3. 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
JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD.
St Louis (USA) • Panama City (Panama) • New Delhi • Ahmedabad • Bengaluru
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®
5. 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.
6.
7. 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
Foreword
8.
9. 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
Preface
10.
11. James V Kasin MD
Chapter four on Pathology, preparation and interpreta-
tion of histological sections (Australia and Virgin Islands).
Eduardo Alfonso MD
For features of a corneal lesion and everything there is to
know so far about external diseases.
(Miami, Florida)
Juan Batlle MD
For developing the Ambiodry technique and sharing his
knowledge of pterygium with others.
(Santo Domingo, Dominican Republic)
Alfonso Equiguieren MD
For his questioning mind and unquestioned loyalty. May
he rest in peace.
(Georgetown, Guyana)
Khalil Fakim MD
For the mucosal graft surgery protocol and complications.
(Mauritius)
Sam Jones (Artist)
Surgical Technique Illustrations
(St Croix, Virgin Islands)
Jean-Christophe Joyaux MD
For encouragement, support and the conjunctival
autograft technique and photos.
(Martinique and Bordeaux, France)
John C Merritt MD
For inspiration, motivation, unwavering support and
repeated reminders to get this work done.
(Clinton, North Carolina)
Basil Morgan MD
For continued interest and suggestions on VEGF research.
(Baltimore, MD)
Raymond Richer MD
For sharing conjunctival autograft cases and exposing the
positives and negatives of our various techniques.
(Fort-de-France, Martinique, France)
Cyril Reifer MD
Of Barbados: First to use conjunctival flaps technique
when it was the merest sclera and stick with it, with good
results. (Bridgetown, Barbados)
Michel Sickenberg MD
For the complicated cases and FRAS and anti-
inflammatory treatments prior to and after surgery.
(Lausanne, Switzerland)
Acknowledgments
12. Pterygium: A Practical Guide to Management
xii
Garth Taylor MD
For his solid support and incredible wisdom to see the
value of trying new techniques. We will never forget him.
(Toronto, Canada)
William Trattler MD
For trying the conjunctival flaps technique with
mitomycin C, realizing its value, expanding on it and
sharing his knowledge with others.
(Miami, Florida)
Sheffer Tseng MD, PhD
Genius of the ocular surface; for the amniotic membrane
graft technique and video and your timely advice with
complicated cases. (Miami, Florida)
Hugh Vaughn MD
For disagreeing (often) and offering alternative solutions
such as transposition and bare sclera with beta radiation.
(Kingston, Jamaica)
The Ophthalmic Society of the West Indies (OSWI)
…for providing a forum in which to discuss controversial
findings, and its members for being so resistant as to make
defining and refining the work a necessity.
(West Indies)
Doctors in Hungary, Tunisia, Libya, Egypt, the
Netherlands and Mexico, who showed enough interest
in the treatment of pterygium to share their views and
cases and provide a forum for discussion.
15. Most books and articles on pterygium focus on
outcomes. This practical guide identifies the features
of a particular case and the reasons for using a
particular method.
All of the management strategies are the surgeon’s
preference and are based on more than 30 years of
experience with large, active, tropical pterygia. The
repeated themes of protection from UV radiation,
inflammation control and restoration of tear film
refer to the elements of pathogenesis which have been
observed as leading directly to prevention and
successful medical and surgical management. Clinical
situations involving preoperative treatments, intra-
operative techniques and postoperative care are
derived from actual patient cases. By following the
basic principles and practices of good medicine, initial
growth and recurrence of pterygia can be prevented.
For the practitioners who see and do 4 or 5 cases a
year as well as those who do more than 100 cases, the
most effective approaches with the lowest acceptable
recurrence rate (<1%) will be highlighted. Recommen-
dations and suggestions are based on observed and
documented results of over 5000 pterygium cases
managed by the author.
For an excellent reference on historical and in-depth
perspectives, the textbook, Pterygium Surgery by Lucio
Burratto and associates is a comprehensive anthology
with excellent information and references and should
be used as such.
Most of the information, suggestions and deductive
findings in this manual are based on empirical data in
the forms of direct and indirect observation of results
as well as research studies and is to be used for clinical
interpretation and management of the individual case.
Much of the content is based on articles written over
the years by the author and others from regions in
which pterygium is prevalent. Some of the information
is anecdotal and will be designated as such. The ideas
and suggestions presented are based on logic and
experience. Some are controversial and may appear
to be circumstantial. This is a clinical, practical guide.
It is comprised of management strategies that work.
However, when the decision on management of a
particular case is made, the practitioner should do
what is the most appropriate and effective in his/her
hands.
I did my first pterygium operation in 1978, upon
my return to the Virgin Islands.
There was a backlog of cases, half of which were
recurrences done elsewhere. I used the bare sclera
technique which was merely suggested in the textbook
without any detailed management and was rewarded
with the customary 50% recurrence rate. On the timely,
advice from a doctor in Puerto Rico with more
experience than I, phenol 30% was tried as an adjunct.
It reduced the recurrence rate to about 20% but left
the eyes white with thin scleras and poor corneal
healing. From that time, prevention made more sense
Introduction
16. Pterygium: A Practical Guide to Management
xvi
than the endless repeated surgeries and dissatisfied
patients. Shortly after, my own pterygium had made
an appearance and was responding positively to low
dose decongestants and tear film replacement, a
regimen that I still use today.
The modified conjunctival flaps technique
developed out of common sense and successful
outcomes. If you cover the sclera, control inflammation
and restore the tear film, you remove the stimulus for
the pterygium to grow back. It works. The statements
and conclusions that appear in this manual that could
seem controversial or circumstantial are derived from
solid observations of improvement in structure and
function of the eye following appropriate pterygium
management.
Pertaining to the layout of the book, note that the
themes of Epidemiology and Pathogenesis are closely
related to Pathology. Understanding the pathology is
essential to the demonstration of behavior of the lesion
which determines its character. By identifying its
character, a classification and staging can be directly
applied to determine the most appropriate surgical
treatment.
A chapter on Prevention has been included in this
manual in response to the many statements in the
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
agreement of those surgeons doing the most cases in
the endemic regions. Newer techniques have been
included and indications for use specified accordingly.
The surgical correction of pterygium has always
commanded all the glory. Likewise, a recurrence
receives the shame and stigma of something done
incorrectly. The section on recurrence, how to prevent
it and how to fix it, is highlighted in Complications.
It includes explicit examples and how to avoid them
as well as how to fix them. In Clinical Correlations,
routine cases are provided so that the practitioner can
apply some of the techniques in management directly
to clinical practice. Unusual cases with successful
outcomes can be used to compare with your own.
Finally, Summary includes a wrap-up of highlights
and pearls.
During the early years of my experience with
pterygia, while on a celebratory trip to London,
I encounterd a set of ancient surgical eye instruments
in the Egyptian section of the British museum. These
instruments along with the alleged words of the 16th
Century French surgeon, Ambroise Paré, (in a different
section) pertaining to pterygium that “it always grows
back”… set me to thinking and trying and striving to
arrive at the perfect (or near perfect) solution to the
pterygium “problem”.
Surgical eye instruments: British museum of
Egyptian artifacts, c. BCE 1000
17. Introduction xvii
The ultimate purpose of this work is to stimulate
interest in pterygium research and publication of
journal articles particularly from practitioners and
scholars in areas of the tropics where it is endemic.
Better methods of prevention should be investigated
and more convenient and effective techniques of
handling difficult cases should be established.
Moreover, those who are presented with challenging
cases should consult with those who have been there
and are willing to share the experience.
In following some of the suggestions included in
this guide, it is my sincere conviction that your
outcomes will be successful.
Second Disclaimer
The author has no financial interest in any of the
products mentioned in this book.
“When you see multiple viewpoints, you are less attached
to your own.”
Questions Most Often Posed by Visiting
Ophthalmologists
1. What is the pathogenesis of a pterygium?
2. Which eyes are most susceptible to pterygium
formation?
3. Which environment has the highest incidence of
pterygium?
4. How does a pingueculum become a pterygium?
5. What can I do to prevent a pterygium from
growing?
6. What are the indications for pterygium surgery
and when can it be left alone?
7. What is the best technique for a specific type of
pterygium?
8. What is the best way to do surgery to prevent
recurrence?
9. What is the best way to gain patient confidence,
ensure the most comfort and get the best results?
10. What is the most important factor in preventing
complications?
11. What is the basic pathology of the average
pterygium?
12. Is mitomycin C as bad as the early articles
portrayed? What is the most effective and safest
dose?
13. Is cosmetic pterygium surgery practical?
14. Why should bare sclera never be done?
15. What are the main causes of postoperative
inflammation and how do I avoid them?
16. How much astigmatism does pterygium cause and
how do I treat it?
17. When do you use adjunctive therapy?
18. What are the causes of recurrence and how do you
prevent them?
19. What are some of the vision threatening
complications of pterygium surgery?
20. Who is to blame when there is a recurrence?
19. 2 Pterygium: A Practical Guide to Management
Figure 1.2: Pterygium crossing arcus senilis
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
20. 3
Features
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 1.3: Inferior pterygium due
to chemical burn
Figure 1.4: Pterygium de novo
21. 4 Pterygium: A Practical Guide to Management
Figure 1.6: Pterygium
Figure 1.5: Pingueculum
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
22. 5
Features
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 1.7: Pingueculum in evolution to
pterygium
Figure 1.8: Raised degenerative lesion may
cause blink interference
23. 6 Pterygium: A Practical Guide to Management
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 1.9: Stage IV pterygium may cause blink
interference with pupil interference
Figure 1.10A: Stage V pterygium with 3.5 D
cylinder in a 30-year-old male
Figure 1.10B: Corneal topography with
induced astigmatism
24. 7
Features
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.
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
25. 8 Pterygium: A Practical Guide to Management
Figure 1.12: Conjunctival hemangioma
Figure 1.13: Foreign body
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.
26. 9
Features
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.
29. 12 Pterygium: A Practical Guide to Management
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)
30. 13
Epidemiology
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
31. 14 Pterygium: A Practical Guide to Management
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.
33. 16 Pterygium: A Practical Guide to Management
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.
34. 17
Pathogenesis
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 3.2: Early tear film and ocular surface
changes
35. 18 Pterygium: A Practical Guide to Management
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
Figure 3.3: Patient IH in 2004
Figure 3.4: Patient IH in 2007
36. 19
Pathogenesis
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 3.5: Pingueculum in evolution
Figure 3.6: Pterygium in situ
37. 20 Pterygium: A Practical Guide to Management
Figure 3.7: Early inflammation in the
subconjunctiva
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.
Figure 3.8: Advancing head of an inflamed
lesion
38. 21
Pathogenesis
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
↓
↓
↓ ↓
↓
↓
↓
↓
↓
↓
↓
39. 22 Pterygium: A Practical Guide to Management
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.
41. 24 Pterygium: A Practical Guide to Management
Figure 4.1: Degenerative pterygium
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.
43. 26 Pterygium: A Practical Guide to Management
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
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
Figure 4.5: Active vascular primary Class Ia
45. 28 Pterygium: A Practical Guide to Management
Figure 4.9: Stage I exposure conjunctivitis
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.
46. 29
Pathology
Figure 4.10: Stage II conjunctival pterygium
Figure 4.11: Stage III limbal pterygium
Figure 4.12: Stage IV corneal pterygium
47. 30 Pterygium: A Practical Guide to Management
Figure 4.13: Stage V compound pterygium
Figure 4.14A: Active limbal stage III Class Ia
Figure 4.14B: Inflammatory cells and collagen
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.
48. 31
Pathology
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
49. 32 Pterygium: A Practical Guide to Management
Figure 4.16B: Lymphocytes and fibroblasts
Figure 4.17A: Degenerative pterygium Stage IV,
Class Ib
Figure 4.16A: Degenerative and proliferative
pterygium
50. 33
Pathology
Figure 4.17B: Less cells, more collagen
Figure 4.18A: Stage V, class IIa fibrovascular
recurrence
Figure 4.18B: Basophilic degeneration
51. 34 Pterygium: A Practical Guide to Management
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
52. 35
Pathology
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.
54. 38 Pterygium: A Practical Guide to Management
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
55. 39
Prevention
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
56. 40 Pterygium: A Practical Guide to Management
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 5.3B: One month after sunglass wear
Figure 5.4: UV-B radiation and glare
57. 41
Prevention
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 5.5: UV400 tinted sunglasses
Figure 5.6A: Before tear film restoration
58. 42 Pterygium: A Practical Guide to Management
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
59. 43
Prevention
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 5.7B: One month after topical with
steroids treatment
60. 44 Pterygium: A Practical Guide to Management
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 5.8: Inflamed preoperative eye
Figure 5.9: Quiet preoperative eye
61. 45
Prevention
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.
63. 48 Pterygium: A Practical Guide to Management
Figure 6.1A: Stage II raised mixed
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
64. 49
Surgery
Figure 6.1B: Heavily pigmented stage II
pterygium pinguculum-nevus with fibrous
components
Figure 6.2A: Inflamed stage II
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).
65. 50 Pterygium: A Practical Guide to Management
Figure 6.2B: Inflamed stage III
Figure 6.3A: Degenerative stage IV
Figure 6.3B: Stage IV “preoperative” pterygium
66. 51
Surgery
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.
67. 52 Pterygium: A Practical Guide to Management
Figure 6.4B: Stage V pterygium with obstructed
pupil
Figure 6.5A: Double-headed pterygium
fibrovascular
Figure 6.4A: Stage V pterygium with induced
astigmatism
68. 53
Surgery
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
Figure 6.5B: Double-headed pterygium
degenerative
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
69. 54 Pterygium: A Practical Guide to Management
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
70. 55
Surgery
Figures 6.6A and B: Initial incision into the body
of a primary stage IV pterygium
Figures 6.7A and B: Excision of the head
A
B
A B
71. 56 Pterygium: A Practical Guide to Management
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.
A
B
72. 57
Surgery
Figure 6.9A: Initial closure at the limbus
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 6.9B: Initial closure at the canthus
73. 58 Pterygium: A Practical Guide to Management
Figure 6.10A: Completed closure
Figure 6.10B: Long and short sutures
Figures 6.11A and B: Subconjunctival mitomycin C application
A B
74. 59
Surgery
Figure 6.12: Initial incision into the head
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.
75. 60 Pterygium: A Practical Guide to Management
Figure 6.14: Harvesting the free graft from the
superior aspect of the conjunctiva
Figure 6.13: Excision of the head
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
76. 61
Surgery
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.
77. 62 Pterygium: A Practical Guide to Management
Figure 6.17: Third recurrence with medial
symblepharon
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.
Figure 6.18: Amniotic membrane graft sutured in
place
78. 63
Surgery
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.
