 mg/ml (0.02%) can be instilled under the graft. An
antibiotic/steroid ointment is applied and the eye is patched.
The postoperative management involves the use of topical antibiotic/steroid ointment and
phenylephrine 2.5% drops t.i.d. for about one month. Sutures are removed after 10 days. Though no dressing
or ointment is needed for the donor site, it should be inspected for signs of infection at which time topical
and oral antibiotics would be used.
5. Transposition for pterygium surgery: This procedure is indicated for multiple recurrences with insufficient
autologous tissue, and after failure of amniotic membrane graft or autograft, as a last resort (Figure 6.19).
It involves the diversion of established recurrent fibrovascular tissue to a point at least 90 degrees
away from the cornea and securing it to the conjunctiva and sclera. In some cases it may be cosmetically
unacceptable but necessary to reduce the continued destruction of the cornea by the lesion. It is done in four
steps.
Figure 6.19: Transposition technique for recurrent pterygium
a. The initial incision is made at the head of the pterygium taking extreme care not to cut too deeply into the
corneal stroma. The head is grasped with a toothed forceps and gently avulsed with assisted blunt
dissection with the Beaver blade. Try to preserve as much cornea as possible.
b. The dissection is carried back to a point on the sclera about 2-4 mm past the limbus taking care not to cut
into the sclera. A small incision is made into the superior edge of the lesion, hemostasis is achieved and
the head is rotated superiorly and sutured to the distal cut edge of the superior conjunctiva.
c. The proximal cut edge of the superior conjunctiva is undermined, a relaxing incision is made and the
resulting flap is brought down and sutured to the corresponding (inferior) edge of the cut conjunctiva.
The resulting overlapping conjunctival flaps are secured to each other and to the sclera with 10 - 0 non-
absorbable sutures.
d. Adjunctive therapy with mitomycin-C is done with a single low dose 0.1 cc of 0.4 mg/ml (0.04%) into the
subconjunctival space and tamponade with a Q-tip. It may be rinsed after 5 minutes.
A topical steroid/antibiotic combination may be instilled and patching for 48 hours may be needed to
achieve full reepithelialization of the cornea. Since no more than 2 or 3 sutures are used, discomfort should be
at a minimum. Careful control of postoperative inflammation is needed.
Comparative Studies: Results
A clear eye that is comfortable, with no discernible blood vessels on the cornea and no fibrovascular activity in
the conjunctiva is considered to be the desired result. A review of the literature reveals that surgeries done
with conjunctival flaps and mitomycin C have a lower recurrence rate than other surgical techniques.3-6, 8-9
Surgery 65
A retrospective study done in house (unpublished) by the author comparing the results of three of the most
common techniques, revealed expected outcomes. Group I consisting of 60 primaries and 20 recurrences had
amniotic membrane grafts (Figure 6.20), 28 with wet biotissue when more cornea was involved and 32 with
dry biotissue when more conjunctival fornix was involved. There were 4 recurrences in the primary subset
(6.6%) and 8 recurrences in the secondary recurrence subset (40%). This was understandable and acceptable
due to the nature of the preoperative lesions. Group II consisting of 56 primaries had conjunctival autograft
surgery (Figure 6.21). There were 3 recurrences (5.4%). Group III consisting of 120 primaries, had conjunctival
flaps surgery (Figure 6.22). There were 2 recurrences (1.6%). All groups had mitomycin C, single dose
intraoperatively without complications.
A comparison of amniotic membrane graft versus conjunctival autograft and topical mitomycin-C treatment
showed similar results, i.e. recurrence rates of 3.8%, 5.4% and 3.7% respectively. The mitomycin C was used as
drops instilled t.i.d. for one week. One case of infectious scleritis occurred in the mitomycin C group receiving
drops.14
Figure 6.20: Amniotic membrane graft at 12

weeks
Figure 6.21: Conjunctival autograft at 12 weeks

Figure 6.22: Conjunctival flaps at 12 weeks
A long-term follow-up of low dose intraoperative mitomycin-C (0.02%) versus conjunctival autograft in
primary pterygium surgery, concluded that both were equally as effective. Three eyes (out of 21) in the
mitomycin-C group with primary excision (15%) had adverse events. Two had delayed corneoscleral epithelial
healing and one had a pyogenic granuloma. Mitomycin-C should not be used topically on a bare sclera.15
A comparative study of intraoperative mitomycin-C and beta-irradiation in pterygium surgery concluded
that the application of 0.04% Mitomycin-C was more effective than the use of beta irradiation as an adjunctive
treatment.16
A comparison of conjunctival autograft versus bare sclera excision in the treatment of pterygium recurrence
showed that the pterygium morphology and size was a significant higher risk when bare sclera was used, and
that conjunctival autograft was more effective.17
In a study comparing conjunctival rotation autograft versus conjunctival autograft the recurrence rates
were found to be so similar (5.88% and 5.55%) that the authors concluded that both techniques were equally
effective. Only 39 eyes were in the study. Significant side effects included delayed healing (11.76%), persistent
congestion (5.88%), a loose graft (5.55%) and dellen formation.18
A comparison of three methods for the treatment of pterygium, amniotic membrane graft, conjunctival
autograft and conjunctival autograft plus mitomycin-C showed all to be equally effective in preventing
recurrence. When choosing which method to use, variables should depend on the size and extent of the excision
required to close the defect and to prevent excessive scleral exposure.19
In a review of treatment of pterygium in Queensland, Australia, where many of the most experienced
ophthalmologists reside, done by primary survey, it was found that more than half the respondents used a
swinging conjunctival flap (50%) for primaries. Another 29% used simple excision with bare sclera and 25% of
all added adjunctive therapies such as Mitomycin-C or β-irradiation. For recurrent pterygia, 33% used adjunctive
therapies with conjunctival autograft.20
In a more straightforward study, the recurrence rates after pterygium excision with sliding conjunctival
flaps (6.9%) were compared to those after free conjunctival graft (18.5%) and found to be more simplified and
significantly better.21
Surgery 67
The results of a single low concentration, intraoperative application of Mitomycin-C versus postoperative
eye drops after pterygium surgery support the efficacy and relative safety of the single dose together with the
use of a conjunctival flap.22
A comparison of conjunctival autografts, amniotic membrane grafts and primary closure for primary pterygia
showed that amniotic membrane grafts are a viable alternative especially for advanced cases of double headed
lesions or those who are at risk for and might need glaucoma surgery later.23
In a randomized controlled study of conjunctival autograft versus amniotic membrane graft in pterygium
excision, amniotic grafting had a higher average recurrence rate (35%) for all types (primary and recurrent)
than conjunctival autograft (15%). The results were skewed as amniotic grafting would be used for larger
lesions, multiple recurrences and double headed lesions, while conjunctival autograft would be reserved for
smaller lesions.24
Healing in conjunctival flaps involves reepithelialization of the cornea and self-adhesion of the flaps to
cover the sclera. It is fast, relatively free of inflammation and involves one intention.
Conjunctival autograft or free graft requires re-epithelialization of the cornea plus revascularization of the
graft (two intentions) and possibility of the new blood vessels being oriented toward the cornea.
Healing in amniotic membrane grafts involves reepithelialization of the cornea, re-epithelialization of the
graft and revascularization of the graft (three intentions).
Adjunctive Therapies
Mitomycin C is the most commonly used adjunctive therapy in modern pterygium surgery. It is an anti-
metabolite which inhibits DNA synthesis, and cellular RNA and protein synthesis, and has antibiotic and anti-
neoplastic properties. The safest and most effective dosage for preventing a pterygium recurrence has been
examined in comparative studies of differing strengths which were effective in reducing the recurrence rate
and low in incidence of side effects. In 1996, it was found that 0.1 cc of 0.5 mg/ml (0.05%) was successful but
still left the eye hyperemic and slightly uncomfortable.25 This dosage was further reduced to 0.1 cc of 0.4 mg/
ml (0.04%) for large primaries and secondary recurrences. The single application of low dose strength of 0.2
mg/ml (0.02%) for most small primaries is still effective and offers little or no complications. The low dose
amount of 0.1 cc or less is consistent in many other studies as well. Each of the outcomes from various studies
concerning conjunctival flaps, free grafts or amniotic membrane grafts, the addition of mitomycin-C yielded
lower recurrence rates. The use of the bare sclera technique with multiple topical drops had higher recurrence
rates and more complications and should not be used. It is a toxic substance and may cause serious damage to
the ocular tissues particularly if burned or injured excessively from the surgery itself.26-33
The preparation of mitomycin-C should be the same for all surgical techniques.
Dilute a 5 mg vial with 12.5 cc of bacteriostatic water, to 0.04% or 25 cc. to 0.02%.
Delivery can be done with 0.1cc soaked into a wek cel sponge and applied to the underside of the conjunctival
flaps or free graft or amniograft. This dose should be rinsed after three minutes. The 0.05 cc dose can be
delivered by cannula directly to the underside of the conjunctiva or graft and tamponaded in place with a
sterile Q-tip. This may be rinsed after 5 minutes depending on the severity of the preoperative pterygium.
There have been no complications from leaving a small amount of mitomycin-C in place.
Since using the single application of low dose MMC, we have experienced one case of scleral melt which
was attributed to a dent in the sclera due to excessive cautery and resultant thinning. We have seen two other
cases recently (referred from elsewhere) in which multiple drops and bare sclera were used (see Complications).
Further longer term follow up with the use of Mitomycin-C is ongoing and no delayed complications have
surfaced to date.
The following are a series of statements regarding the use of mitomycin-C in pterygium surgery.
Results from Florida: Quote
William Trattler, MD…Center for Excellence in Eye Care, Miami, Fla.… “The source of a pterygium recurrence
is the subconjunctival tissue after removing the head and the affected subconjunctival tissue, I make relaxing
incisions in the conjunctiva and suture the superior and inferior margins together so there is no bare sclera.
Then (I) inject less than 0.1cc of 0.02% mitomycin-C into the subconjunctival space. I had only one recurrence
in five years of doing this technique.”
Results from the Caribbean: Article
Pterygium Surgery with Mitomycin C: Ten Year Results. A.L.Anduze, MD, “870 cases with conjunctival flaps
and Mitomycin-C, …0.35% recurrence rate”.4
Results from New York: Article
Serious complications of mitomycin C using bare sclera and multiple drops.26

Note that Almost all complications with Mitomycin C have been recorded with the use of bare sclera technique and
multiple topical drops.
Results from Turkey: Article
Intraoperative application of mitomycin C in the surgical treatment of pterygium with bare sclera and recurrence
rate of 5.9%.27
Results from Canada: Article
Use of Mitomycin C with conjunctival autograft in pterygium surgery in Asian-Canadians reveals a lower
recurrence rate (9%)in the group in which MMC was used versus the group in which it was not used (18%).
The difference was noted especially in the more advanced pterygia.28
β-irradiation with a strontium 90 plaque at 1200 to 6000 rads in a single dose or divided over several weeks
applied directly to the bare sclera reduces the recurrence rate to between 10-15%. Together with the evidence
of late complications (12% in one study) of scleral necrosis (melt) and scleromalacia (abnormal thinning) at the
site of application, excessive pain (possibly due to the bare sclera itself), early cataract, and endophthalmitis,
its continued use is being reduced.34 There is no doubt that in experienced hands it works well, but when
considering the cost issue and availability being largely in academic settings and hospitals with a radiology
department its use has diminished further.
Surgery 69
Thiotepa (triethylene thiophosphoramide) is an alkylating agent similar to nitrogen mustard. When applied
to the bare sclera (0.05% drops daily for 6 - 8 weeks) it reduces the recurrence rate to between 8 and 15%.
However, it is toxic. Along with reactive conjunctivitis, photophobia, and scleral necrosis, it is most often
associated with deposits of black pigment on the conjunctiva and eyelids. It has largely been discontinued.29
5 FU (fluorouracil) is a good, effective adjunct which reduces the recurrence rate significantly (11%). It may
be used in the same way as mitomycin-C. Complications include conjunctivitis, scleral granuloma, scleral
necrosis and conjunctival necrosis.35 In some regions it is difficult to obtain.
Postoperative Management Using Surgeon’s Preferences

The low incidence of infection after pterygium surgery is probably due to the presence of tear enzymes, the
external site, good preoperative care, basic hygiene and good health. Many recurrences occur in those with
poor lifestyle habits, debilitated individuals, and in cases with identifiable high risk factors. All efforts in the
postoperative period should be directed toward primary wound healing.
The immediate postoperative care should consist of a one-time application of a steroid/antibiotic ointment,
a patch for 24 hours and oral medications for sleep and possible discomfort. A mild irritation may be due to
the suture tips which may be in contact with the inner surface of the eyelid. A call to the home and check in
with a family member concerning the patient’s status is good practice and an adjunct to postoperative care.
Once the patch is removed and the eye is opened and blinking, this irritation is easily tolerated and even
disappears. The 9-0 sutures are smaller than the eyelashes. The oral analgesics are optional and are given for
one to two days. Upon removal of the patch, the eye is treated with artificial tears and decongestants at least
four times daily. The use of sunglasses and a hat is encouraged especially when outdoors. Topical NSAIDs or
steroid drops are optional in the first two weeks. It may be unorthodox, but in order to promote primary
wound healing, they may be withheld until the cornea is re-epithelialized and the basic wound edges are
secure. They may be used after this period or in the interim mainly in the presence of persistent hyperemia
and discomfort. The infection rate is very low as the restoration of “normal” tears and regular use of the
postoperative drops is a sufficient preventative. (Conjunctival infection is seen in about one in one hundred
cases and endophthalmitis has not been seen in over 3000 cases in the Virgin Island).
Avoidances include not rubbing the eye; no direct fan into the face; no swimming or exposure to salt water
or chlorine pools; reduce sun exposure by wearing sunglasses; no chemical sprays and no exposure to cigarette
or cigar smoke.
In the interim, irritating tips of the sutures may be trimmed and any irregular suture can be removed early.
The flaps or free graft must remain in place and cover the sclera for at least two weeks to keep the chance of
recurrence at a minimum.
Suture removal is recommended at 2 weeks (Figures 6.23 and 6.24). The sclera should be covered and the
blood vessels oriented vertically away from the cornea. The eye should be mildly hyperemic and the flaps or
graft stable. Use topical anesthesia with 4% xylocaine, a jeweller’s forceps and iris stitch scissors. Remove the
shorter sutures first. If the flaps begin to pull apart (1 - 2 mm), leave one or two of the longer sutures in place
for another 7 - 10 days. If they are more than 3 mm or more apart, then resuture immediately. A wound
dehiscence increases the risk of recurrence since the edges of the flaps serve as irritation points for the movements
of the eyelid and the sclera that is exposed serves as a nidus or stimulus for the fibrovascular response. A
covered sclera at 2 weeks ensures a low recurrence risk of almost zero. If the hyperemia is minimal and the
Figure 6.23: Sutures at 2 weeks postoperative
Figure 6.24: Six weeks postoperative
flaps are intact at 2 weeks, the chance of recurrence will be very low.8 After suture removal maintain the
frequency of topical drops at q.i.d. for one more week and reduce accordingly. Refraction may be done at 1
month; wait 4 - 6 months if significant preoperative astigmatism in a young individual was present (see
Complications) (Figures 6.25A to D).
Figure 6.25A: Preoperative stage IV pterygium

Surgery 71
Figure 6.25B: Two weeks postoperative with

sutures in place
Figure 6.25C: One month postoperative healing
Figure 6.25D: Three months postoperative

healing
Wound healing may be enhanced with good anti-inflammation dietary measures to boost the immune system.
The use of omega-3 fatty acids and anti inflammation spices like turmeric and ginger taken orally, Vitamin C
and lots of water may help with the overall healing process.36-39
Corneal wound healing is the primary objective after surgery. Keratocytes become fibroblasts and repopulate
the wound. In the first week following surgery, adjacent epithelial cells in the cornea move over one layer at a
time to cover the defect. In the second week, proteins fill the intracellular spaces to form tight junctions and
secure cells to the basement membrane. Any disruption here may lead to the formation of aberrant collagen
and extracellular matrix and the cells may fail to adhere properly. Just as inflammation can cause excessive
scarring through overstimulation of the fibroblasts, suppression of inflammation with high doses of steroids
may interfere with normal cell function (keratocytes) and delay wound healing. Similarly, overuse of antibiotics
can kill cells outright, interfere with barrier functions of the epithelium, slow collagen synthesis and stimulate
more inflammation. Care should be taken not to overuse these medications in the postoperative period.40,41
Suggested Healing Regimens
1. Decongestant with naphazoline 0.012% and artificial tears preoperatively b.i.d. and postoperatively q.i.d.
Designated as “Natural “ (no steroids or antibiotics) healing. This is an unorthodox method and a sample
outcome is shown in Figure 6.26A.
2. Oral vitamin C 500 mg, one tablet b.i.d., Omega-3 capsule 1000 mg. b.i.d., topical tears and Naphazoline
0.012% .both q.i.d. This is an example of Immunoenhancement healing and the results are shown in Figure
6.26B.
Figure 6.26A: Natural healing at 2 weeks after

surgery
Figure 6.26B: Immuno-enhanced healing at

2 weeks after surgery
Surgery 73
Figure 6.26C: Immuno-suppressed healing at 2

weeks after surgery
3. Topical dexamethasone: 1% and/or diclofenac and/or tobramycin drops each t.i.d. preoperatively and q.i.d.
postoperatively. This is Immunosuppression healing and a sample outcome is shown in Figure 6.26C.
All three regimens give successful outcomes.
Mission Work: A Suggested Travel Set for Itinerant Surgery
The instruments, medicines and accessories needed are dependent on the destination.
Most missions are offered in developing countries where high-tech medical facilities are lacking. A general
list of necessities for pterygium surgery to be packed and transported are presented in Table 6.2. It may be a
good idea to have a customs form available and a letter of invitation from the host country.
Sample Cases
1. Figure 6.27A to C explains the eye of a 60-year-old fisherman, who imbibed alcohol daily, never wore
sunglasses, and presented for the first time for and eye exam. This was an actively inflamed, stage IV, class
Ia lesion which was considered to be at extremely high risk for recurrence as he had five out of six risk
factors. He was male, with red-fair complexion, cumulative outdoor exposure, chronic dehydration and no
eye protection. Following preoperative treatment with the protocol to reduce inflammation, he underwent
a large excision with conjunctival flaps and mitomycin-C, 0.1 cc at 0.04% strength. He did not comply with
postoperative instructions and did not use topical steroids or antibiotics given at the time. He did use
decongestants because they “felt good”. Though he did show up to have the sutures removed at two weeks,
he did not keep his other follow up appointments until six months later.
At the time of suture removal there was +4 hyperemia but no discharge or dehiscence.
He did surprisingly well. Success was attributed to the integrity of the flaps as a barrier and functional
scleral cover, and to the mitomycin-C in controlling the inflammatory reaction and keeping the activity of
aberrant myofibroblasts in check.
Table 6.2: Travel Set for Itinerant Surgery
Informed consent forms

Loupes
Anesthesia: Topical: tetracaine 0.5%, 4% xylocaine,
2% Carbocaine and 0.5% marcaine (for peribulbar if needed)
22 Gauge and 30 gauge needles, 3 cc and 1 cc syringes
Preoperative Medications: atropine 1%, * antibiotic,
Prep: Betadine solution, alcohol swabs, sterile drapes (non-fenestrated and fenestrated) caps, gowns, masks, surgical gloves
Surgical instruments: (3 packs)
Sterilizing pouches for dry clave
Sterile cotton tip applicators
Sterile gauze sponges (3X3 or 4X4)
Disposable cauteries
Suture: 9-0 nylon. 10-0 nylon
Intraoperative medications
Phenyephrine 2.5%, BSS irrigation, mitomycin-C (5 mg vial diluted to 0.04% (0.4 mg/ml) with 12.5 ml of bacteriostatic water.
Postoperative medications: *antibiotic ointment (one dose only) topical decongestants, tears; ibuprofen, aminophen and
flurazepam.
Eye pads, tape
Postoperative instructions
When visiting a foreign country for purposes of providing health care, there are some basic principles of cultural medicine that
should be observed. The local eye care providers and professionals should always be contacted and involved in the procedures
of patient care. Together, these services become invaluable. Apart, there may be animosity and hostility. Always leave the area
better than you found it. Impart compassion, information and service, but take some knowledge back with you. It is common
courtesy that “the teacher can be taught”. Everyone is worth something and every opportunity is a chance for learning. Show
respect whenever and wherever it is due and never forget to smile.
*without the benefit of preoperative prevention of inflammation measures, a good broad spectrum antibiotic should be instilled
in the eye before and after surgery.
Figure 6.27A: Preoperative stage IV, class Ia

inflamed pterygium
Surgery 75
Figure 6.27B: Postoperative at 2 weeks
Figure 6.27C: Follow up at 6 months time of

suture removal
2. Figure 6.28A is a Stage V, active pterygium with impaired vision due to astigmatism and pupil encroachment.
There is restricted movement of the globe due to symblepharon. Note that the semilunar fold is obliterated.
An amniotic membrane graft or a conjunctival autograft, both with mitomycin-C, 0.1cc at 0.04% single
intraoperative dose are the suggested techniques. Incise the body of the pterygium at the limbus and let it
retract distally toward the canthus. Measure and place the graft from the edge of the retracted conjunctiva
to the limbus. The postoperative Figure 6.28B shows excellent results with the reformation of the semilunar
fold and no signs of inflammatory regrowth. Having less area to cover yields better results.
Figure 6.28A: Stage V pterygium
Figure 6.28B: Same eye postoperative with

induced astigmatism at 6 months
New Treatments in Pterygium Management
Fibrin surgical glue is a useful alternative to sutures in securing the grafts in pterygium surgery. Concern over
the irritability of sutures prompted its use in the attempt to secure the graft (conjunctival and amniotic) in
place. It consists of human fibrinogen and thrombin and bovine aprotinin and calcium chloride in a dual
syringe system. The contents mix upon exiting the ports and the sealing component is activated to form a clot
with adhesive properties that holds the graft in place. Advantages of fibrin glue include its avoidance of the
suturerelated problems of irritation (nonabsorbable) and premature dissolution leading to wound dehiscence
(absorbable). The application is fast, easy, reduces surgical time and there is less pain reported.42-44 The
disadvantages lie in its relatively high cost and low availability especially in areas endemic to pterygium. In
securing the conjunctiva firmly to the sclera, the healing is unnatural and the sliding effect of the conjunctiva
Surgery 77
over the sclera is curtailed, at least for a while. The glue is self-limited and eventually the scarred conjunctiva
will assume its natural position. In some cases, it may cause a hypersensitivity type inflammation and discomfort
which may lead to eye rubbing.45 Other possible complications include graft displacement, graft dehiscence,
and inability to hold tissue that is under tension. The immediate postoperative symptoms are similar to those
with sutures and include pain, photophobia, irritation, epiphora, local hyperemia but are less intense than
with some sutures.46 In all fairness, the intensity of most of these symptoms may be due to the inherent nature
of the surgical procedure, and not to the glue itself. Most grafts are done on large, advanced lesions which
may result in a longer and more difficult healing period, hence a higher tendency for the graft to dislodge. The
procedure requires the use of steroids, sometimes prolonged, with the possibility of delayed healing, increased
intraocular eye pressures and secondary infections. It may have a higher recurrence rate in some studies (12%
vs 7.7%) than with graft and sutures.47 In one study, the recurrence rate was lower with fibrin glue (5%) than
with sutures10 when autografts were used.48 Improvements in the product and better availability are needed.
Surgical contact lenses applied postoperatively are larger in diameter than normal (17 to 19 mm) and have
custom curvatures for normal tear film circulation so they can be worn for two to three weeks at a time. The
cornea heals faster, there is less inflammation and the recurrence rate of pterygium is reduced.49
In an unpublished study, anecortave acetate showed great promise in the inhibition of neovascularization
after surgery on previously recurrent lesions. Its safety and efficacy ratings were very high using topical
drops. The use of topical bevacizumab, formerly known as anti-VEGF, to interfere with the growth of new
vessels in the subconjunctival and corneal tissue can be considered for postoperative use as well.50
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40. Pflugfelder SC. Surgical Wound Healing. A look at the basics. Refractive Eye Care for Ophthalmologists. Issues in Ocular
Infection. Ethics Communication, inc Mar 2004.
41. Netto, et al. Wound Healing in the Cornea: a review of refractive surgery complications and new prospects for therapy.
Cornea 2005;24(5):509-22.
42. Marticorena J, et al. Pterygium surgery: conjunctival autograft using fibrin adhesive. Cornea 2006;25(1):34-6.
Surgery 79
43. Koranyi G, Seregard S, Kopp ED. Cut and paste: a no suture, small incision approach to pterygium surgery. Br J Ophthalmol.
2004;88(7):911-4.
44. Uy HS, et al. Comparison of fibrin glue and sutures for attaching conjunctival autografts after pterygium excision.
Ophthalmology 2005;112(4):667-71.
45. Srinivasan S, Slomovic AR. Eye rubbing causing conjunctival graft dehiscence following pterygium surgery with fibrin glue.
Eye 2007;21(6):865-7.
46. Bahar I, et al. Fibrin glue versus vicryl sutures for primary conjunctival closure in pterygium surgery: long-term results. Curr
Eye Res 2007;32(5):399-405.
47. Khierkhah A, Casa V, Sheha H, Raju VK, Tseng SC. Role of conjunctival inflammation in surgical outcome after amniotic
membrane transplantation with or without fibrin glue for pterygium. Cornea 2000;27(1):56-63.
48. Jiang J, et al. Comparison of fibrin sealant and sutures for conjunctival autograft fixation in petrygium surgery: one year
follow-up. Ophthalmologica 2008;222(2):105-11.
49. Arenas E, Garcia S. A scleral soft contact lens designed for the postoperative management of pterygium surgery. Eye Contact
Lens 2007;33(1):9-12.
50. IIiev ME, et al. Intravitreal bevacizumab (Avastin) in the treatment of neovascular glaucoma. Am J Ophthalmol 2006;
142(6):1054-6.
Complications
Preoperative complications arise in part from inadequate attention to risk factors and poor preoperative care.
This is a case that is potentially troublesome: the individual is in poor health, has fair to red pigmented skin, a
history of prolonged intense exposure to UV radiation, dry eyes, a pterygium that is inflamed or is positioned
at the lateral aspect or other unusual presentation, or is a recurrence. Recognition of the risk factors for recurrence
is essential for a successful outcome. Reduction of inflammation is the most important step before surgery,
followed by prevention of inflammation postoperatively. Preoperative instructions and postoperative follow
up must be clarified and adhered to strictly. Many complications can be avoided or repaired with patient
cooperation and timely follow up exams. The most feared complication is recurrence. Figure 7.1 is an eye with
a recurrent pterygium, which is at high risk for further recurrence after a re-operation.
Intraoperative complications begin with the anesthesia. A deep scleral injection may lead to globe penetration
and serous retinal fluid leakage. A superficial subconjunctival injection near the limbus and with the tip of the
needle always in view is the safest method of administering anesthesia for pterygium. Figure 7.2 shows the
case of an eye in which the incision was made too deeply into the cornea. Incision directly into the head may
start too deeply and damage vital corneal tissue. This may lead to delayed healing, and result in dellen formation
which leads to prolonged inflammation and increases the chances of recurrence (The initial incision should be
Figure 7.1: Stage IV vascular inflamed high risk

recurrence
Figure 7.2: Surgical ulceration of the cornea sets

up a nidus for inflammation
Complications 83
into the body). Excess cautery may cause excess postoperative pain and focal ulcerations which lead to areas
of scleral thinning which may become nidi for inflammatory cells. Removing too much Tenons capsule or
disturbing the muscle sheath indicates that the dissection is too far posterior and may result in reactive
inflammation. Injured or disrupted subconjunctival tissues usually respond with an overproduction of errant
fibroblasts and neovascular proliferation. Excess hemorrhage as in Figure 7.3, leads to delayed healing which
also results in persistent inflammation (It should be noted that a favorite locale for initial recurrence is at the
site of a persistent hemorrhage). Over dosage with adjunctive therapy may also contribute to serious
postoperative complications.1 Leaving too much bare sclera is a complication in that it serves as a stimulus for
the sequellae that lead to inflammatory recurrence. The placement of irregular or an over abundance of sutures
can also lead to inflammation.
Acute inflammation in response to excessive surgical trauma and resulting hemorrhage is manifested by
grossly dilated blood vessels with changes in permeability which leads to fluid and cellular exudates throughout
the excision site. Inflammatory cells move in and the risk and sequence for recurrence is increased. The cell
membranes release phospholipids which produce arachidonic acid. This product takes two pathways, one to
leukotrienes and the other to prostaglandins. Under the action of Cox-1 and 2 enzymes, both proinflammatory
and protective prostaglandins are formed. The former result in increased vascular permeability, disruption of
the healing process and pain.
Postoperative complications begin with the initial symptoms of pain and inflammation. Potent oral
painkillers may cause blood thinning which may result in further local hemorrhaging at the site. They should
be given with care. Try cold compresses and increased hydration both topically and systemically. A mixture of
0.5% Tetracaine diluted to 50% in tears used for a few days only should provide some relief. High doses of
topical steroids will reduce inflammation but should be carefully monitored due to their possible detrimental
effect on initial wound healing and propensity to cause increased intraocular pressure and secondary infections.
NSAIDs block both Cox-1 and Cox-2 enzymes and suppress prostaglandin formation. Their effect on wound
healing is less than that of steroids and their use in acute inflammation would be more appropriate in pterygium
Figure 7.3: Intraoperative hemorrhage and

inflammation in an autograft
surgery. Loteprednol and cyclosporine are also effective and have lower side effects. The appearance of
purulence prompts the immediate use of antibiotics.2
Some complications may be associated with suppression of the immune system and delayed wound healing
and may be directly related to recurrence:
Persistent hyperemia and pain past the first ten days of healing can be treated with the addition or
continuation of low dose steroids, especially after the cornea is healed. This is usually associated with high
risk preoperative signs or intra operative excesses. Figure 7.4 shows an eye with well positioned, healing
conjunctival flaps and abnormal redness at 3 weeks. The hemorrhages inferiorly may be nidi for recurrence at
the limbus.
Figure 7.5 shows hyperemia somewhat reduced but still in the active phase. This eye had a large lesion as
seen by the extensive corneal scar.
Dellen may result from extensive corneal dissection and/or excessive cautery. Its presence increases the
risk of recurrence since the subconjunctival tissues will release inflammatory factors toward the defective
area.3 Its presence may also affect the corneal curvature and result in significant postoperative astigmatism.
Figure 7.4: Intense hyperemia at three weeks

postoperative
Figure 7.5: Persistent hyperemia at 6 weeks

Complications 85
Treatment should be directed toward restoring the corneal surface. Initial patching may be followed by tear
film substitutes and possible topical cyclosporine. Oral vitamin C and zinc may contribute to wound healing.
Amniotic tissue grafting may be considered to stimulate epithelial growth into the defect. Figures 7.6 and 7.7
shows poor corneal healing leading to dellen and high risk for recurrence at the site.
The resolution of traumatic dellen may depend on the depth of the insult. Injury at the stromal level usually
results in permanent scarring. Figure 7.8 shows dellen within a corneal scar in the outlined bed of a previous
pterygium. Figure 7.9 shows the hypertrophic scar tissue of a healed dellen over a long period of time. Both
had been treated conservatively with topical medications.
Graft slippage and wound dehiscence are risk factors for impending failure. The newly placed tissue requires
a sufficient blood supply in order to survive and grow. A sclera that is devoid of all blood vessels due to
overuse of cautery and/or adjunctive therapy will often not support the adhesion of new tissue. Insufficient
or incorrect suturing and absorbable sutures that dissolve too soon can lead to graft slippage and flap dehiscence.
The wound then converts to bare sclera which is a high risk factor for recurrence. If the slippage leaves a gap
of or if the flaps are wider than 2 mm, then simple re-suturing will restore the essential coverage of the sclera
as in Figure 7.10.
If the flaps are less than 2 mm apart at the time of suture removal (2 weeks) such as in Figure 7.11A, then the
open area of the wound will generally granulate in without adverse sequel (Figure 7.11B) and can be observed.
Figure 7.6: Poor corneal healing at 1 week
Figure 7.7: Bilateral dellen at 2 weeks

Figure 7.8; Classic dellen scar at 6 months
Figure 7.9: Postoperative dellen after 10 years
Figure 7.10: Flap dehiscence of more than 3 mm

at 2 weeks postoperative (sutures retained)
Complications 87
Figure 7.11A: Wound dehiscence of 2 mm at

two weeks
Figure 7.11B: Same eye at 6 weeks
Larger gaps with graft or flap tissue already adherent to the sclera should be covered with a free graft or
amniotic membrane graft as soon as possible.
Bare sclera is a major cause of postoperative complications and has a similar pathogenesis and adverse
results as graft failure and wound dehiscense (Figure 7.12). It leaves too much area to be re-epithelialized and
serves as a stimulus for inflammation and delayed healing. Recurrence rates for bare sclera surgical technique
range from 30 to 50%. The surface that remains exposed has a rough, uneven exterior, which leads to the
release of inflammatory cells, which stimulate the proliferation of aberrant fibroblasts and results in abnormally
active scar tissue. The addition of adjunctive therapy reduces the rate somewhat but it is still too high.
Scleral necrosis or scleral melt can result from several causes, the most common of which is excessive adjunctive
therapy, i.e. Beta irradiation that is too strong (more than 6000 rads) and too frequent and mitomycin-C at a
strength of more than 0.4 mg/ml or a dose of more than 0.1 cc. or when applied as multiple drops over a
period of weeks on to a bare sclera. It occurs early with mitomycin-C and later with beta radiation1,4 (Figure
7.13).
Figure 7.12: Flap dehiscence at 3 weeks

becomes bare sclera
Figure 7.13: Scleral necrosis 5 years after β

radiation
Conjunctival epithelium will not adhere to a completely avascular sclera. Hence, excessive cautery and
adjunctive therapies that cause a thinning of the sclera will usually not heal properly. Acute necrosis in which
the sclera appears as white and edematous can also occur from too much excision of tissue and overuse of
cautery. It appears usually in the first week. Scleral melt like in Figure 7.14A, appears at 2 to 3 weeks in the
postoperative period. The initial treatment in this case of scleral melt was done with topical aloe vera drops
(gel diluted to 50% with bacteriostatic water) to promote healing, artificial tears with high methylcellulose
content to reduce mechanical irritation and oral Vitamin A, C and E (10,000 IU, 1000 mg, and 400 IU) combination
for healing. Figure 7.14B shows complete healing within three weeks of treatment. If there is insufficient
response, then a free graft or amniotic membrane graft is indicated to cover the defect and preserve the globe.5,6
The risk of scleral melt is greatly reduced when the strength of mytomycin-C is less than 0.1 cc of 0.04% and a
single intraoperative dose is used.
In a sensitive eye without recurrence, the best dose is 0.05 cc at 0.02%.
Practical surgeons and skeptics are still waiting for the long-term results of the use of mitomycin-C due to
its purported radiomimetic effects.7
Complications 89
Figure 7.14A: Scleral melt after use of

mitomycin-C drops
Figure 7.14B: Same eye healed after topical

treatment for 3 weeks
Figure 7.15 shows a case of scleral necrosis which appeared at about one year after the application of 8000
rads to the bare scleral surface following removal of a large primary pterygium.
Figure 7.15A shows a case of a large scleral melt after the removal of a primary pterygium and use of
mitomycin-C drops of unknown dosage and for 3 weeks.
The patient complained of swollen lids, a painful eye, excess tearing and blurred vision. Topical artificial
tears and aloe vera drops worsened the symptoms. An amniotic membrane graft (without mitomycin-C) gave
good results (Figure 7.15B).
Granuloma formation is associated with retained foreign body, usually cotton fibers from the applicators or
silk from a suture. Many of the granulomas I have encountered were associated with the concomitant overuse
of topical steroids (Figure 7.16). How much this may have lead to a delay or interference in the healing process
sufficient to promote the formation of granuloma remains to be investigated. If the granuloma persists and
interferes with the lid function or is cosmetically unacceptable, it can be removed by simple excision when
most if not all of the inflammation has subsided.
Symblepharon occurs in relation to the amount of loss of Tenon’s capsule or disruption of the muscle sheath
which when coupled with hypersensitivity issues, then leads to severe contracture of the palpebral conjunctiva
Figure 7.15 A: Scleral melt after mitomycin-C

drops
Figure 7.15 B: Same eye 6 weeks after amniotic

membrane graft
Figure 7.16: Granuloma at 3 weeks

postoperative
and shortening of the fornix. The resulting tissue is thick, fibrovascular and prone to high recurrence rate after
excision. The most effective treatments are large amniotic membrane grafting and conjunctival autograft, with
mitomycin-C and strict inflammation control.8
Complications 91
Figure 7.17A is the second recurrence for this 40 year old male athlete whose stereovision was severely
impaired by a large pterygium and restrictive symblepharon. His astigmatism was measured at 17 diopters
and his vision was barely 20/400. Despite his residence in the northern hemisphere, the pterygium was relentless
in its destruction of palpebral and bulbar conjunctiva and its advancement into the cornea. Conjunctival flaps
with 0.1 cc of 0.04% mitomycin-C were done in conjunction with limbal relaxing incisions. His visual acuity
improved to 20/25 on the first postoperative day. At 3 months, the cornea remained clear but the symblepharon
returned. The visual acuity regressed and at 6 months had returned to 20/200 with 4.5 diopters of astigmatism
(Figure 7.17B).
A fourth surgery with amniotic membrane graft tissue and mitomycin-C was done a year later. The visual
results were again encouraging but the symblepharon reformed after 2 months this time. The patient’s
inflammation profile was examined by FRAS testing for antioxidant levels and was found to be out of normal
range. He was started on a strict anti inflammation diet, avoiding omega-6 products and avoiding toxins and
pollutants like cigarette smoking and topical NSAIDs. After three months, his FRAS-3 levels were within the
normal range. A second amniotic graft (fifth surgery) was done using a larger graft anchored further into the
superior fornix than the previous one.
Figure 7.17A: Recurrent pterygium and

symblepharon (2nd surgery)
Figure 7.17B: Recurrent symblepharon (3rd

surgery)
Figures 7.17C and D shows that the results were acceptable. The symblepharon did not recur. The initial
vision gain regressed and remained at 20/70 with a residual astigmatism of 4.0 diopters that was reduced
with additional refractive surgery.
Postoperative astigmatism occurs when too much cornea has been removed and contracture of the stromal
fibers occurs during the healing process, which results in deep scar formation. Just to what extent and degree
pterygium surgery has on the corneal topography has been well studied.9-11 Corneal topography showing
pterygium induced astigmatism improves following pterygium surgery in the early period. The restoration of
normal patterns, however, does not occur until later in the postoperative period. In my own observations of
changes in astigmatism following surgical removal of the lesion, younger corneas resume a normal corneal
curvature sooner than older corneas.
Sixty (60) eyes with stage V pterygia and greater than 2.0 diopters of astigmatism were followed after
conjunctival flap surgery with mitomycin C with external photos, corneal topography, automated keratometry
and manifest refractions for one year. There were thirty-eight (38) males and eighteen (18) females, ranging in
age from 34 to 70 years old. The preoperative corrected visual acuities ranged from 20/20 to 20/400. There
Figure 7.17C: Amniotic membrane graft in place
Figure 7.17D: No symblepharon after second

amniotic graft
Complications 93
were forty-nine (49) primary and eleven (11) secondary pterygia. All measured 2 mm or more of advancement
into the cornea. In all patients with unilateral corneal pterygium, there was a greater than 2.0 diopteric difference
between the eyes. Preoperative topography revealed the expected with the rule astigmatism in most of the
younger patients and more bizarre patterns in the older patients, with incomplete scanning presumably due
to the opacification caused by the relative density and location of the pterygium head. The larger the pterygium,
the more distorted the scan. Though fifty-eight (58) eyes showed the characteristic with-the-rule pattern, there
were two cases of against the rule patterns which were apparently caused by the downward pulling action of
the pterygium head from an eccentric origin at the 4 o’clock meridian and orientation was more oblique than
horizontal. This adds credence to the theory of directional forces of exertion.
Figure 7.18A and B shows the corneal topography of a 34-year-old male in which the 3.5 diopter astigmatism
returned to normal over 6 months after pterygium surgery.
Figure 7.19A to C shows the corneal topography of a 62-year-old male in which the 3.0 diopter astigmatism
persists over 1 year after pterygium surgery.
Figure 7.18A: Preoperative astigmatism
Figure 7.18B: 6 months postoperative

Figure 7.19A: Preoperative astigmatism
Figure 7.19B: 8 months postoperative
Figure 7.19C: 1 year postoperative

Complications 95
Twenty-one eyes showed significant improvement (defined as better than 1.5 diopters) in refraction and
visual acuity as well as a visible shift in corneal topography toward the spherical. These changes were often
noted within the first 3 months postoperatively in 34.4% of cases; another eight (8) eyes improved after 6
months (13.3%); 5 improved after 9 months and twenty-two (22) showed no improvement at 1 year. 13 eyes
worsened at 3 months then improved and 3 eyes remained with a postoperative vision worse than before
surgery at 1 year. 10 eyes initially improved but then returned to the preoperative astigmatism level after 1
year. Table 7.1 shows the astigmatism variations after pterygium surgery.
Table 7.1: Visual acuity results of pterygium surgery patients
Total 60 eyes (unpublished data)
Postoperative Improvement Percent

> +1.5D
Astigmatism
3 months 21 eyes 34.4
6 months +8 eyes 48.3
9 months +5 eyes 56.6
12 months +1 eye 58.3
Improvement < +1.5D

Worsened >+1.5D
6 months 3 eyes 5.0
9 months 3 eyes 5.0
Significant changes in astigmatism occur up to one year following pterygium surgery. Corrective refractive
surgery can be done when the healing process has been completed. Older eyes are likely to have more permanent
changes in corneal curvature and less likely to show improvement following pterygium surgery. An
improvement in spherical shape of the corneal surface results when corneal stroma is released from forces
exerted by the pterygium. Surgical technique, depth of incision, degree of use of cautery, a smooth limbal area
with minimal scar tissue and the individual’s healing ability are all contributing factors. In some cases after
bare sclera technique or excision combined with mitomycin-C, the spherical power increases and the cornea
steepens. Surgery with the limbal-conjunctival autograft technique produced the least induced astigmatism.12
Since these changes appear to be dependent on age of the patient, size of the pterygium and inherent
elasticity of the cornea, it is recommended that further surgical correction be delayed until complete healing
has occurred. The indication and optimal time to perform corrective refractive surgery should be at least 1
year postoperatively in younger patients (< 50) as they exhibit positive changes and 6 to 9 months in older
patients as they exhibit less change. Corrective surgery with limbal relaxing incisions is the simplest procedure
and gives good results. Trapezoidal keratotomy may also be used.13
Recurrence
Recurrence after pterygium surgery is mainly due to a combination of persistent inflammation and abnormal
stress. Surgery is stressful. Stress leads to the release of cortisol and adrenalin hormones that in turn release
activation and inhibitory factors, which lead to inflammation. Inflammation is the fuel of a recurrence. The
worse case scenario is the 2 months postoperative patient with an active, symptomatic, vascular, inflamed
lesion sitting in the waiting room in obvious pain and complaining that it is “growing back”.
A recurrence may be defined as the postoperative growth of fibrovascular tissue 2mm or more onto the
clear cornea in the area of previous pterygium excision.14 It usually begins at the edge of the cut “subconjunctival”
layer nearest the limbus where there is bare sclera or damaged unhealed cornea. The recurrence tissue has a
blunt head and thick, fleshy, more fibrovascular body and is more aggressive in growth pattern than the
primary. It is usually tightly attached to the sclera and bleeds more easily and more profusely. It may be
superficially attached to the cornea and is lifted easily, like a pseudo-pterygium, or may be deeply embedded
into the corneal stroma. As it reaches the cornea and contracts, it usually pulls and displaces the semilunar
fold or likewise, causes a symblepharon.
Risk factors for recurrence are indicated by the presence and progression of inflammation as related to
repeated overexposure, individuals with red-fair complexion and a poor diet high in inflammation promoting
omega-6 fatty acids such as processed foods, the presence of Type I hypersensitivity factors in the blood,
excessive cautery associated with dellen, a disrupted Bowman’s membrane that acts as a lure for
neovascularization of the cornea, excessive tenonectomy, failure to restore the corneo-scleral junction barrier,
poor wound healing, overuse and overdose of adjunctive chemicals, persistent aqueous deficient dry eyes,
irritation due to absorbable or irregularly placed sutures or tissue glue, and bare sclera. Recurrence is not
genetic. Family members of a pterygium patient who reside in the Northern climes do not show the same
inclination to pterygium formation or recurrence.15
The usual time of recurrence is in the first month after surgery.16 Follow up visits should include this time
period. If the eye is quiet, the sclera is covered and there are no signs of recurrence, most likely it will not recur
thereafter barring any unforeseen incident or episode of intense exposure. The earliest sign of recurrence is the
appearance of a wisp of fibrovascular tissue at an unhealed area of cornea or limbal sclera in an inflamed eye.
A persistent hemorrhage in this area increases the chance that a recurrence is underway. When the flaps are
loose or retracted or a dehiscence has occurred or graft shows gap of more than 2mm, this is bare sclera and
the chances of recurrence is increased. This may be due in part to poor wound healing from a number of
factors (steroids, antibiotics, Type I hypersensitivity, repeat injury) or weakening of the wound due to premature
absorption of sutures.
The mechanisms of formation are related to the release of inflammatory mediators, which alter or destroy
the normal stromal keratocytes. Instead of the normal fibroblasts in the wound producing new collagen and
extracellular matrix, these abnormal myofibroblasts produce abnormal products, which prevent the adherence
of new epithelial cells to the wound site and lead to the formation of excess fibrovascular tissue, wound
contracture and aberrant healing. The process is marked by intense and prolonged inflammation. Figure 7.20A
to D show the sequence of a typical pterygium recurrence.
Prevention measures for recurrence are again directed at the control of inflammation.
Complications 97
Figure 7.20A: Onset of recurrence at 4 weeks
Figure 7.20B: Recurrence at 8 weeks
Figure 7.20C: Recurrence at 12 weeks
Preoperative reduction of inflammation with anti inflammatants and good hydration provides a quieter
eye for surgery. Good basic surgical technique in which less is better (less tissue removal with dissection and
less destruction with cautery) and sutures are placed in a comfortable line with tips trimmed or buried.17
Figure 7.20D: Recurrence at 1 year
Promotion of faster and more complete healing in surgery for recurrence can be done with conjunctival
flaps and its single wound and intact blood supply. Conjunctival autograft gives similar results especially if
the recurrence is small and old.18
The proper use of adjunctive therapy at the time of surgery significantly reduces the recurrence rate. The
basic common sense postoperative instructions of no rubbing of the eye and continued protection form exposure
and irritants should be followed. The promotion of healing with Vitamin C and other supplements and the
restoration of the aqueous tear film through topical and systemic hydration can help.
At the earliest sign of recurrence (after the initial wound healing process has been completed), NSAIDs and
topical steroids can be used to reduce the persistent inflammation and hopefully stem the progression.
Decongestants and tears should be increased as well. It is at this point that the new therapies such as anti-
VEGF drugs and anecortave acetate could be used to inhibit neovascularization.
The management of recurrence should begin with the acknowledgement of its presence and likelihood of
progression. Make sure that the informed consent contains a risk of recurrence and refer to it as needed. Do
not blame the surgeon (if it is a referral) or the patient. Recurrence is a natural result of the of pterygium
surgery. Maintain a positive attitude. There is good healing and less good healing. Strive for good healing.
Formulate a treatment plan together. Be realistic in what can be done by both the surgeon and the patient.
The goal of the treatment of an initial recurrence is first to suppress the fibrovascular process. If the cornea
is not healed properly, consider a bandage contact lens, vitamin C and E supplementation and aloe vera drops
to promote healing. If the sclera is bare, cover it. If the recurrence is well established, then plan the surgical
approach.
Conjunctival flaps with mitomycin-C is a good choice for first and small recurrences with ample normal
conjunctiva both superiorly and inferiorly. Amniotic membrane graft with mitomycin-C is good for second,
large, symblepharon and double headed recurrences. If not available and if no significant glaucoma is present
Complications 99
or anticipated, a conjunctival autograft with mitomycin-C is a good choice.19,20 If insufficient tissue is available
to cover the defect in any case, then a buccal mucosal graft can be done.
Treating with large doses of topical steroids in the immediate postoperative period may lead to impaired
healing response and possible rebound inflammatory response. Use the steroids for reduction of inflammation
preoperative, then sparingly in the postoperative period in order to control inflammation and promote
postoperative healing.
Recommended Technique for Recurrence Surgery (Surgeon’s Preference)
Incise the body of the pterygium at the limbus. Allow the bulk of the tissue to retract distally. Careful dissection
is in order as a recurrence is more likely to be tightly adhered to the sclera. Do not take too much tissue in the
dissection as this leaves a larger area to cover and prolongs the healing. Expect more hemorrhage than with a
primary. Moderate hemostasis can be accomplished with very light cautery taking care not to dent the sclera,
topical phenylephrine 2.5%, cold BSS and/or one to two drops of mitomycin-C. It will not harm an intact
sclera. Leave some small scleral blood vessels intact to encourage postoperative graft adherence but not heme,
which will be prohibitive. Avoid dehiscence or graft slippage by using short sutures for positioning and long
sutures for maintaining traction. Use a single dose of Mitomycin-C 0.1cc at 0.04% strength applied
intraoperatively to the underside of the graft and rinse after 5 minutes.
If conjunctival flaps or graft cover the sclera, remain in place at the time of suture removal and
inflammation is minimal, the risk of recurrence will be low.
Specific complications of amniotic membrane grafting include failure of reepithelialization and subsequent
sloughing; recurrence of the pterygium over the graft; hemorrhage under the graft (which would prevent
normal epithelialization as the graft needs contact with a partially vascularized sclera in order to survive); and
increased or abnormal scarring. Complications of mucosal grafting include postoperative pain (buccal and/or
excision site); graft necrosis and failure; recurrence; granuloma (about 10% of cases); persistent hyperemia
(past 1 month); and abnormal pigmentation of the graft.
Sample Cases
1. Double-headed second recurrence: Figures 7.21A to D show the eye of a 28 year old mentally challenged
fisherman’s helper, with extreme exposure, red-fair complexion, no eye protection, no topical medications,
poor diet, high soda and junk food intake, no alcohol, and history of episodes of intense rubbing. He had
bare sclera technique done to the left eye on two occasions. The last surgery was five years prior. The fellow
eye had the same presentation after one similar surgery. Visual acuity was barely 20/400 in either eye.
He used decongestants (0.012% Naphazoline), tears (Carboxymethyl cellulose 0.5%) and a topical steroid
(Dexamethasone 0.1% ) q.i.d. for ten days preoperative. Surgery was done with bilateral conjunctival flaps
and mitomycin-C. The initial incisions were made at the limbus and the flaps fashioned from the superior
and inferior “normal” conjunctiva which included the affected conjunctiva distal to it. With the flaps directed
vertically, the blood vessels and affected tissue was parallel to the limbus insteadof perpendicular to it. The
cornea was cleaned being extra careful not to go too deep. Due to the patient’s young age re-epithelialization
Figure 7.21A: Preoperative double-headed

inflamed recurrent pterygium
Figure 7.21B: Postoperative at 2 weeks
Figure 7.21C: Corneal healing at 6 weeks’

conjunctival migration in progress
was consistent and complete. Mitomycin C at a dosage of 0.1 cc of 0.04% was applied to the subconjunctiva
of each side and rinsed after five minutes. Postoperative care was with tears and decongestant q.i.d., and
cold compresses q4 hours on the first day postoperative. No steroids were used during the entire
postoperative period. There was initial concern over the wide (> 2 mm) space between the leading conjunctival
Complications 101
Figure 7.21D: Healing at 6 months
edge and the limbus. However, this granulated and re-epithelialized well due to good promotion of healing
without steroids. Visual acuity improved to 20/40. Postoperative instructions were followed and the patient
remained comfortable.
The gap is still present as “bare sclera”, but healthy conjunctival subepithelial cells have filled the space and
the inflammatory reaction is less. Healing appears to be going along well. The patient continues to do well
at ten years postoperatively. He is still using the decongestant in the mornings and the tears in the evenings.
He now wears a brimmed hat and UV400 protective lenses when outdoors. His BCVA improved to 20/25.
2. Multiple recurrences: Figure 7.22A to D is the eye of a 42 year old male, night security guard whose free
daytime is spent at the beach. He has had four surgeries for recurrent pterygium, which include bare sclera,
free graft, conjunctival flaps with mitomycin-C and amniotic membrane graft. He presents with the fourth
recurrence and a plea to do something successful for a change. His BCVA is 20/60. The anti- inflammatory
diet was started and topical prevention of inflammation measures were taken. He complied with all
instructions and made his follow up visits.
Figure 7.22A: 4th recurrence, 1 year after 4th

surgery, amniotic graft
Figure 7.22B: Two days after transposition, 5th

surgery
Figure 7.22C: 10 weeks after transposition
Figure 7.22D: Fibrous scar at 6 months after

surgery
Complications 103
A surgical transposition of the existing tissue was done by rotating the main pterygium head superiorly
and suturing it to the stationary conjunctiva with 10-0 nylon. This put it into a position parallel to the
limbus. A thin flap of normal conjunctival tissue was brought down and sutured to its proximal edge. No
tissue was removed. Mitomycin-C at dose of 0.1cc at 0.04% was injected under the conjunctiva and rinsed
after five minutes. A lot of prayers were said.
His vision improved. The inflammation subsided. There are no blood vessels in the cornea. This is a
happy patient.
3. Mega-pterygium with corneal penetration (2nd recurrence): Not all cases have perfect outcomes. Figure
7.23A and B shows the eye of an 80 year old lady who presented with a 33 history of pterygium problems.
The first surgery resulted in a recurrence in the first month. The second surgery was so painful that she
resisted seeking attention for the next 25 years.
She presented with a huge fibrovascular scar and severely impaired vision of finger counting due in
part to the presence of a significant cataract. The plan was for a large amniotic membrane graft with
mitomycin-C. The initial incision was made along the limbus and the bulk of the conjunctival scar tissue
was allowed to retract distally. The graft would be placed between it and the limbus. During the excision of
the head, the corneal scar tissue was found to occupy the full thickness of the cornea. To avoid imminent
Figure 7.23A: Stage V pterygium recurrence
Figure 7.23B: Quiet fibrous scar 1 year after 3rd

surgery
perforation, the plane of dissection was changed to the middle stroma. The graft was then sized to include
the fornices and half of the cornea to provide a template for re-epithelialization.
Healing was uneventful. While the visual acuity improved to 20/100, the patient opted to forego
further surgery. A corneal endothelial transplant would be considered.
4. Isolated lateral: Figure 7.24A and B shows the eye of a 34-year-old male with a history of trauma with a
stick to left eye 15 years prior. There was a bruise but he thought nothing of it and it cleared after “a while”.
The lesion appeared “a few months later” and grew on to the cornea within a year. No treatment was
undertaken at the time as he hoped it would go away. It became bothersome and symptomatic about 5
years ago. He exhibits high risk factors 4 out of 6, male, young, red-fair complexion (lightly pigmented eye),
and no eye protection. In addition, the presence of scar tissue would perhaps cause the lesion to behave like
a recurrence.
In the postoperative period as predicted, it took longer for the hyperemia to subside. This is perhaps
due to the nature of the injury and the fact that the lateral aspect of the bulbar conjunctiva is more exposed
to ultraviolet-B radiation, which could impede healing to some degree through persistent inflammation.
Figure 7.24A: Lateral pterygium only
Figure 7.24B: Same eye at 3 weeks

postoperative
Complications 105
Figure 7.25A: Stage V primary after

preoperative treatment
Figure 7.25B: Same eye 3 months postoperative
4. Figure 7.25A and B is the eye of a 60 year old male with a stage IV, primary, with mixed fibrovascular
activity and high risk with more than four risk factors. His vision is impaired due to the size and location of
the lesion. There was little or no induced astigmatism. The eye would have been pre-treated with the reduce
inflammation protocol and simple conjunctival flaps, autograft, amniotic membrane graft or mucosal graft
with mitomycin-C 0.1cc at 0.04% could have been done to give a successful outcome. A quiet preoperative
eye gives good postoperative results.
REFERENCES
1. Anduze AL, Burnett JM. Indications for and complications of mytomycin-C in pterygium surgery. Ophthalmic Surgery and
Lasers 1996;27(8):667-73.
2. Hsaio CH, et al. Intrascleral dissemination of infectious scleritis following pterygium excision. Br J Ophthalmol 1998;82:29-
34.
3. Starck T, Kenyon KR, Serrano F. Conjunctival autograft for primary and recurrent pterygia: surgical technique and probem
management. Cornea 1991;10(3):196-202.
4. Alsagoff Z, Tan DTH, Chee SP. Necrotising scleritis after bare sclera excision of pterygium. Br J Ophthalmol 2000; 84:1050-2.
5. Esquenazi S. Autogenous lamellar scleral graft in the treatment of scleral melting and corneal perforation in recalcitrant
infectious scleral and corneaoscleral ulcers Cornea 2002;21(3):275-83.
6. Ma DH, See LC, Hwang YS, Wang SF. Comparison of amniotic membrane graft alone or combined with intraoperative
mytomycin-C to prevent recurrence after excision of recurrent pterygium. Cornea 2005;24(2):141-50.
7. Ucakhan OO, Kanpolat A. Combined “symmetrical conjunctival flap transposition” and intraoperative low dose mitomycin-
C in the treatment of primary pterygium. Clin Experiment Ophthalmol 2006;34(3):219-25.
8. Shimazaki J, Shinozaki N, Tsubota K. Transplantation of amniotic membrane and limbal autograft for patients with recurrent
pterygium associated with symblepharon. Br J Ophthalmol 1998;82:235-40.
9. Cinal A, et al. The effect of pterygium surgery on corneal topography. Ophthalmic Surg and Lasers 2001;32(1).
10. Ozdemir M, Cinal A. Early and Late effects of pterygium surgery on corneal topograpography. Ophthalmic Surg Lasers
Imaging 2005;36(6):451-6.
11. Errais K, et al. Effect of pterygium surgery on corneal topography. Eur J Ophthalmol 2008;18(2):177-81.
12. Yilmaz S, Yuksel T, Maden A. Corneal topographic changes after four types of pterygium surgery. Refract Surg 2008;24(2):160-
5.
13. Ibrahim O, et al. Trapezoidal Keratotomy for correction of naturally occurring astigmatism. Arch Ophthal 1991;109:1374-81.
14. Gris O, et al. Limbal-Conjunctival Autograft transplantation for the treatment of Recurrent Pterygium. Ophthalmology
2000;107(2):270-3.
15. Frucht-Pery J. Proliferative activity and p53 expression in primary and recurrent pterygia. Ophthalmology 2001;108(5):985-
8.
16. Hirst LW, Sebban A, Chant D. Pterygium recurrence time. Ophthalmology 1994;101(4):755-8.
17. Akura J, et al. Measures for preventing recurrence after pterygium surgery. Cornea 2001;20(7):703-7.
18. Mutlu FM, et al. A comparative study of recurrent pterygium surgery: limbal conjunctival autograft transplantation versus
mitomycin-C with conjunctival flap. Ophthalmology 1999;106(4):817-21.
19. Shimizaki J, Kosaha K, Shimmura S, Tsuboto K. Amniotic membrane transplantation with conjunctival autograft for recurrent
pterygium. Ophthalmology 2003;110(1):119-24.
20. Solomon A, Pires RTF, Tseng SC. Amniotic membrane transplantation after extensive removal of primary and recurrent
pterygia. Ophthalmology 2001;108(3):449-59.
Appendix
SUGGESTED ANSWERS TO QUESTIONS IN CHAPTER ONE
1. Main causes of pterygium: Cumulative exposure to UV-B radiation, dehydration and chronic inflammation.
2. High risk for pterygium formation: Red-fair complexion, high exposure to UV radiation, young males
with outdoor hobbies or occupation, dehydration/dry eyes, pro-inflammation diet.
3. High incidence environment includes low lying islands with white sandy beaches, minimal cloud cover
and dry, dusty terrain.
4. Pingueculum becomes pterygium with the addition of persistent inflammation.
5. Prevention measures: Protection, hydration and inflammation control.
6. Indications for surgical excision are: Stage II for cosmetics and/or contact lens wear and stages III, IV and
V symptomatic; any lesion that touches the cornea should be removed.
7. Best technique depends on size, location, amount of inflammation present and above all, the surgeon’s
familiarity and comfort with the procedure.
8. Prevent recurrence through minimal tissue damage during surgery, the proper use of adjunctive therapy,
and good preoperative and postoperative care to reduce inflammation.
9. Gain patient confidence with proper preoperative reduction of inflammation, comfortable, complete
anesthesia, proper technique and good postoperative care.
10. The most important factor in preventing recurrence is inflammation control.
11. The basic pathology of pterygium is a combination of basophilic degeneration, collagenization and
inflammatory cells.
12. Mitomycin C is very toxic when used incorrectly. Proper use and efficacy has made it the most commonly
used adjunctive therapy in modern pterygium surgery. A single, intraoperative, subconjunctival, low dose
of 0.05cc of 0.02% to 0.1cc of 0.04% is deemed safe and effective. Long-term effects of more than 15 years
are yet to be determined.
13. Removal of a cosmetic pterygium is safe and practical.
14. Bare sclera is a nidus for intense inflammatory reaction, prolonged healing and high recurrence rate. It
should never be done even with adjunctive therapy. Always cover the sclera.
15. Main causes of postoperative inflammation are preoperative inflammation, bare sclera, dellen, excessive
cautery, dry eyes, irregular or absorbable sutures, poor health and continued exposure to irritants and UV
radiation.
16. Pterygium can cause up to 20 diopters of astigmatism through contracture of corneal stromal fibers and
extreme warping. It can be treated with refractive surgery a year after removal in young patients and a
few months after in older patients due to differences in healing patterns.
17. Use adjunctive therapy intraoperatively, single dose and when indicated by the stage and severity of the
pterygium.
18. Use conjunctival flaps with mitomycin C for small or first time recurrences, amniotic membrane graft for
large or multiple recurrences, conjunctival autograft for older patients with large recurrences and no
indications of glaucoma needing filtration, and mucosal graft if neither of the above are available.
Appendix 109
19. Vision threatening complications of pterygium surgery include globe perforation from anesthesia
administration or excess dissection, overuse of β-radiation in dose and frequency, and over use of mitomycin-
C as multiple drops on a bare sclera or high doses over 0.1cc and 0.05%.
20. Blame no one for a recurrence, especially not the patient. There are behavioral factors that contribute to
recurrence but most occur as part of the natural healing or non-healing process.
SUGGESTED HIGHLIGHTS AND RECOMMENDATIONS

Risk Factors for Pterygium (Primary)
1. Male gender (occupational)

2. Age < 40
3. Exposure to UV radiation (cumulative)
4. No protective eyewear
5. Red-fair complexion
6. Adverse lifestyle (chronic dehydration, irritants)
Figure A.1: Classic pterygium
Suggested Pterygium Prevention Plan
1. UV-B protection: UV400 protective sunglasses, with gray-green tint for the tropics; brimmed hat; visor;
umbrella; avoid peak sun exposure 10 a.m. to 2 p.m; avoid mechanical and chemical irritants.
2. Hydration: Topical tears, drink water 6-8 glasses daily; decrease alcohol intake; increase blinking; punctum
plugs; cyclosporine drops.
3. Inflammation control: Topical phosphate steroids, NSAIDs (use short term for acute hyperemia);
Fluorometholone drops for longer term: Decongestants (0.012% Naphazoline and cold eyewash) daily
(prevent congestion). Systemic anti-inflammatory diet of omega-3 fatty acids, vitamin C, turmeric, ginger,
flaxseed oil. Avoid pro-inflammatory omega-6 trans fats, saturated fats, partially hydrogenated fats (junk
food).
Suggested Preoperative Care

Reduce Inflammation
1. Decongestants and tears b.i.d.

2. Cyclosporine or dexamethasone phos.0.1% or loteprednol q.i.d. for 5 - 7 days, then use preventive immune
enhancers.
4. Sunglasses with UV 400 gray tint.
5. Hydration (water 6 - 8 glasses daily).
Prevent Inflammation
1. Decongestants and tears b.i.d.

2. Omega-3 fish oil capsules 1000 mg, and Vitamin C 500 mg, b.i.d. for four weeks stop all junk food.
3. Sunglasses UV400 gray tint.
4. Hydration (6 - 8 glasses water daily).
Anti-inflammation Diet
1. Omega-3 fish oil (whole food and supplements) 1000 mg daily.

2. Flaxseed (fresh and or oil) 500 - 1000 mg daily.
3. Antioxidants (vegetables and fruits, berries; or supplements).
4. Olive oil (extra-virgin) daily.
5. Ginger 500 mg (fresh added to food or supplements).
6. Turmeric 500 mg (powder or supplements).
7. Vitamin C 500 - 1000 mg (fresh citrus or supplements).
Optional
1. Echinacea 450 mg (extract or supplements)
2. Green tea
3. Garlic
4. Boswellia
5. Cat’s claw
6. Devil’s claw
7. Cayenne
8. Evening primrose oil
9. Astragalus
10. Medical mushrooms (Maitake, Shiitake, Reischi)
11. Aspirin (low dose 81 mg).
Avoid or reduce intake of inflammation producing foods
1. Fried foods and dairy products
Appendix 111
2. Red meat
3. Yeast and white sugar
4. Excess alcohol and tobacco
5. Caffeine, peanuts, processed wheat (gluten)
6. Unsaturated vegetable oils.
Suggested Surgical Management for Clinical Stages
Stage I and II: No surgery; preventive medical treatment

Stage III, Ia: Conjunctival flaps with Mitomycin C
Stage III, Ib: Conjunctival flaps
Stage IV, Ia: Conjunctival flaps with Mitomycin C
Stage IV, Ib: Conjunctival flaps or autograft
Stage V, Ia: Conjunctival flaps with Mitomycin C or amniotic membrane graft
Stage V, Ib: Conjunctival flaps or amniotic membrane graft
Stage IV or V, IIa (First recurrence): Conjunctival flaps with Mitomycin C (second recurrence): amniotic
membrane graft with Mitomycin C (third recurrence): transposition with Mitomycin C or mucosal graft
Stage VI , Ib (Inactive fibrous scar): Conjunctival flaps, amniotic membrane graft, or mucosal graft
Primary Objectives of Pterygium Surgery
a. Reduce inflammation, then

b. Promote corneal healing, and
c. Tear film restoration, to get a
d. Clear quiet eye.
Figure A.2: Ideal postoperative healing

Surgical Pearls in Pterygium Management
a. Good preoperative preparation to reduce inflammation

b. Cover the sclera/do not use bare sclera
c. Use single intraoperative low dose mitomycin-C/ not drops
d. Use appropriate technique for type of pterygium
e. Do not use excessive cautery
f. Do not disturb the muscle sheath
g. Good postoperative care to prevent inflammation
h. Good anesthesia
i. Mitomycin-C dosage: 0.05cc of 0.02% to 0.1cc of 0.04%
j. 9-0 or 10-0 non-absorbable suture
k. Tissue glue for conjunctival autograft.
Comparison of Common Techniques
Conjunctival flaps vs Conjunctival autograft vs Amniotic membrane graft
Feature: Same blood supply needs new blood supply needs new blood supply
same tissue attached needs new tissue needs new tissue
Ease: Very easy technically difficult technically difficult
Time: 20 - 25 minutes 45 - 60 minutes 30 - 45 minutes
Physical: Single wound two wounds single wound

little tissue damage most tissue removed medium tissue removed
Closure: Few sutures many sutures required many sutures

no tissue glue possible tissue glue possible tissue glue
Healing time: 2 - 4 weeks 6 - 8 weeks 8 - 10 weeks
Cosmesis: Excellent fair fair
Cost: Low low high
Tissue: Attached availability of graft tissue regional availability
Limits: Size of lesion availability of tissue availability of tissue
Indications: Primary primary more versatile, recurrence
first recurrence first recurrence and all epithelial defects

Appendix 113
Pocket Guide to Conjunctival Flaps in Pterygium Surgery
Figure A.3
Suggested Recommended Dosages of Mitomycin C
For small primaries, 0.05 cc of 0.02 mg/ml

low inflammation (0.02%).
For large primaries, 0.05 cc of 0.04 mg/

small recurrences, and ml(0.04%).
medium inflammation
For multiple and 0.1 cc of 0.04 mg/ml

large recurrences, and (0.04%)
high inflammation
Postoperative Instructions for the Pterygium Surgery Patient
Sleep for at least 8 hours, eyes closed (oral medications prn) patch removal in the morning apply topical
decongestants and tears q.i.d. cold compresses to lids as needed vitamin C supplements (citrus, immune
boosters, oatmeal, etc.) suture removal in 14 days.
Risk Factors for Pterygium (Recurrence)
High Low
1. Previous pterygium surgery Primary pterygium surgery

2. Fibrovascular, class Ia Degenerative, class Ib
3. Broad base, blunt head Dark complexion
4. Type I hypersensitivity Narrow base, pointed head
5. Fair-red complexion Indoor activity
6. Outdoor activity
7. Dry eyes/ dehydration
8. Bare sclera technique
9. Dellen, surgical injury
10. Poor general health
11. Age group <50
Common Complications in Pterygium Surgery
Persistent hyperemia Scleral necrosis

Dellen Granuloma
Wound dehiscence Symblepharon
Graft slippage Astigmatism
Bare sclera Recurrence
Average Rates of Recurrence of Pterygium
Surgery Recurrence rate
Conjunctival flaps 1-3%

Auto or free graft 5-15%
Amniotic membrane graft (primary) 5-8%
Amniotic membrane graft (recurrent) 15-25%
Mucosal graft 20-30%
Appendix 115
Figure A.4: 15 years after pterygium surgery with mitomycin-C
Innovations and Controversies
1. Preoperative reduction of inflammation

2. Intra operative excision of less tissue
3. Postoperative promotion of healing without steroids
4. Use of diet and supplements to promote healing
5. Leaving low dose mitomycin-C on subconjunctiva without rinsing
6. Use of tissue adhesives and wound healing.
Index
A Dry spots 5 Phlyctenule 9

Dry spots on fluorescein stain 16 Pingueculum 2, 7, 13, 16
Astigmatism 6
Pre-pterygium 16
F Proliferative pterygium 24
B Pseudopterygium 7
Foreign body 8
Barbados eye study 14 Pterygium 2, 16, 12, 38
Basophilic degeneration 33 astigmatism 6
G
Blink interference 5 blink interference 5
Granuloma 8 causative factor 16
C cell destruction 17
I conjunctival hemangioma 8
Classification of pterygium 26
control of inflammation 42
Clinical staging of pterygium 28 Induced astigmatism 5, 31
corneal edema 17
Complications 82 Inflammatory lymphocytes 24
dermoid 9
astigmatism 92 Instruments for pterygium surgery 53
dietary supplement 43
bare sclera 87 Irregular astigmatism 7
differential diagnosis 7
dellen 85
effects of ultraviolet B 17
granuloma 89 L
hyperemia 84 environment 12
hypertrophic scar 85 Limbal catarrh 9 environmental pterygium 19
intraoperative complications 82 Limbal pterygium 30 foreign body 8
postoperative astigmatism 84 geographic location 12
postoperative complications 83 M granuloma 8
preoperative complications 82 induced astigmatism 5
Maintaining a healthy tear film 40
recurrence 91, 96 irregular astigmatism 7
scleral necrosis 87, 89 limbal catarrh 9
N
stage V pterygia 92 limbal stem cell destruction 19
symblepharon 89 New medical treatments 43 maintaining a healthy tear film 40
technique for recurrence surgery 99 New treatments 76 new medical treatments 43
wound dehiscense 87 Nodular episcleritis 9 nodular episcleritis 9
Conjunctival hemangioma 8 papilloma 8
Control of inflammation 42 phlyctenule 9
O
Corneal pterygium 31 pingueculum 7
Ocular effects associated with ultraviolet
prevention 38
radiation 22
D pseudopterygium 7
Ocular effects of ultraviolet radiation 22
squamous cell carcinoma 9
Degenerative changes of pterygium
formation 34 ultraviolet protection 38
P
Degenerative pterygium 24, 31 VEGF 43
Dermoid 9 Papilloma 8 visual disturbances 4, 20
Dietary supplement 43 Pathogenesis of a pterygium 20 with-the-rule astigmatism 6
S postoperative management 69 U
preoperative care 48
Squamous cell carcinoma 9 Ultraviolet protection 38
results 64
Surgery 48 V
techniques 54
adjunctive therapies 67
VEGF 43
instruments for pterygium
surgery 53
T W
new treatments 76 Travel set for Itinerant surgery 74 With-the-rule astigmatism 6

Pterygium - A Practical Guide To Management - 9788184487251

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A PRACTICAL GUIDE TO MANAGEMENT

JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD.

North America Office

First Edition: 2009

My colleagues and scholars who believe in good basic

James V Kasin MD Jean-Christophe Joyaux MD

For features of a corneal lesion and everything there is to John C Merritt MD

Of Barbados: First to use conjunctival flaps technique

Garth Taylor MD Hugh Vaughn MD

William Trattler MD The Ophthalmic Society of the West Indies (OSWI)

Chapter 1 Features ................................................................................................................................................ 1

Chapter 2 Epidemiology ................................................................................................................................... 11

Chapter 3 Pathogenesis ..................................................................................................................................... 15

Chapter 4 Pathology ........................................................................................................................................... 23

Chapter 5 Prevention ......................................................................................................................................... 37

Chapter 6 Surgery ............................................................................................................................................... 47

Chapter 7 Complications .................................................................................................................................. 81

Appendix ........................................................................................................................................... 107

Index .................................................................................................................................................. 117

Figure 1.1: Pterygium crossing the midline

Figure 1.2: Pterygium crossing arcus senilis

Figure 1.3: Inferior pterygium due

The Pingueculum and the Pterygium

Figure 1.4: Pterygium de novo

Figure 1.5: Pingueculum

Figure 1.6: Pterygium

Figure 1.7: Pingueculum in evolution to

Figure 1.8: Raised degenerative lesion may

Figure 1.9: Stage IV pterygium may cause blink

Figure 1.11A: Stage V pterygium with 3.0 D

Figure 1.11B: Corneal topography with irregular

Results from a corneal injury or ulceration at or near the limbus.

Figure 1.12: Conjunctival hemangioma

Figure 1.13: Foreign body

Squamous Cell Carcinoma

Figure 1.14: Squamous cell carcinoma

Geographic Location (Figure 2.1)

Figure 2.1: World distribution of pterygium

Figure 2.2: Pingueculum in a pigmented eye

Figure 2.3: Pterygium in a blue eye after 6 years’

Figure 3.1: Dry spots on fluorescein stain

Figure 3.2: Early tear film and ocular surface

Table 3.1*: The Electromagnetic Spectrum

Infrared C 10,000-3000 nm (retina RPE)

How does a Stage I Pingueculum become a Stage IV Pterygium?

Figure 3.3: Patient IH in 2004

Figure 3.4: Patient IH in 2007

Figure 3.5: Pingueculum in evolution

Figure 3.6: Pterygium in situ

Figure 3.7: Early inflammation in the

Figure 3.8: Advancing head of an inflamed

Figure 3.9: Active pterygium onto the cornea

Figure 3.10: Classic corneal pterygium

Table 3.2: Pathogenesis of Pterygium Pathway

Exposure to UV-B radiation + Altered Tear film

Table 3.3: Other Ocular Effects of Ultraviolet Radiation

Figure 4.1: Degenerative pterygium

Figure 4.2: Stromal collagenization

Figure 4.3: Proliferative pterygium

Figure 4.4: Inflammatory cells

Table 4.1: Classification of Pterygium

Primary active (Class Ia) (Figure 4.5)